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Table Of Contents:
What’s included: Ready-to-study anatomy, physiology and pathology notes of the nervous
system & special senses presented in succinct, intuitive and richly illustrated downloadable PDF
documents. Once downloaded, you may choose to either print and bind them, or make
annotations digitally on your iPad or tablet PC.

Free Bonus: ‘Neurology’, ‘Neurosurgery & ‘Ophthalmology’ chapters of Toronto Notes for
reference and further detailed reading.

File List:
• Development & Organisation of the Nervous System
• The Nervous System In Detail
• Blood Vessels of the Brain
• Neurotransmission
• Memory
• Neurobiology of Emotions
• Somatosensory Processing
• Motor Processing
• The Peripheral Nervous System
• Cranial Nerves & Their Pathways
• Special Senses; Vision, Taste, Smell, Hearing & Equilibrium
• Pain & Nociception
• Important Clinical Neurological Things
• Brain Tumours
• Central Nervous System Infections
• Dementias
• Ear Pathology
• Epilepsy
• Equilibrium Disorders
• Guillian-Barre Syndrome
• Hearing Disorders
• Herpetic Neuralgia (Shingles)
• Huntingtons Disease
• Intracranial Haemorrhages
• Ischaemic Encephalopathy
• Motor Neurone Diseases & Polio
• Multiple Sclerosis & Leukodystrophies
• Myaesthenia Gravis
• Neurosyphilis
• Overview of Disorders of the Special Senses
• Parkinsons Disease
• Peripheral Neuropathies
• Prion Diseases
• Raised Intracranial Pressure
• Spinal Cord Syndromes
• Strokes
• Traumatic Brain Injuries
• Vision Disorders
• TORONTO - Neurology & Neurosurgery
• TORONTO - Ophthalmology
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Week 1
Neuroscience Notes
Development & Organisation of the Nervous System

The Nervous System - Overview:

• Macro Structures:
o Brain
o Spinal Chord
o Peripheral Nerves
o Sense Organs
§ Eyes
§ Ears
§ Tongue
§ Olfactory bulbs
§ Skin
• Functions:
o Detection of stimuli (external/internal)
o Response to stimuli
o Coordinates activity of other organs & systems

Organisation of the Nervous System:

• Central Nervous System (the “CPU” & “Motherboard”)
o Brain
o Spinal Cord
• Peripheral Nervous System (the “Cables”)
o Cranial Nerves & Spinal Nerves
o Communication between CNS & rest of body

Nervous
System

Central Nervous Peripheral

System Nervous System
(Brain & Spinal (Cranial Nerves
Cord) & Spinal Nerves)

Afferent
Efferent
(Incoming)
(Out-going)
- Sensory

Somatic
(Voluntary) Autonomic
(Involuntary)
- Motor Function

Sympathetic NS Parasympathetic NS
(Fight/Flight) (Rest & Digest)

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General Embryonic Development is Described as Either:
• Trimesters (3x 3-Month Periods):
o First: - Foundations of Major Organs
o Second: - Development of Organs
o Third: - Rapid Growth & Fully Functional Organs.
• OR... Anatomical Stages: **(These are more relevant)
o Pre-Embryonic Period: 0-2 Weeks
§ Fertilisation
§ Blastocyst Formation & Implantation
§ Gastrulation
o Embryonic Period: 3-8 Weeks
§ Development & Differentiation of 3 Germ Layers into foundations of Organs.
o Foetal Period: 9 Weeks à Birth.
§ Period of Growth, NOT Differentiation.

Embryonic Development of the Nervous System:

1. Blastocyst: (Pre-Embryonic Period)
a. A fertilised egg reaches the Morula stage (Day 3), differentiates into a Blastocyst (Day 7) and then
implants in the endometrium.
b. The implanted Blastocyst consists of an ‘Inner-Cell Mass’ surrounded by Trophoblasts.
c. This ‘Inner-Cell Mass’ differentiates to form the ‘Bilaminar Disc’ (2 layers of cells)
i. Epiblast Layer: The top layer of Columnar Cells.
ii. Hypoblast Layer: The bottom layer of Cuboidal Cells.

2. Gastrulation: (Embryonic Period [wk 3+])

a. Gastrulation = the process that establishes the 3 Primary Germ Layers in the Embryo.
b. Begins with formation of the Primitive Streak (a shallow midline groove) along the caudal/tail half of
bilaminar disc.
c. At the cephalic/head end of the Primitive Streak is the Primitive Node which surrounds the small
Primitive Pit. Cells of the Epiblast proliferate & migrate through the Primitive pit into the gap
between the Epiblast & the Hypoblast. This is known as Invagination.
d. The Epiblast then becomes the Ectoderm, the invaginated cells become the Mesoderm and the
Hypoblast becomes the Endoderm.

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3. Neurulation:
a. Neurulation = Where the ectoderm around the midline thickens to form an elevated Neural Plate.
b. This Neural Plate invaginates to form a Neural Groove down the midline, flanked by 2 Neural Folds.
The Notochord, a flexible rod of mesoderm-derived cells, defines the primitive axis of the embryo.
c. The outer edges of the 2 Neural Folds continue folding towards the midline where they fuse
together to form the Neural Tube. (NB: Initially this happens around the centre of the embryo,
leaving open Neural Grooves at both the Cephalic & Caudal ends. However, these Neural Grooves,
aka Neuropores, close off by around wk 6 of development. Failure of a Neuropore to close can result
in Neural Tube Defects such as Spina-Bifida )
d. The hollow part inside the Neural Tube is called the Neurocoele.
e. The Neural Tube then separates from the Ectoderm and sinks down to the level of the Mesoderm.
i. The Mesoderm that flanks the sunken Neural Tube develops into The Somites, which
eventually become the Skin, Skeletal Muscle & Vertebrae+Skull.
f. Next, some cells on the top of the Neural Tube differentiate and separate to form the Neural Crest.
Cells of the Neural Crest eventually migrate & give rise to Peripheral Sensory Neurons, Autonomic
Neurons & Sensory Ganglia of the spinal nerves.

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The Somites:
• Somites = The Mesoderm Tissue directly adjacent to Neural Tube.
o The Mesoderm that flanks the sunken Neural Tube develops into The Somites, which eventually
become the Skin, Skeletal Muscle & Vertebrae+Skull.
• Somites grow in association with the developing nervous system à establish early connections.
• Somites differentiate into 3 regions:
o Sclerotome: Becomes the Vertebral Column & Skull
o Myotome: Becomes Skeletal Muscle
o Dermatome: Becomes Skin
• Hence, the Somites determine the distribution of Nervous Supply to all Mesoderm-Derived Tissue.

Development of the Neural Tube Into the Spinal Cord:

1. Once the Neural Tube closes, the cells differentiate into Neuroblasts.
2. These Neuroblasts give rise to 2 concentric layers, The Mantle Layer (Inner) and The Marginal Layer (Outer).
a. Mantle Layer: Later forms the Grey-Matter of the Spinal Cord. (Ventral & Dorsal ‘Horns’)
b. Marginal Layer: Later forms the White-Matter of the Spinal Cord.
3. The Dorsal & Ventral regions of the Mantle Layer thicken forming 2xBasal Plates, and 2xAlar Plates.
a. Basal Plates: (Motor Plates) Develop into Motor Neurons innervating skeletal muscles.
i. Become the Ventral Horns
b. Alar Plates: (Sensory Plates) Develop into Sensory Neurons.
i. Become the Dorsal Horns
- NB: The Lateral Horns in the Thoracic & Lumbar Regions of the Spinal Cord are Autonomic Motor Neurons
and their Axons exit via the Ventral Roots.

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Development of the Neural Crest cells Into the Sensory (‘Dorsal-Root’) Ganglia of PNS:
1. Neural Crest Cells also differentiate into Neuroblasts which become the Sensory (‘Dorsal-Root’) Ganglia.
2. The Neuroblasts of the Dorsal-Root Ganglia develop 2 processes:
a. Penetrates into the Alar Plate of the Neural Tube AND/OR into the Marginal Layer & up to brain.
b. Grows distally (outwards) and integrates with the Ventral Motor Root, forming the Trunk of the
Spinal Nerve. These neurons eventually terminate in the sensory receptors in skin/muscle/tendons.
NB: These Dorsal-Root Ganglia Processes form the ‘Sensory PseudoUnipolar’ Nerve-Type.

NB: By Wk 7 we have a Nearly-Functional Nervous System very similar in Organisation to Adult Anatomy.

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Development of the Head & Brain:

1. Neural-Tube Enlargement (Cephalic End):
a. At around 3-4wks, the Cephalic portion of the Neural Tube enlarges to form 3 regions; the Primary
Brain Vesicles:
i. Prosencephalon (Fore Brain)
ii. Mesencephalon (Mid Brain)
iii. Rhombencephalon (Hind Brain)
NB: The Cephalic Flexure between the Prosencephalon & Mesencephalon – important in humans for
Bipedalism (Brain @ 900 to Spinal Cord).

b. By around 4-5wks, the Primary Brain Vesicles develop further:

i. Prosencephalon (Fore Brain) develops into:
1. Telencephalon (Future Cerebral Hemispheres)
2. Diencephalon (Future Thalamus & Hypothalamus)
ii. Mesencephalon (Mid Brain)
iii. Rhombencephalon (Hind Brain) develops into:
1. Metencephalon (Future Pons & Cerebellum)
2. Myelencephalon (Future Medulla)

2. Brain Formation:
a. At around 11wks, there is massive Proliferation of Neuroblasts in Cephalic Neural Tube, causing
folding due to lack of space within the cranium.

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3. Pharyngeal Arches & Cranial Nerves:
a. Pharyngeal Arches = Similar to the Somites in lower parts of embryo. Each Pharyngeal Arch consists
of:
i. Ectoderm Tissue à Cranial Nerves & Skin of Face.
ii. Mesenchyme (Mesoderm) Tissue à Musculature of Face & Neck
iii. Endoderm Tissue à Pharyngeal Epithelium.
b. NB: Essentially, this results in Segmental Development of the Head & Neck, similar to Somites.

4. Formation of Ventricles:
a. The Neurocoel of the Neural Tube becomes the Ventricles of the Adult Brain.

i. Lateral Ventricles (Vent. 1 & 2):

1. Sits in the Cerebral Hemispheres (Telencephalon)
2. Are shaped due to folding of brain during development.
3. Each Consists of:
a. An Frontal (Anterior) Horn
b. A ‘Body’
c. An Occipital (Posterior) Horn
d. A Temporal (Inferior) Horn
ii. Third Ventricle:
1. Sits in the Diencephalon
2. Lateral Walls formed by Thalamus & Hypothalamus
3. Connects with the 4th Ventricle via the Cerebral Aqueduct.
iii. Fourth Ventricle:
1. Sits in the Brainstem
2. Is Continuous with the Spinal Canal (Central Canal).

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 GLS STUFF:
Terminology:
- “Rostral” = Head
- “Caudal” = Tail
- “Dorsal” = Back
- “Ventral” = Front
- “Ganglia” = Groups of Nerve-Cell Bodies
- “Gyrus” = Elevations (Crests) of the folds on the Cerebral Cortex.
- “Sulcus” = Grooves / Furrows between the Gyri on the Cerebral Cortex.

Anatomy of the Brain:

- Surface Anatomy
o Dorsal Landmarks:
§ Longitudinal Fissure: Separates Left & Right Hemispheres
§ Central Sulcus: Separates the Frontal & Parietal Lobes.
§ Lateral Sulcus: Separates the Temporal Lobe from the Other Lobes.
§ Occipital Lobe: Most Caudal Lobe (Visual Cortex)
§ Colliculi: Nestled in between the Cerebrum & Cerebellum.
• 2x Superior: Controls eye movements
• 2x Inferior: Part of Auditory Pathway

Brain Stem (Note the Colliculi – Superior & Inferior)

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o Ventral Landmarks:
§ Optic Chiasm (“Optic Crossing”): ‘X’-shaped crossing-over of Optic Nerves.
§ Hypothalamus:
§ Infundibulum: Connection between Pituitary & Hypothalamus.
§ Pituitary:
§ Olfactory Bulbs:
§ Mamillary Bodies:

o Medial Landarks (Ie. On Sagital Section):

§ Cingulate Gyrus
§ Corpus Callosum
§ Lateral Ventricle
§ Pineal Body
§ Thalamus
§ Hypothalamus

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o Coronal Section Landmarks:
§ Cortex (Grey Matter)
§ White Matter
§ Lateral Ventrcile
§ Caudate Nucleus
§ Corpus Striatum
§ Thalamus
§ Massa Intermedia: The Bridge between the Left & Right Thalamus.
§ Hippocampus

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 System: Neurological

Nervous System:
- Central Nervous System (CNS)
o Brain & Spinal Chord
o Integrating command centre
- Peripheral Nervous System (PNS)
o Outside the CNS
o Nerves extending to and from the periphery and CNS

The Neuron:
Structural Features:
a) Receptive Field: Dendrites
o Stimulated by inputs
b) Cell Body: Soma
o Responds to graded inputs
c) Efferent Projection: Axon (and axon hillock)
o Conducts nerve impulses to target
o Myelinated and unmyelinated
d) Efferent Projection: Myelin Sheath
e) Efferent Projection: N de f Ra ie
f) Output: Synaptic Terminals

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Supporting Cells:
Neuroglia (Glia)
o Smaller support cells of NS
o Outnumber neurons 10:1
o Structural & mechanical support
o Roles in maintaining homeostasis
o Myelination
o Immune responses via phagocytosis.
o Types of neuroglia:
CNS:
Astrocytes
o Nutrient bridge between neuron & capillaries
o Guide migrating young neurons
o Synapse formation
o Mop up excess K+ ions + neurotransmitters
Oligodendrocytes
o Myelin formation in CNS
Microglia
o Long thorny processes
o Monitors neuron health
o Senses damaged neurons
o Migrates to damaged neuron
o Phagocytoses microbes & debris (immune cells are denied access to CNS)
Ependymal Cells
o Lines central cavities of brain + spinal chord
o Blood-brain barrier
o Beating cilia circulates cerebrospinal fluid
PNS:
Schwann Cells
o Myelin Formation – wrap around axon
o Regeneration of damaged neurons
Satellite cells
o Surround neuron bodies

tructure, nutritional support & protection.

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Connective Tissue Sheaths on Peripheral Nerves:
Endoneurium
o Delicate connective tissue layer
o Surrounds each axon
Perineurium
o Coarser connective tissue layer
o Bundles groups of fibres into fascicles
Epineurium
o Tight, fibrous sheath
o Bundles fascicles into a single nerve.
o Houses blood vessels

Grey Matter & White Matter:

Grey Matter
o Neuron bodies (Soma)
o Imbedded in neuroglial cells
o Eg:
Cortex of Brain
Centre of Spinal Chord
Ganglia/nuclei

White Matter
o Neuron fibres (axons & dendrites
o White due to myelin
o Eg:
Peripheral Nerves & Plexuses
Central fibre tracts

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 Anatomy of the Brain:

Surface Anatomy
- Dorsal Landmarks:
o Longitudinal Fissure: Separates Left & Right Hemispheres
o Central Sulcus: Separates the Frontal & Parietal Lobes.
o Lateral Sulcus: Separates the Temporal Lobe from the Other Lobes.
o Occipital Lobe: Most Caudal Lobe (Visual Cortex)
o Colliculi: Nestled in between the Cerebrum & Cerebellum.
2x Superior: Controls eye movements
2x Inferior: Part of Auditory Pathway

- Ventral Landmarks:
o O ic Chia m O ic C o ing ‘X’-shaped crossing-over of Optic Nerves.
o Hypothalamus:
o Infundibulum: Connection between Pituitary & Hypothalamus.
o Pituitary:
o Olfactory Bulbs:
o Mamillary Bodies:

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- Medial Landarks (Ie. On Sagital Section):
o Cingulate Gyrus
o Corpus Callosum
o Lateral Ventricle
o Pineal Body
o Thalamus
o Hypothalamus

- Coronal Section Landmarks:

o Cortex (Grey Matter)
o White Matter
o Lateral Ventrcile
o Caudate Nucleus
o Corpus Striatum
o Thalamus
o Massa Intermedia: The Bridge between the Left & Right Thalamus.
o Hippocampus

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Blood Vessels & Blood Flow to the Brain

Arterial Supply of the Brain:

- Brain is Supplied by 2 Arterial Systems:
o 2x Vertebral Arteries 1x Basilar Artery Circle of Willis
o 2x Internal Carotid Arteries Circle of Willis
- Ci cle of Willi The Ana omo i of he B ain
o (The Ro ndabo of Arteries on the underside of the Brain with multiple Roads coming off it)
o (Encircles the Optic Chiasma, The Pituitary Gland & the Mammillary Bodies.)
o The R ad : (Anterior Posterior)
2x Anterior Cerebral Arteries
1x Anterior Communicating Artery
2x Internal Carotid Arteries
2x Middle Cerebral Arteries
2x Posterior Communicating Arteries
2x Posterior Cerebral Arteries
1x Basilar Artery
o NB: Communicating Arteries are always patent, but generally not functional (no blood flow) when
blood flow from both Carotids & Basilar Arteries is normal. However, if blood flow from one of the
major arteries is impeded, blood is shunted through the Communicating Arteries to compensate.

Distribution of Cerebral Arteries:

- Anterior Cerebral Arteries:
o (Travels up and over the Corpus Callosum, sprouting branches outwards towards the cortex)
o Medial Portion of Frontal Lobe (Incl. Cortex)
o Medial Portion of Parietal Lobe (Incl. Cortex)
o Corpus Callosum
- Middle Cerebral Arteries:
o (Travels through the Lateral Fissure/Sulcus and emerges onto the Lateral Surface of the Brain)
o Lateral Portion of the Frontal Lobe (Incl. Cortex)
o Lateral Portion of the Parietal Lobe (Incl. Cortex)
o Entire Temporal Lobe (Incl. Cortex)
- Posterior Cerebral Arteries:
o (Travels along the Inferior brain surface between the Cortex and the Cerebellum)
o Inferior Portion of Temporal Lobe (Incl. Cortex)
o Posterio-Medial Portion of Parietal Lobe (Incl. Cortex)
o Entire Occipital Lobe (Incl. Cortex)

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Venous Drainage of the Brain Via D al Sin e
- Venous Drainage begins with venous blood collecting in small venous channels known as “Dural Sinuses”.
- Sinuses Sit Within The Dura-Mater:
o The Dura-Mater is the thickest & outermost of the 3 Meninges of the brain. It extends deep into
the brain in 2 locations, the Falx Cerebri & the Tentorium Cerebelli:
1. Falx Cerebri:
The Dura Mater folds deep into the Longitudinal Fissure (Falx Cerebri) of the brain,
where it forms 2 Sinuses:
o 1. A Triangular S e io Sagi al Sin at the top of the dural fold.
o 2. A lower Infe io Sagi al Sin at the bottom of the dural fold.

2. Tentorium Cerebelli:
The Dura Mater folds deep into the Transverse Cerebral Fissure (Tentorium
Cerebelli) of the brain, where it forms a pair of sinuses:
o The R L T an e e Sin e .
o NB: All blood from Sup. & Inf. Sagittal Sinuses and the Straight Sinus
empties into these Transverse Sinuses.
o The L.&R. Transverse Sinuses then become the L.&R. Sigmoid Sinuses (Respectively).
o These Sigmoid Sinuses turn Inferiorly and become the Internal Jugular Veins.

Reabsorption of CSF into the Dural Sinuses:

- NB: CSF is constantly being produced, and therefore must also be constantly drained to prevent a rise in
intracranial pressure. Therefore:
- CSF is Reabsorbed into the Venous System via diffusion through Arachnoid Villi.
o Arachnoid Villi are invaginations of Arachnoid Mater through the Dura Mater and into the
Superior Sagittal Sinus.

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• Cerebral Blood Flow And Intracranial Pressure:
• Cerebral blood flow is carefully regulated under normal conditions.
• Cerebral Blood Flow:
• What percentage of cardiac output goes to the cerebral circulation at rest?
• 750ml/min (15% of cardiac output)
• Relationship Between Cerebral Blood Flow & Arterial Pressure:

• Autoregulation of Cerebral Blood Flow:

• What effect does a high PCO2 have on cerebral blood flow?
• Hypercarbia Vasodilation ↑Cerebral Blood Flow.
• What effect does a very low and very high PO2 on cerebral blood flow?
• Very High O2 Vasoconstriction
• Very Low O2 Vasodilation
• What implication does this have for the management of a patient with an acute head
injury/cerebral oedema?
• You want to prevent any hypercapnia because any vasodilation will Takes up
more room ↑Intracranial Pressure.
• You want to maintain PO2

• Kelly-Monroe Doctrine:
• States that the Cranial Compartment is Incompressible, and the Volume is Fixed.
• The Cranial Constituents (Blood, CSF, and Brain Matter) create a state of Volume
Equilibrium:
• Any increase in Volume of one of the constituents must be compensated by a
decrease in volume of another.
• Volume Buffers:
• Both CSF and, to a lesser extent, Blood Volume.
• (Eg. In Extradural Haematoma CSF & Venous Blood Volumes are Decreased)
• Maintain normal ICP
• Buffer Capacity ≈ 100-120mL

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Ganglia
Collections of neuron cell bodies in PNS
o Afferent Spinal Nerves:
Cell bodies of sensory neurons
‘Dorsal root ganglion’
o Efferent Spinal Nerves:
Cell bodies of autonomic nerve fibres
‘Sympathetic trunk ganglion’
o In Central Nervous System:
Called: Basal Nuclei / Nuclei

Spinal Nerves:
Innervation of the Skin:
o Dermatomes:
A portion of the mesoderm (skin, sensory receptors, sebaceous glands, blood vessels)
innervated by the cutaneous branches of a single spinal nerve.

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Neuronal Action Potentials:
4 Phases:
1 Resting Phase:
o Membrane is much more permeable to K+ than to Na+.
o Greater diffusion of K out than Na in
o Therefore inside is negative/Ouside is positive.
o Both Na & K voltage gated channels are CLOSED.
2 Depolarisation Phase:
o Mechanical/chemical/vibratory/other stimulus opens some Na+ channels such that Na+ flows into
the cell.
o Therefore membrane potential becomes less negative (ie. It depolarises)
o If the MP reaches approx. -55mV (threshold), the voltage gated Na+ channels open.
o Na+ influx increases dramatically – until MP reaches approx. +30mV where the voltage-gated Na+
channels close.
3 Repolarisation Phase:
o @ approx. +30mV K+ voltage gated channels open. (perm. of K increases & Na decreases)
o Large outflow of K+ membrane potential becomes more negative (repolarises) and returns to -
70mV.
4 Hyperpolarisation (undershoot) Phase:
o K+ channels remain open past -70mV and MP becomes more negative than at rest.
o K+ channels close and Na/K ATPase returns the MP to normal (-70mV)

Refractory Periods During the Action Potential:

Basically the total time between a stimulus creating an action potential and the MP returning to rest.
o Determines how soon a neuron can respond to another stimulus.
Divided into 2 sub-periods:
o Absolute Refractory Period no additional stimulus (no matter how large) can initiate a further
action potential.
o Relative Refractory Period If an additional stimulus is to initiate another action potential during
this time, it must be larger in order to reach threshold.

Speed of impulse: Dependent upon:

- 1. Axon Diameter Larger = Quicker
- 2. Presence of Myelin (white matter) Impulse jumps from exposed axon-region to the next instead of
having to open & close ion channels across the axon’s entire length (which would be slow)

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Phases of Neurotransmission:
1. Action potential reaches axon terminal, opens voltage-gated Ca+ channels.
- Influx of Ca+ into axon terminal causes vesicles of neurotransmitter to migrate to the axon terminal.
- ‘Ne o an mi e released by exocytosis from the sending (pre-synaptic) neuron.
- Neurotransmitter (acetylcholine/nor adrenaline/dopamine/glutamate/gaba/etc) diffuses across synaptic
cleft between 2 neurons.
2. Neurotransmitters bind to ligand-gated ion channels, causing change in MP of post-synaptic neuron (dendrite)
creating graded potentials.
-Short-lived, localised changes in membrane potential.
-Current flow decreases in magnitude with distance.
-The stronger the stimulus, the greater the GP (and further distance)
If GP depolarises membrane, it is excitatory
If GP hyperpolarises membrane, it is inhibitory.

- The sum of the GP may cause MP to reach threshold, triggering an action potential on the next neuron.
3. Neurotransmitter Inactivation stops continued stimulation of post-synaptic neuron.
- Neurotransmitter is either broken down by enzymes (eg. ACh-Esterase) or reabsorbed by pre-synaptic
terminal.

2 Types of Post-Synaptic Receptors:

- Ionotropic: (Ligand-Gated Ion Channels)
o Mech: Binding of Neurotransmitter Opening of Ion Channel Excitation/Inhibition of Cell.
Excitatory: Na+/Ca+ Channel – opening Na+/Ca+ Influx Depolarisation of Membrane
E ci a o Po -S na ic Po en ial (EPSP)
Inhibitory: Cl- Channel – opening Cl- Influx Hyperpolarisation of Membrane
K+ Channel – opening K+ Efflux Hyperpolarisation of Membrane
Inhibi o Po -S na ic Po en ial (IPSP)
- Metabotropic: (G-Protein Linked Receptors)
o Mech: Binding of Neurotransmitter Activates G-Protein Activates ‘Effector’ Proteins
Activate secondary Messengers (Eg. cAMP) Regulates Ion Channels/Activates Enzymes/Alters
Metabolism.

Actions of Neurotransmission:
- Direct Physiological Action:
o Eg. Neuromuscular Junction Muscle Contraction
o Eg. Sympathetic Synapse @ SA-Node ↑Heart Rate
- Links in a Chain:
o Eg. Peripheral Sensory Neuron Spinal Cord Ascending Sensory Pathways Thalamus
Cortex
- Modulation:
o Ie. Exerting a +ve/-ve influence on transmission by another neuron.

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 The Neurotransmitters

The Major Neurotransmitters (Classified by Structure):

- Amine Cla ical Ne o an mi e
o Acetylcholine (ACh)
o Dopamine
o Noradrenaline/Norepinephrine (NA/NE)
o Serotonin/5-Hydroxyl Tryptamine (5-HT)
- Amino Acids:
o Glutamate (#1 Excitatory Neurotransmitter of the Brain)
o GABA (γ-Amino Butyric Acid) (#1 Inhibitory Neurotransmitter of the Brain)
o Glycine
- Peptides:
o Cholecystokinin
o Enkephalins (Eg. Endorphins, Opioids) (Turn off Nociceptive/pain Pathways)
o Vasoactive Intestinal Peptide (VIP)

Memories
Short-Term Memory (STM):
- Based in Hippocampus.
- Lasts Seconds Several Hours MAX. (AKA: “Crammers” Memory)
- Limi ed o - Ch nk of Info.
- Amnesia ≈ Damage to Connection between STM & LTM.
Long-Term Memory (LTM):
- Limitless Capacity:
- Usually Requires STM Input:
o Generally LTM-Creation requires the info to pass through STM first.
- LTM Creation Improved by:
o Positive/Powerful Emotional State
o Rehearsal
o Association of New data with Old Data.
o The Belief that the Memory is Important
- By Remodelling the Neuron (Functionally/Structurally)
- More Specifically, Synaptic Remodelling:
- Long-Term Potentiation (LTP):
o Definition: “A Long-Lasting Post-Synaptic Depolarisation, induced through Repetitive Stimulation &
Summation of Excitatory Post-Synaptic Potentials.”
Simply – “A Persistent Increase in Synaptic Strength”
o The #1 Neurotransmitter:
Glutamate binds to NMDA and/or AMPA Receptors.
o 3 Phases of LTP:
1. Induction - (Synaptic Plasticity)
2. Expression - (Synaptic Augmentation)
3. Maintenance - (Long Term Loss/Continuation of LTP)
- 2 Types of Long-Term Memory:
o 1. Declarative (EXPLICIT):
Brain Regions:
Hippocampus
Para-Hippocampal Regions (Medial Temporal Lobe)
Areas of Cerebral Cortex
Thalamus + Hypothalamus
Learning WHAT :
Facts/Words/Ideas/Concepts/Events
o 2. Non-Declarative (IMPLICIT):
Learning HOW : - How to do things/How to recognise things.
Motor: Motor Cortex, Cerebellum,
Emotional Responses: Amygdala

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- Se en Sin of Memo (Types of Memory Deficits):
o 1. Transience
– Memory ‘Fade’
o 2. Absent-Mindedness
– Brushing teeth when already brushed them
o 3. Blocking
– When a memory is on the ‘Tip of the tongue’.
o 4. Misattribution
– Where you Misremember where you saw/heart something, or even if.
o 5. Suggestibility
- Where someone suggests that you saw/heard something (when you didn’t) and you
‘remember’ seeing/hearing it.
o 6. Bias (Negative Bias)
- Tend to recall only the Negative Things.
o 7. Persistence
- Remember a Single Failure rather than multiple successes (eg. Post Exam Briefings)
o ...8. Confabulation When you elaborate on a memory.

Intelligence - Theories:

- Theory of Multiple Intelligences:

o 7 Intelligences:
Linguistic: - Good with words/dates/names/places.
Logical-Mathematical - Good with numbers/abstract/puzzles/logic/computers
Spatial - Good with pictures/directions/jigsaws/construction/drawing
Musical - Good with sounds/notes/rhythms.
Bodily-Kinaesthetic - Good with motor/sports/mimicking/fine craft
Interpersonal - Good with people/leading /manipulation/streetwise/team/Co-op
Intrapersonal - Independent/Loner/sense of self-worth/individual/opinionated

- Emotional Intelligence:
o Properties:
Knowing your feelings/strengths/weaknesses.
Managing your emotions/motives/behaviour
Persisting despite setbacks
Empathy (good at reading other’s emotions)
o Indicators of EI:
Optimism
Taking Initiative
Achievement Motivation
o 3 Adaptive Abilities:
Appraisal & Expression of Emotion
Regulation of Emotion
Utilisation of Emotion

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 Neurobiology of Emotions
Neuroanatomy of Emotion The Limbic System:
- The Papez Circuit:
o 1. Thalamus relays Sensory Input to Cingulate Cortex.
o 2. Cingulate Cortex - gives you the Emotional Experience
- also relays to the Neocortex, which gives Context/Colouring to the Emotion.
- also relays to the Hippocampus
o 3. Hippocampus Relays to the Hypothalamus – Causes the Emotional Expression (Visceral
Response)

- ***Amygdala***:
o #1 Structure involved in Emotion The “Heart” of the Limbic System.
o “The Fight/Flight Centre”
o Linked to all but 8 areas of the Cortex :. Thought to be #1 integrator of Cognitive & Emotional
Info.
o Regulates:
Fear & Aggression
Vigilance & Attention
Recognition of Emotion (in Self & Others)
Emotional Contribution to Memory. (Emotional Implicit Memory)

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Neurotransmitters & Emotion:
- *Noradrenaline:
o Activated By:
Novel, Unexpected Stimuli
o Released By:
Locus Coeruleus (A Nucleus
In the Pons involved with
physiological responses to
stress & panic.)
- *Serotonin: What we target in treating Depression.
o Activated By:
General activity/arousal
o Released By:
Raphe Nuclei (A group of
Nuclei In the brainstem)
- *Dopamine:
o Activated By:
Pleasurable Activities
o Released By:
Ventral Tegmental Area (VTA)
Substantia Nigra
- Glutamate & GABA:
o Reduces Anxiety

Fear:
- Brain Structures Involved:
o Thalamus
Amygdala
o Thalamus
Primary Sensory Cortex
Association Cortices
- Long & Short Pathways:
o Long:
Info processed by higher brain centres & Hppocampus.
Results in a more complex response
o Short:
Info sent straight to Amygdala
Results in a basic response (Recoil from stimulus/Freeze)
Advantage = No cortical processing means quicker reaction times S i al

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 AfraTafreeh.com exclusive

Somatosensory Processing

Sensory Receptors:
- Classifying Sensory Receptors:
Type of Stimulus:
Mechano: deformation & mechanical force (touch/pressure/vibration/stretch)
Thermo: temperature changes
Photo: light energy
Chemo: changes in aqueous chemistry of interstitial fluid/smell/taste
Nociceptor: sense potentially damaging stimuli pain (heat/cold/pressure/chemicals)
Location in Body:
Exteroceptors: near the body surface – touch/pressure/pain/temperature/ the senses
Interoceptors (visceroceptors): stimuli within the body [viscera/blood vessels] – (chemical
changes/tissue stretch/temperature) pain/discomfort/hunger/thirst
Proprioceptors: occur in skeletal muscles/tendons/joints/ligaments/muscle sheaths
Structural Complexity:
Simple: absolute majority – modified dendritic endings of sensory neurons.
Complex: minority – sense organs = collections of cells associated with the “special senses”
(vision/hearing/smell/taste)
- Once sensory input enters CNS, it travels to the Thalamus (sorting station of the brain)
Impulses are sorted on the basis of where they came from and the type of sensation
They are then sent to their relative functional areas on the cortex (brain surface).
- Response: If a response is required, then a discrete area of the brain will activate it.
Primary motor cortex: voluntary motor
Language & Speech Centres: vocalisation
Hypothalamus & Brain Stem: visceral responses (chest/abdominal – pulse/sweat/B.Pressure)

Receptor Types:

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Receptors: Nature of Activity:
- When Are They Active?
o Tonic Receptors:
Continually Firing
– Eg. Proprioceptors
o Phasic Receptors:
Fire only with a Change in the Environment.
– Eg. Thermoreceptors
- When Do The Inac i a e Ho Q ickl do he Ada
o NB Ada a ion Time Taken for receptor to Stop Firing during Sustained Stimulation
RARs Rapidly Adapting Receptors:
Receptor quickly stops firing under continuous stimulus
- Eg. Touch Receptors (Can’t feel clothes after a while)
SARs Slowly Adapting Receptors:
Receptor maintains firing under continuous stimulus
- Eg. Muscle Stretch Receptors (Proprioceptors)

Receptive Fields:
- A Receptive Field: The Area Monitored by 1x Receptor.
o Ie. Touch anywhere in that field, the sensation will come from the entire receptive field.

Functional Sensory Areas of the Brain:

Primary visual area – receives visual information from the retina of the eye.
Primary motor area – controls voluntary skilled movements of our skeletal muscles
Pre-motor cortex – controls learned motor skills (musical instruments/typing/etc)
Primary auditory area – sound energy stimulates hearing receptors and is interpreted as
pitch/vol/location.
Primary somatosensory area – receives information from the general (somatic) sensory receptors.
Primary gustatory area – perception of taste stimuli.
Primary Olfactory area – info from smell receptors

Sensory Association Areas info flows from sensory receptors to a specific primary sensory cortex, then to a
specific association area. Association areas give meaning to the received information, store it in memory, relate it
to past experiences & decide on plan of action

Somatosensory Processing:
- Somatosensory Cortex:
o Roles:
Detection of Sensation & Conscious Awareness of Sensation
Feature/Quality Recognition (ie. Texture/Size/Shape)
o Exhibits S a (Body Mapping)
– ie. Specific Cortical Areas responsible for Particular Body Regions
o Receptor Density in a Body Region determines the Size of the respective Cortical Area. – See Below:

- Somatosensory Association Area:

o The Somatosensory Cortex has Connections to the Somatosensory Association Areas
o Role:
Compares Received Stimulus to Past Experiences.

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Somatosensory Pathways:
- First Order Neurons (Peripheral Afferent Nerves):
o (Eg. Dorsal Root of Spinal Nerves & Sensory Cranial Nerves)
o Enter Spinal Cord via Dorsal Nerve Root Terminate in Dorsal Horn.
o NB: Cell-Bodies of the Pseudounipolar-Neuron Receptors culminate in the Dorsal Root Ganglion

- Second Order Neurons (Ascending Pathways of Spinal Cord):

o Once inside the Spinal Cord, 1st-Order Neurons Synapse with 2nd-Order Neurons
o 2nd-Order Neurons:
Often responsible for Decussation (Crossing of Fibre-Tracts to the Other Side of the Body)
Different Sensory Info takes Different Ascending Pathways to the Brain.

- Third Order Neurons:

o NB: 3rd-Order Neurons are only Relevant to the Posterior Column & The SpinoThalamic Pathways.
The SpinoCerebellar Pathway terminates in the Cerebellum with 2nd-Order Neurons.
o Carry Sensory Info from Thalamus to Primary Somatosensory Cortex in Parietal Lobe.
Thalamus Sorts incoming Sensory Info Sends it to Cortex.

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- Neurotransmitters & Receptors:
o NTs/Receptors @ The Sensory Nerve:
*TRPV1-Receptor (Ca+ Channel TRP Vanilloid Rece o 1 O ened b
Capsaicin (from hot chillies)
Heat
Mechanical (Mechanism unclear)
H+ (Acid)(Often a result of inflammation)
Bradykinin Receptors:
Bradykinin Receptor Activates TRPV1-Receptor Depolarisation Nociception.
Prostanoid Receptors:
Sensitive to Prostaglandins.
Open Na+ Channels
Inhibit K+ Channels ↑MP :. Lowers Threshold ↑Sensitivity
Open TRPV1-Receptors
ASIC Acid Sen i i e ga ed Ion Channel
Acid ASIC-Stimulation Depolarisation of Cell Nociception
Opiate/Cannabinoid Receptors:
Sensitive to Opioid & Cannabinoids.
Open K+ Channels K+-Efflux ↓MP (Hyperpolarises Cell) ↓Sensitivity

o NTs/Receptors @ The Dorsal Horn:

Afferent Pathway:
*Substance-P
*Glutamate (AMPA & NMDA Receptors)
Efferent Pathway Sensory Modulation Via Pain-Gate Mechanism:
*OPIOIDS*:
o Activate Descending Inhibitory Pathways & Directly inhibit Dorsal Horn
Synapse.
*Noradrenaline
o Directly Inhibits Dorsal-Horn Synapse
*Serotonin (5-HT):
o Directly Inhibits Dorsal-Horn Synapse
*Enkephalins:
o Directly Inhibits Dorsal-Horn Synapse
NB: Low-Dose Tri-Cyclic Anti-Depressants can treat Neuropathic pain by blocking
re-uptake of NE, 5-HT, & Enkephalins in Dorsal Horn Synapse.

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 Motor Processing

Motor Processing Hierarchy - The Levels of Motor Control:

- 1. Ready (Strategy) Deciding Wha o do
o Prefrontal Cortex
o Basal Ganglia (NB: Basal Ganglia are the interface between ‘Strategy’ & ‘Tactics’.)
- 2. Set (Tactics) Deciding Ho o do i
o Pre-Motor Area (PMA)
- 3. Go (Execution) Ac ion
o Primary Motor Cortex (M1)
o Cerebellum
o Brainstem
o Descending Tracts
o Spinal Nerves
o Peripheral Motor Neurons

Descending Tracts Involved in Motor Function:

- Descending Motor Pathways:
o Lateral Pathways:
Roles:
Both Tracts – Voluntary Movement of Distal Extremities (Particularly Hands & Feet)
2 Divisions:
Corticospinal Tract:
o Originates in Primary Motor Cortex
o Run through the Internal Capsule to the Brainstem.
o Decussate in Medullary Pyramids (Medulla)
Rubrospinal Tract:
o Originates in Red Nucleus of Midbrain.
o Decussate immediately below Red Nucleus (In the Pons)

o Continue down the spinal cord in the Lateral White Matter.

o Terminate in Ventral Horn of Spinal Grey Matter

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 o Ventromedial (Indirect/Extrapyramidal) Pathways:
4 Divisions:
Tectospinal (AKA: Colliculospinal) Tract
Vestibulospinal Tract
Pontine Reticulospinal Tract
Medullary Reticulospinal Tract
Specific Functions:
Tectospinal/Colliculospinal: Visual Tracking (Head/Eye Coordination)
Vestibulospinal: Maintain Balance During Standing & Moving
Pontine Reticulospinal: Maintains Muscle Tone & Visceral Motor Functions
Medullary Reticulospinal: Maintains Muscle Tone & Visceral Motor Functions

Reflexes:
- Rapid, automatic responses to stimuli.
- Occur over neural pathways called reflex arcs.
- Components of a reflex arc:
Receptor Sensory neuron CNS integration centre Motor neuron Effecter

Visceral Reflexes:
- Similar to the Somatic-NS, the ANS also has reflex arcs;
- Visceral Reflex Arcs Components:
o Visceral Sensory Neurons (Chemical Changes/Stretch/Irritation of Viscera) Integration Centre
Motor Neuron Effector

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 The Autonomic Nervous System:

Divisions of the Autonomic NS:

- The 2 Divisions of the ANS (Sympathetic & Parasympathetic) serve the same visceral organs, but cause
Opposite Effects. This Dual Innervation counterbalances each division’s activities Maintains
Homeostasis.
- Sympathetic:
o “Fight/Flight”
o Mobilizes the body during activity
o Effects are Widespread
- Parasympathetic:
o “Rest/Digest”
o Conserves Body Energy & Promotes Maintenance Functions.
o Has relatively Short-Lived Effects (Due to short-acting nature of Acetylcholine)
o Effects are relatively Localised

Effectors:

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Efferent Pathways & Ganglia:
- As opposed to the Somatic-NS which uses a mono-synaptic system (& Hence Lacks Ganglia), the
Autonomic-NS uses a 2-Neuron-Chain system.
- 1. The Pre-Ganglionic Neuron:
o The Cell-Body of the first neuron
o Resides in the Brain or Spinal Cord
o Synapses with a Ganglionic Neuron.
- 2. The Ganglionic Neuron:
o Resides in an ‘Autonomic Ganglion’ outside the CNS.
o Extends from the Ganglion to the Effector Organ.

Sympathetic & Parasympathetic Divisions Differ Anatomically in 3 Ways:

- 1. Site of Origin
- 2. Fibre Lengths
- 3. Location of Ganglia

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Anatomy: The Parasympathetic (Craniosacral) Division:
- Fibres originate from:
o Brain Stem
o Sacral Region of Spinal Cord
- Fibre Lengths:
o Preganglionic Fibres – Extend nearly all the way to the structures to be innervated.
o Postganglionic Fibres – Very Short; Extend from the Terminal Ganglia & synapse with Effector
Cells.
- Ganglia Location:
o The Te i a Ga g ia are located Very Close To or Within the Target Organs.

- The Cranial Outflow:

o Fibres Originate From Cranial-Nerve Nuclei in the Brain Stem.
o Fibres Extend to their Terminal Ganglia via 4 of the paired Cranial Nerves:
III – Oculomotor Nerves Pupil Constriction & Lens Accommodation (close sight)
VII – Facial Nerves Stimulate large Glands in the head
(Nasal/Lacrimal/Submandibular & Sublingual Salivary)
IX – Glossopharyngeal Nerves Stimulate Parotid Salivary Glands
X – Vagus Nerves Serves virtually all organs of the thoracic & abdominal
Cavities (Except Distal Large Intestine)
- The Sacral Outflow:
o Fibres Originate from Neurons in the Lateral Gray Matter of Spinal Cord Segments S2-S4.
o Fibres Extend to their Terminal Ganglia via Splanchnic Nerves of the Pelvic Plexus.
o Serve Distal Large Intestine & the Pelvic Organs (Bladder, Ureters, Repro. Organs)

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Anatomy: The Sympathetic (Thoraco-Lumbar) Division:
- NB: Sympathetic-NS innervates more organs than the Parasympathetic, and its effects are longer-lasting.
- Fibres originate from:
o Cell bodies of Preganglionic Neurons in the Lateral Horns Spinal Cord Segments T1 L2.
- Fibre Lengths:
o Preganglionic Fibres – Exit the Spinal Cord via the Ventral Root Then pass through a White
Ramus
Communicans Synapse adjoining Sympathetic Trunk (Chain) Ganglion.
(NB: These fibres are short)
o Postganglionic Fibres – Exit the Sympathetic Ganglion at/below/above their spinal level via a Gray
Ramus Communicans Then enters the Ventral Spinal Nerve at that level

Effector Organs.

NB: The Colour of the Rami Communicans reveals whether or not their fibres are myelinated.
Preganglionic Fibres = Myelinated Postganglionic Fibres = Unmyelinated

- Ganglia Location:
o Sympathetic Trunks (Chains of Ganglia) Flank each side of the Vertebral Column from the Neck to
Pelvis.

NB: Although the Sympathetic Trunks exist along the length of the spinal cord, the Fibres arise only
from Thoracic & Lumbar cord segments.

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 Physiology of the Autonomic NS:

Neurotransmitters of the PNS:

- Afferent (Sensory): *Glutamate*/Calcitonin-Gene-Related Peptide/Substance
P
- Efferent (Motor):
o Somatic/Voluntary (Skeletal Muscle): Acetylcholine (ACh)
o Autonomic:
Sympathetic:
Preganglionic: Acetylcholine (ACh) Stimulates Ganglia & Adrenal
Medulla
Postganglionic: Norepinephrine
Adrenal Medulla: Stim. by Acetylcholine (ACh) to release Epinephrine & NE
into Blood.
Parasympathetic:
Preganglionic: Acetylcholine (ACh)
Postganglionic: Acetylcholine (ACh)

Sympathetic & Parasympathetic Tone:

- Sympathetic (Vasomotor) Tone:
o The continual state of Partial Constriction of the Vascular System that Maintains BP (even @ rest)
o During Activity, a Higher BP is needed the Vasomotor Fibres fire more rapidly
Vasoconstriction.
o NB: Alpha-Blockers dull the effects of the Sympathetic/Vasomotor Tone Control Hypertension.
- Parasympathetic Tone:
o Slows the heart, sets the Normal activity levels of the Digestive & Urinary Systems, & Stimulates
Glandular Secretion (Except Adrenal Glands & Skin Glands)
o NB: The Sympathetic division an override this during times of stress.
o NB: Drugs that block Parasympathetic Responses ↑HR, Faecal/Urinary Retention & ↓Glandular
Secretion.

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 Cranial Nerves:

I. Olfactory
Smell
II. Optic
Vision (Visual Acuity)
III. Oc lomo o e e-mo e
Controls 4 of the 6 eye muscles.
IV. T ochlea lle
Controls 1 of the extrinsic eye muscles – pulley shaped
V. Trigeminal
3-branched (Opthalmic, Maxillary, Mandibular) sensory fibres to the face & cornea + Mastication
VI. Abd cen abd c
Controls the extrinsic eye muscle that abducts the eyeball (lateral rotation)
VII. Facial
Facial expression (Furrow Brow, Shut Eyes, Smile)
VIII. Vestibulocochlear
Hearing and balance (formerly the auditory nerve)
IX. Glossopharyngeal ong e ha n
Sensory Tongue and pharynx (Gag reflex)
X. Vag he ande e
Mouth motor + parasympathetic effects in the thorax & abdomen.
XI. Accessory
Neck and shoulder muscles
XII. H oglo al nde - ong e
tongue movement – Poke tongue out

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Nerve Functional Location of Nerve Cranial Exit Functions (major)
Components Cell Bodies Point
I Olfactory nerve Special Sensory Olfactory Cribriform Plate Smell
Epithelium of The Ethmoid
Bone
II Optic nerve Special Sensory Retinal Ganglion Optic Canal Vision and associated reflexes
III Oculomotor Somatic Motor Midbrain Movements of eyes
nerve Superior Orbital (Superiorly, Inferiorly &
Fissure Medially)
Visceral Motor Presynaptic: Pupillary constriction and lens
(parasympathetic) Midbrain accommodation
Postsynaptic: (parasympathetic)
Ciliary Ganglion
IV Trochlear nerve Somatic Motor Midbrain Superior Orbital Movements of eyes
Fissure (Inferolaterally)
V Trigeminal nerve
- V1 Opthalmic General Sensory Trigeminal Ganglion Superior Orbital Sensation from Cornea, & V1
Division Fissure Dermatome

- V2 Maxillary Foramen Sensation from Maxillary

Division Rotundum Teeth, Nasal Mucosa, Maxillary
Sinuses, Palate, & V2
Dermatome

- V3 Foramen Ovale Sensation from Mandibular

Mandibular Teeth, Mucosa of Mouth,
Division Tongue & V3 Dermatome

Branchial Motor Pons Muscles of Mastication &

Swallowing

VI Abducent nerve Somatic Motor Pons Superior Orbital Lateral Rectus Muscle -
Fissure Abduction (Lateral Rotation) of
the Eye
VII Facial nerve Branchial Motor Pons Internal Facial Muscles + Some Muscles
Acoustic of Mastication
Special Sensory Geniculate Ganglion Meatus; Facial Taste (Anterior 2/3 of Tongue)
Visceral Motor Presynaptic: Canal; Stimulation of Submandibular
(Parasympathetic) Pons Stylomastoid & Sublingual Salivary Glands, &
Postsynaptic: Foramen Lacrimal Glands.
Pterygopalatine
Ganglion;
Submandibular
Ganglion

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VIII Vestibulocochlear
- Vestibular Special Sensory Vestibular Ganglion Internal Position of the Head & Balance
Division Acoustic Meatus (The body’s Gyro)
- Cochlear Special Sensory Spiral Ganglion Hearing (Via Spiral Organ)
Division
IX Branchial Motor Medulla Jugular Foramen Stylopharyngeus Muscle
Glossopharyngeal (Assists with swallowing)
Visceral Motor Presynaptic: Stimulates Parotid Salivary
Medulla Gland
Postsynaptic:
Otic Ganglion
Visceral Sensory Superior Ganglion Visceral Sensation from
Parotid Gland, Carotid Sinus,
Pharynx & Middle Ear
Special Sensory Inferior Ganglion Taste(Posterior 1/3 of Tongue)
General Sensory Inferior Ganglion Cutaneous Sensation of
External Ear
X Vagus Branchial Motor Medulla Jugular Foramen Constrictor Muscles of
Pharynx, Muscles of Larynx,
Palate & Upper 2/3 Esophagus
Visceral Motor Presynaptic: Maintains Smooth Muscle
Medulla Tone in Trachea & Bronchi,
Postsynaptic: Peristalsis in GIT & ↓HR.
Viscera
Visceral Sensory Superior Ganglion Visceral Sensation from Base
of Tongue, Pharynx, Larynx
Trachea, Bronchi, Heart,
Esophagus, Stomach &
Intestine L-Colic Flexure.
Special Sensory Inferior Ganglion Taste (Epiglottis & Palate)
General Sensory Superior Ganglion Sensation from the External
Ear.
XI Spinal Somatic Motor Spinal Cord Jugular Foramen Sternocleidomastoid &
Accessory Trapezius Muscles
XII Hypoglossal Somatic Motor Medulla Hypoglossal Intrinsic & Extrinsic Muscles of
Canal the Tongue.

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 Spinal Cord
o Extends from Foramen Magnum
o Resides in the vertebral canal
o Bathed in cerebrospinal fluid
o Terminates at the ‘conus medullaris’ (cone of medulla) – approx L1 in adults.
o Cauda Equina:
Nerve rootlets of lower-lumbar & sacral regions extend further down vertebral canal.
o Filum Terminale:
Conn. Tissue anchors Cauda Equina to the base of vertebral canal.

Internal Structure: External Structure:

Grey Matter: Spinal Nerves:
o All neuronal cell bodies o Merging of the Dorsal & Ventral root
o 2 Dorsal Horns fibres
Nerve cells that receive sensory o Carry mixed sensory & motor info to
information from body relevant body area
Via the dorsal root fibres. Branches of Spinal Nerves:
o 2 Ventral Horns o Ventral Rami: “ventral branch”
Contain motor nerve cells o Dorsal Rami: “dorsal branch”
Cell axons leave through ventral Sympathetic Chain
root fibres. Sympathetic Ganglia:
o Lateral Horns:
Present in thoracic & upper
lumbar regions
Autonomic motor nerves from
sympathetic nervous system
Exit spinal cord through the
ventral roots
White Matter:
o Ascending and descending fibre tracts.

Information Pathways: Central Peripheral

Somatic:
Afferent (Sensory Info) Efferent (Skeletal Muscle)
o Receptor cells in periphery o Neuronal cell bodies in ventral horn of grey
o Info conveyed along peripheral axon Soma (in matter.
dorsal root ganglion) o Cell axon leaves spinal cord through ventral root
o Info conveyed along proximal axon spinal spinal nerve
cord (CNS) o Axon flows out of Ventral Rami
o Info ascending fibres (white matter) brain o Directly innervates muscle @ neuromuscular
for processing junction

Visceral:
Afferent (Sensory Info) Efferent (Smooth Muscle)
o Receptors in viscera o Neuronal cell bodies in lateral horn of grey
o Info conveyed along peripheral axon Soma matter.
(in dorsal root ganglion) o Cell axon leaves spinal cord through ventral root
o Info conveyed along proximal axon spinal spinal nerve
cord (CNS) o Axon flows out of Ventral Rami
o Info ascending fibres (white matter) brain o Axon synapses with peripheral ganglia
for processing o Peripheral ganglia innervates internal viscera:
smooth muscle/glandular tissue/cardiac
muscle

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 Shoulder Girdle Nerves

(Ant) Musculocutaneous
o Innnervates:
Flexors of Arm:
Biceps Brachii
Brachialis
Coracobrachialis
Skin of Anterio-Lateral Forearm

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(Ant) Median
o Innervates:
Flexors of Anterior Forearm:
Palmaris Longus
Flexor Carpi Radialis
Flexor Digitorum Superficialis
Lateral ½ of Flexor Digitorum Profundus
Flexor Pollicis Longus
Pronator Teres
Pronator Quadratus
Thenar Muscles (Intrinsic muscles of Lateral Palm)
Lumbricals #1 & #2
Digital Branches to Fingers
Skin of Lateral 2/3 of Hand, Palm Side & Dorsum of Fingers 2 & 3

(Ant) Ulnar
o Innervates:
Flexors of Anterior Forearm:
Flexor Carpi Ulnaris
Medial part of Flexor Digitorum Profundus
Majority of Intrinsic Muscles of Hand
o Adductor Pollicis
o Flexor Digiti Minimi Brevis
o Abductor Digiti Minimi
o Opponens Digiti Minimi
o Lumricals #3 & #4
o Interossei
Skin of Medial 1/3 of Hand (Ant & Post).

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(Post) Axillary
o Innervates:
Deltoid
Teres Minor
Skin & Joint Capsule of Shoulder
(Post) Radial
o ALL Posterior Upper-Arm & Forearm Muscles.
Extensor Muscles of Arm, Forearm & Hand:
Triceps Brachii
Anconeus
Supinator
Brachioradialis
Extensor Carpi Radialis Brevis
Extensor Carpi Radialis Longus
Extensor Carpi Ulnaris
Abductor Pollicis Longus
Extensor Pollicis Brevis
Extensor Pollicis Longus
Extensor indicis
Extensor Digitorum
Extensor Digiti Minimi
Skin of Entire Latero-Posterior Arm & Forearm & Hand (except dorsum of fingers 2 & 3)

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Lumbar Plexus:

NB: Know:
Lumbosacral Trunk – Communicates between Lumbar & Sacral Plexus

o Femoral Nerve:
Branches off L2, L3 & L4
Runs between Psoas Major & Iliacus beneath Inguinal Ligament Thigh Splits in 2:
Anterior Division
o Cutaneous Branches
o Muscular Branches Pectineus & Sartorius
Posterior Division
o Cutaneous Branch – Saphenous Nerve
o Muscular Branches Quadriceps Femoris
Innervates:
Pectineus
Sartorius
Rectus Femoris
Vastus Lateralis
Vastus Intermedius
Vastus Lateralus
Skin of Anterio-Medial Thigh & Lower Leg + Medial Aspect of Foot

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NB: Cutaneous Innervation In blue

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o Obturator Nerve:
Branches off L2, L3 & L4
Runs medial to Psoas Major, down along the inside wall of lesser pelvis through
Obturator Canal (in obturator membrane) through Obturator Foramen Thigh
Innervates:
External Obturator
Adductor Longus
Adductor Brevis
Adductor Magnus
Gracilis
Skin of medial aspect of thigh

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Sacral Plexus:

o Superior Gluteal Nerve:

Branches off L4, L5 & S1
Runs from Dorsal Roots leaves pelvis through Greater Sciatic Foramen above Piriformis
Gluteus Medius, Gluteus Minimus & Tensor Fasciae Latae.
Accompanied by Superior Gluteal Vein & Artery.
Innervates:
Gluteus Medius
Gluteus Mimimus
Tensor Fasciae Latae

o Inferior Gluteal Nerve:

Branches off L5, S1 & S2
Runs from Dorsal Roots leaves pelvis through Greater Sciatic Foramen above Piriformis
Gluteus Maximus.
Innervates:
Gluteus Maximus

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o Sciatic Nerve:
Branches off L4, L5, S1, S2 & S3
Runs from inside pelvis through Greater Sciatic Foramen (below piriformis) descends
along the posterior thigh to about its lower third Divides into 2 Branches: Tibial &
Common Fibular Nerves. (some variation)
Innervates:
Hamstrings
½ of Adductor Magnus

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Sciatic Nerve: Common Fibular (Peroneal) Nerve:
Branches off Sciatic Nerve
Runs obliquely along the lateral side of the Popliteal Fossa Head of the Fibula
Adjacent to the Medial Margin of the Biceps Femoris Winds around neck of
Fibula divides into Deep & Superficial Fibular (peroneal) Nerves
Innervates:
o Skin of Lateral Aspect of Lower Leg
o Skin of Dorsum of Foot
Deep Fibular Nerve:
o Innervates:
Tibialis Anterior
Extensor Digitorum Longus
Fibularis Tertius
Extensor Hallucis Longus
Superficial Fibular Nerve:
o Innervates:
Fibularis Longus
Fibularis Brevis

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Tibial Nerve:
Branches off Sciatic Nerve
Runs through Popliteal Fossa Then follows the Tibia to the ankle passes into
Foot (below medial malleolus) Terminates as Medial & Lateral Plantar Nerves
Innervates:
o Gastrocnemius
o Popliteus
o Soleus
o Plantaris
o Tibialis Posterior
o Flexor Digitorum Longus
o Flexor Hallucis Longus

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 Week 2
Neuroscience Notes
Blood Vessels & Blood Flow to the Brain

Why Does the Brain Need Blood?

- Consumes 15-20% of the body’s total energy needs, (and receives 15% of Cardiac Output), despite being
only 2% of total body mass.
- Neurons require high ATP to:
o Maintain Ion Gradients across Plasma Membrane
o Regulate Neurotransmitter synthesis/re-uptake.
- Neurons have NO ANAEROBIC CAPACITY à Therefore the brain absolutely depends on Oxygenated Blood.
o Hence, any deficit in blood supply is detrimental (≈30+sec lack of blood/O2 to brain à unconscious)

Blood Supply to the Brain is an ANASTOMOSIS:

- Anastomosis: Where Multiple Arteries Supply the Same Region of Tissue. Ie. A Dual Blood-Supply.
- The Advantage: If one of the arteries becomes blocked/damaged, the other artery will compensate for it.

Arterial Supply of the Brain:

- Brain is Supplied by 2 Arterial Systems:
o 2x Vertebral Arteries à 1x Basilar Artery à Circle of Willis
o 2x Internal Carotid Arteries à Circle of Willis
- ‘Circle of Willis’, The Anastomosis of the Brain:
o (The ‘Roundabout’ of Arteries on the Ventral Surface of the Brain with multiple ‘Roads’ coming off it)
o (Encircles the Optic Chiasma, The Pituitary Gland & the Mammillary Bodies.)
o The ‘Roads’: (Anterior à Posterior)
§ 2x Anterior Cerebral Arteries
§ 1x Anterior Communicating Artery
§ 2x Internal Carotid Arteries
§ 2x Middle Cerebral Arteries
§ 2x Posterior Communicating Arteries
§ 2x Posterior Cerebral Arteries
§ 1x Basilar Artery

o NB: Communicating Arteries are always patent, but generally not functional (no blood flow) when
blood flow from both Carotids & Basilar Arteries is normal. However, if blood flow from one of the
major arteries is impeded, blood is shunted through the Communicating Arteries to compensate.

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Distribution of Cerebral Arteries:
- Anterior Cerebral Arteries:
o (Travels up and over the Corpus Callosum, sprouting branches outwards towards the cortex)
o Medial Portion of Frontal Lobe (Incl. Cortex)
o Medial Portion of Parietal Lobe (Incl. Cortex)
o Corpus Callosum

- Middle Cerebral Arteries:

o (Travels through the Lateral Fissure/Sulcus and emerges onto the Lateral Surface of the Brain)
o Lateral Portion of the Frontal Lobe (Incl. Cortex)
o Lateral Portion of the Parietal Lobe (Incl. Cortex)
o Entire Temporal Lobe (Incl. Cortex)

- Posterior Cerebral Arteries:

o (Travels along the Inferior brain surface between the Cortex and the Cerebellum)
o Inferior Portion of Temporal Lobe (Incl. Cortex)
o Posterio-Medial Portion of Parietal Lobe (Incl. Cortex)
o Entire Occipital Lobe (Incl. Cortex)

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The Blood-Brain Barrier:
- Isolates Brain from Blood to provide a Stable Environment, necessary for control & function of CNS Neurons.
- How?:
o 1. The Endothelial Cells of the CNS Capillaries are seamlessly joined by Tight Junctions.
§ This prevents diffusion of most materials except dissolved gasses & lipid-soluble compounds.
§ Therefore, any required water-soluble compound must be transported across the BBB.
o 2. Thick Basement Membrane of Capillary

o NB: In the 2 Choroid Plexuses, the BBB is formed by Tight Junctions between Glial (Eppendymal)
Cells as the capillaries in this region are Fenestrated & highly leaky.

- The BBB exists everywhere except:

o Hypothalamus – (Monitors chemical composition of blood. Ie. Hormone levels, water balance, etc)
o Vomiting Centre - (Monitors poisonous substances in blood)

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Venous Drainage of the Brain – Via “Dural Sinuses”:
- Venous Drainage begins with venous blood collecting in small venous channels known as “Dural Sinuses”.
- Sinuses Sit Within The Dura-Mater:
o The Dura-Mater is the thickest & outermost of the 3 Meninges of the brain. It extends deep into the
brain in 2 locations, the Falx Cerebri & the Tentorium Cerebelli:
§ 1. Falx Cerebri:
• The Dura Mater folds deep into the Longitudinal Fissure (Falx Cerebri) of the brain,
where it forms 2 Sinuses:
o 1. A Triangular ‘Superior Sagittal Sinus’ at the top of the dural fold.
o 2. A lower ‘Inferior Sagittal Sinus’ at the bottom of the dural fold.
§ NB: Inf. Sagittal Sinus merges to form the ‘Straight Sinus’.

§ 2. Tentorium Cerebelli:
• The Dura Mater folds deep into the Transverse Cerebral Fissure (Tentorium
Cerebelli) of the brain, where it forms a pair of sinuses:
o The R.&L. “Transverse Sinuses”.
o NB: All blood from Sup. & Inf. Sagittal Sinuses and the Straight Sinus empties
into these Transverse Sinuses.

o The L.&R. Transverse Sinuses then become the L.&R. Sigmoid Sinuses (Respectively).
o These Sigmoid Sinuses turn Inferiorly and become the Internal Jugular Veins.

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Regulation of Blood Flow to the Brain:
- Blood Flow to the Brain is AUTOREGULATED:
o Ie. BP in the Brain is kept constant, despite systemic BP fluctuations.
o It also means different areas of the brain control their blood flow depending on metabolic activity.
- The Myogenic Autoregulation of Blood Flow to the Brain:
o When Mean Arterial Pressure rises, the SNS constricts the larger arteries of the brain to prevent
damaging high pressures in the smaller, more delicate vessels. (Important for preventing Stroke)
- The 3 Metabolic Autoregulatory Factors Affect Blood Flow to the Brain:
o **1. Blood [CO2]:
§ ↑[CO2] à Vasodilation (to ↑ Blood Flow)
§ ↓[CO2] à Vasoconstriction (to ↓ Blood Flow)
o 2. Blood/CSF pH:
§ ↑[CO2] à ↑[H+] via carbonic anhydrase à ↓pH à Vasodilation (to ↑ Blood Flow)
+
§ ↓[CO2] à ↓[H ] via carbonic anhydrase à ↑pH à Vasoconstriction (to ↓ Blood Flow)
o 3. Blood/CSF [O2]:
§ ↓[O2] à Vasodilation (to ↑ Blood Flow)
§ ↑[O2] à Vasoconstriction (to ↓ Blood Flow)

Reabsorption of CSF into the Dural Sinuses:

- NB: CSF is constantly being produced, and therefore must also be constantly drained to prevent a rise in
intracranial pressure. Therefore:
- CSF is Reabsorbed into the Venous System via diffusion through Arachnoid Villi.
o Arachnoid Villi are invaginations of Arachnoid Mater through the Dura Mater and into the Superior
Sagittal Sinus.
- Water Diffuses from Arachnoid Villi à Sup. Sagittal Sinus Due To:
o 1. Higher Hydrostatic Pressure in Sub-Arachnoid Space.
o 2. Higher Colloid-Osmotic Pressure of the Venous Blood in the Sinus.

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Intracranial Pressure:
- What is it?
o The pressure within the cranium created by the cerebrospinal fluid (CSF), and exerted on the brain
tissue & the brain's blood circulation vessels.
- Determinants:
o CSF Production/Resorption (Eg. ↑Production + ↓Resorption)
o Brain Tissue (Eg. Tumour / Inflammation)
o Blood (Eg. Haemorrhage)
- High Intracranial Pressure:
o Compresses the Cerebral Arteries à Decreased Blood Supply à Brain Damage
o Can also displace the brain.
- Symptoms of High ICP:
o Altered Consciousness
o Changes in BP & HR
o Changes in Eye Responses
o Changes in Motor Function

Cerebral Oedema:
- What is it?
o An excess accumulation of water in the intracellular and/or extracellular spaces of the brain.
- Types of Cerebral Oedema:
o Vasogenic:
§ (Extracellular Oedema)
§ Due to a breakdown of tight endothelial junctions which form the BBB.
§ Eg. Hydrostatic Cerebral Oedema – where acutely high cerebral capillary pressure results in
fluid moving from Capillary to ECF.
o Cytotoxic:
§ (Intracellular Oedema)
§ Due to a defect in cellular metabolise à inadequate functioning of the Na/K-ATPase in the
cell membrane à cellular retention of H2O
o Osmotic:
§ (Extracellular Oedema)
§ Where a drop in Plasma Osmolality (compared to CSF Osmolality) causes water to flow from
the Venous Sinuses back into the Sub-Arachnoid Space.

Migraines:
- What are They?
o Incapacitating Neurovascular disorder characterized by unilateral, throbbing headaches,
photophobia, phonophobia, nausea & vomiting.
- What Causes Them?
o Decrease in Serotonin Levels à ↑Sensitivity to Migraine Triggers + Cerebral Vasoconstriction à
↓cerebral blood flow à Raphe Nuclei in Brain-Stem release Serotonin à Cerebral Vasodilation +
Release of ProInflammatory Mediators from Trigeminal Nerve & Spinal Nerves à Perivascular
Cerebral Inflammation à Pain.
- Classic Vs. Common:
o Classic:
§ Associated with ‘Aura’. (A visual symptom, such as an arc of sparkling (scintillating) zig-zag
lines or a blotting out of vision or both)
o Common:
§ Migraine without ‘Aura’ (Only 20% of sufferers experience aura. Most bypass the aura
phase)
- Migraines as a Risk Factor:
o ↑ Risk of Silent Post. Cerebral Infarcts.
o ↑ Risk of Stroke & CVD (Women)
o ↑ Risk of MI (Men)

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CVA’s – Cerebro-Vascular Accidents (Strokes):
- 3rd largest cause of death
- What is it?
o “The rapidly developing loss of brain function(s) due to disturbance in the blood supply to the brain.”
o The specific functional loss caused by a stroke depends on which artery/s and functional areas of the
brain are affected/occluded.

- 2 Forms of Stroke:
o Ischaemic:
§ Thrombotic
§ Embolic
o Haemorrhagic:
§ Bleeding à short-circuits blood flow + increases Intra-Cranial Pressure à Compresses other
Cerebral Arteries à Stroke.
• NB: Haemorrhages in the brain can lead to perfusion deficits à ↑CO2 + ↓pH à
Vasodilation of cerebral arteries à More blood flow to the bleeding area à more
bleeding à ↑Intracranial Pressure.

- 3 Common Causes of Stroke:

o Atherosclerosis –
§ Atherosclerotic Plaque within a cerebral artery ruptures causing thrombosis (blood clotting)
à ↓Blood Flow à Cerebral Ischaemia à Stroke.
§ Part of an Atherosclerotic Plaque that has broken off lodges in a cerebral artery à ↓Blood
Flow à Cerebral ischaemia à Stroke
o Heart Disease –
§ Eg. Atrial Fibrillation can cause clotting à thrombo-emboli lodging in cerebral artery à
↓Blood Flow à Cerebral ischaemia à Stroke
o Hypertension –
§ Puts high stress on blood vessel walls à blood vessel to thicken and break downà stroke.
§ Can cause clots or plaques to break off artery walls à block a brain artery à stroke.
§ In rare cases it can cause a haemorrhagic stroke in people who were born with irregular
formation of the blood vessel walls in the brain.

Measuring Brain Injury – The Glasgow Coma Scale:

- A scale that measures the conscious state of a person against certain criteria, and the resulting points give a
patient score between 3 (indicating deep unconsciousness) and 15 (full consciousness).

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Pictures for Your Interst/Reference:

Flow & Production of CSF

Venous Sinuses:

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 Meninges of the Brain

Summary of Arterial Supply of the Brain

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 Week 3
Neuroscience Notes
Neurotransmission

What is Neurotransmission?:
- Neuron à Neuron/Cel/Organ/Muscle/Etc. Communication
- Point of ‘Communication’ = The “Synapse”

Terminology:
- Pre-Synaptic Neuron: The ‘Sender’ Neuron
- Synaptic Cleft: The ‘Gap’ Between cells
- Post-Synaptic Cell: The ‘Receiver’ Cell
- Synaptic Potential: The ‘Drive’ for Transmission (that mobilizes the synaptic vesicles to pre-synaptic
membrane).

Neuron-Neuron Neurotransmission:
- NB: Neurons Synapse with Each Other in 3 Ways
- 3 Types of Synapses:
o 1. Axo-Somatic: Axon à Cell Body (For Modulatory Effects)
o 2. Axo-Axonic: Axon à Axon (For All/Nothing Signals)
o 3. Axo-Dendritic: Axon à Dendrite (For Multiple Inputs to a Neuron)

2 Types of Post-Synaptic Receptors:

- Ionotropic: (Ligand-Gated Ion Channels)
o Mech: Binding of Neurotransmitter à Opening of Ion Channel à Excitation/Inhibition of Cell.
§ Excitatory: Na+/Ca+ Channel – opening à Na+/Ca+ Influx à Depolarisation of Membrane à
à “Excitatory Post-Synaptic Potential” (EPSP)
§ Inhibitory: Cl- Channel – opening à Cl- Influx à Hyperpolarisation of Membrane à
K+ Channel – opening à K+ Efflux à Hyperpolarisation of Membrane à
à “Inhibitory Post-Synaptic Potential” (IPSP)
- Metabotropic: (G-Protein Linked Receptors)
o Mech: Binding of Neurotransmitter à Activates G-Protein à Activates ‘Effector’ Proteins à Activate
secondary Messengers (Eg. cAMP) à Regulates Ion Channels/Activates Enzymes/Alters Metabolism.

Actions of Neurotransmission:
- Direct Physiological Action:
o Eg. Neuromuscular Junction à Muscle Contraction
o Eg. Sympathetic Synapse @ SA-Node à ↑Heart Rate
- Links in a Chain:
o Eg. Peripheral Sensory Neuron à Spinal Cord à Ascending Sensory Pathways à Thalamus à Cortex
- Modulation:
o Ie. Exerting a +ve/-ve influence on transmission by another neuron.

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Process of Neurotransmission:
1. Action Potential reaches axon terminal.
2. Voltage Gated Ca+ Channels open in response to Action Potential à Ca+ influx into Axon Terminal.
a. NB: the amount of Ca+ influx can be influenced by neuromodulators.
3. Migration of Neurotransmitter-Filled Vesicles due to Ca+ influx à Vesicles fuse with Presynaptic Membrane.
a. NB: The number of vesicles mobilised is Directly Proportional to the amount of Ca+ Influx.
4. Excytosis of Vesicles à Neurotransmitter release into Synaptic Cleft
5. Diffusion of Neurotransmitter Across Synapse à to the Post-Synaptic Membrane.
6. Binding of Neurotransmitter to Post-Synaptic Receptors:
a. Receptors may be:
i. Ionotropic – Ligand Gated Ion Channels.
ii. Or Metabotropic – G-Protein Linked Receptors.
b. Neurotransmitter may be:
i. Excitatory – Depolarise Post-Synaptic Membrane (By causing Na+ Influx)
ii. Or Inhibitory – Hyperpolarise Post-Synaptic Membrane (By causing Cl- Influx)
7. Termination of Signal – Either by Neurotransmitter Destruction/Inactivation or Re-Uptake into the Neuron.

Key Ions Involved in Neurotransmission:

- Na+: - Influx - To depolarise membrane to initiate/propagate an Action Potential
- K +: - Efflux - To repolarise the membrane to resting potential once the Action Potential has passed.
+
- Ca : - Influx - To trigger the Exocytosis of Neurotransmitter into Synaptic Cleft.

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For a Chemical to be a ‘Neurotransmitter’, it must have:
1. Dedicated Synthesis
a. NB: Amine & Amino-Acid Neurotransmitters are synthesized in the Axon-Terminal, HOWEVER,
Peptide Neurotransmitters are synthesized in the Cell Body & Transported to the Axon Terminal.
(This is because Peptide Synthesis requires Gene Transcription & Translation which require a Nucleus
& Rough Endoplasmic Reticulum.)
b. NB: There is a Rate-Limiting Step for all Neurotransmitter Synthesis.
(Eg. Activity/Amount of an Enzyme, Substrate Availability)
2. Active Packaging
a. Amine & Amino-Acid NT’s Actively Packaged Into Vesicles, Driven by H+ Gradient within Vesicle.
(Ie. H+-Filled Vesicles exchange H+ for Neurotransmitter)
b. Peptide NT’s Packaged by Golgi Apparatus & transported to Axon Terminal

(Notice The Different Pathways of Synthesis of Peptide-NT’s Vs. Amine/Amino-Acid -NT’s.)

3. Controlled Release
a. Various Proteins involved in Vesicle Mobilisation are activated by Ca+ Influx.
(NB: Many such proteins are destroyed by Botox, giving Botox recipients expressionless faces)
b. Vesicle-Membrane fuses with Presynaptic-Membrane, Creating a Release-Pore à NT Diffuses across
Synaptic-Cleft. Often some NT’s end up in other neighbouring synapses.

à à
4. Receptive Post-Synaptic Cell
a. Neurotransmitter Activates either:
i. Ionotropic Receptors: (Ligand-Gate Ion Channels)
ii. Metabotropic Receptors: (G-Protein Linked Receptors à Secondary Messengers)
5. Signal Termination Mechanism
a. To Prevent Over-Release of NT, Autoreceptors exist on Pre-Synaptic Membrane.
i. Provide –ve feedback by inactivating Adenylate Cyclase à ↓cAMP à Closes Ca+ Channels
à Stops Vesicle Mobilisation & Release
b. To Prevent On-Going Stimulation, a NT’s signal is terminated by either:
i. Synaptic Enzyme: (Destroys the NT in the Synapse)
ii. Rapid Re-Uptake: (Transport of NT Back into Pre-Synaptic Cell)
NB: For NT’s taken back up, there are 2 fates:
1. Recycling (Repackaged into Synaptic Vesicles)
2. Enzymatic Degradation (NT is broken down into Metabolites)

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Regulation of Receptor Response:
- If NT is Over-Released and/or Not Terminated à On-Going Stimulation à Receptor Activity is Altered:
o Desensitisation: ↓Response to NT due to ↓Sensitivity of the Receptor.
o Down-Regulation: ↓Response to NT due to ↓# of Receptors.
NB: This functions to block out “Noise”.
- If NT is Under-Released or if Antagonist is Administered for Too Long à Receptor Activity is Altered:
o Supersensitisation: ↑Response to NT due to ↑Sensitivity of the Receptor.
o Up-Regulation: ↑Response to NT due to ↑# of Receptors.

Neuromodulation:
- Ie. The Fine-Tuning (“Volume Control”) of a signal.
- A Neuromodulator can be conceptualized as a neurotransmitter that is not reabsorbed by the pre-synaptic
neuron or broken down into a metabolite. Such neuromodulators end up spending a significant amount of
time in the CSF (cerebrospinal fluid), influencing (or modulating) the overall activity level of the brain.
- Hence creates a Broad Signal across the brain à Synchronous activation of Separate Regions à Elicits
markedly different level of responses from Synaptic Activity.
- Neuromodulators may either be released into a Synaptic Cleft, or Extracellular Fluid.
- Types of Neuromodulators:
o Metabolic Products (Eg. Adenosine, ATP, H+)
o Hormones (Eg. Oestrogen)
o Gases (Eg. Nitric Oxide, CO2)
o Amines (Eg. Dopamine, Serotonin, Histamine, Acetylcholine)
o Proteins
o Prostaglandins
o Etc.Etc. (ie. There are loads!)

The Neurotransmitters

The Major Neurotransmitters (Classified by Structure):

- **Amines (“Classical Neurotransmitters”):
o Acetylcholine (ACh)
o Dopamine
o Noradrenaline/Norepinephrine (NA/NE)
o Epinephrine
§ (NB: NE is the Neurotransmitter, while Epinephrine is the Hormone)
o Serotonin/5-Hydroxyl Tryptamine (5-HT)
o Histamine
- Amino Acids:
o Glutamate (#1 Excitatory Neurotransmitter of the Brain)
o γ-Amino Butyric Acid (GABA) (#1 Inhibitory Neurotransmitter of the Brain)
o Glycine
o Aspartate
- Peptides:
o Cholecystokinin
o Enkephalins (Eg. Endorphins, Opioids) (Turn off Nociceptive/pain Pathways)
o Neuropeptide Y (Regulates Food Intake/Hunger)
o Somatostatin
o TRH
o Vasoactive Intestinal Peptide (VIP)

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Acetylcholine/ACh (Cholinergic Nerves):
- Roles:
o Brain Functions:
§ Voluntary Motor Control
§ Memory & Learning Pathways
§ Arousal
§ Sleep/Wake Cycles
o Peripheral Functions:
§ Contraction of Skeletal Muscle
§ Parasympathetic Activity in the
Heart/GI/Eye/Salivary Glands/Lacrimal
(Tear) Glands

- ACh Synthesis:
o Choline + Acetyl-CoA are combined by Choline-Acetyl-Transferase (CAT) to form Acetylcholine + CoA
§ (Hence, Choline & the Acetate group from the Acetyl-CoA combine à ACh)
§ NB: This occurs in the cytosol of the Neuron at the Axon-Terminal.
- ACh Packaging:
o ACh is concentrated into Vesicles by an ACh-Transporter
- ACh Release:
o Via Ca+ Mediated Vesicular Exocytosis
- Cholinergic Receptors (2 Types):
o 1. Muscarinic: - G-Protein Linked/Metabotropic Receptors (Parasympathetic NS)
o 2. Nicotinic: - Ligand-Gated Ion Channels/Ionotropic Receptors (Neuromuscular Junction/CNS/PNS)
- ACh Signal-Termination:
o ACh is degraded within the synapse by Acetyl-Choline Esterase à Choline + Acetate
o The Choline released is Actively Transported back into the Pre-Synaptic Cell by a Choline Transporter
- Rate-Limiting Step:
o The Reuptake of Choline; Because the availability of Choline determines the amount of ACh synthesis

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Catecholamines (Dopamine/Nor-Epinephrine(Nor-Adrenaline)/Epinephrine(Adrenaline):
- Dopamine:
o Roles:
§ Brain Functions:
• Voluntary Motor Control
• Cognition
• Reward Centre
• Emotions & Behaviour
• Vomiting
§ Peripheral Functions:
• Cardiovascular Function (↑HR &
Contraction)
• Renal Vasodilation @ JG
Apparatus (↑Filtration)

o Synthesis:
§ Starts with Tyrosine (Amino Acid)
§ Tyrosine is converted to Dopa by
Tyrosine-Hydroxylase
§ Dopa is converted to Dopamine by Dopa-Decarboxylase
o Packaging:
§ Dopamine is packaged into vesicles in Axon Terminal.
o Release:
§ Via Ca+ Mediated Vesicular Exocytosis
o Dopaminergic Receptors:
§ - Are Metabotropic (G-Protein Linked Receptors)
NB: All Catecholamine Receptors are Metabotropic.
o Dopamine Signal-Termination:
§ Active Re-Uptake into the Axon via Na+-Dependant Transporters à Repackaged/Destroyed.
• NB: If Destroyed – Via enzymatic degradation by Mono-Amine Oxidase (MAO).
o Rate-Limiting Step?:
§ Conversion of Tyrosine à Dopa by Tyrosine-Hydroxylase
§ Hence, the activity of Tyrosine-Hydroxylase is ‘rate-limiting’ for All Catecholamine Synthesis.

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- Nor-Epinephrine:
o Roles:
§ Brain Functions:
• Attention/Arousal (Fight/Flight
Response)
• Sleep-Wake Cycle
• Learning & Memory
• Anxiety
• Pain
• Mood
§ Peripheral Functions:
• Sympathetic Responses
• ↑HR + BP
• ↑Glycolysis + Gluconeogenesis +
Fat Metabolism
• ↑Blood flow to Muscles
• ↑Blood Flow to Coronary
Circulation
o Synthesis:
§ Starts with Tyrosine (Amino Acid)
§ Tyrosine is converted to Dopa by Tyrosine-Hydroxylase
§ Dopa is converted to Dopamine by Dopa-Decarboxylase
§ Dopamine is packaged into vesicles in Axon Terminal.
§ Dopamine is converted to Nor-Epinephrine (Nor-Adrenaline) by Dopamine-Hydroxylase
inside the Vesicles.
o Packaging:
§ Dopamine is packaged into vesicles in Axon Terminal before conversion to Nor-Epinephrine.
o Release:
§ Via Ca+ Mediated Vesicular Exocytosis
o Adrenergic Receptors:
§ - Are Metabotropic (G-Protein Linked Receptors)
NB: All Catecholamine Receptors are Metabotropic.
o Signal-Termination:
§ Active Re-Uptake into the Axon via Na+-Dependant Transporters à Repackaged/Destroyed.
• NB: If Destroyed – Via enzymatic degradation by Mono-Amine Oxidase (MAO).
o Rate-Limiting Step?:
§ Conversion of Tyrosine à Dopa by Tyrosine-Hydroxylase
§ Hence, the activity of Tyrosine-Hydroxylase is ‘rate-limiting’ for All Catecholamine Synthesis.

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Serotonin:
o Roles:
§ Brain Functions:
• Pain
• Wakefulness/Arousal
• Sleep-Wake Cycle
• Mood & Emotions
• Vomiting
• Circadian Rhythm (Indirectly
by conversion to Melatonin)
§ Peripheral Functions:
• GI Tract
• Platelet Function

o Synthesis:
§ Starts with Tryptophan
§ Tryptophan is converted to 5-HTP by Tryptophan Hydroxylase
§ 5-HTP is converted to 5-HT (Serotonin) by 5-HTP-Decarboxylase.
o Packaging:
§ Serotonin is packaged into vesicles in Axon Terminal.
o Release:
§ Via Ca+ Mediated Vesicular Exocytosis
o Serotonergic (5-HT) Receptors:
§ “5-HT” Receptors (Can have Ionotropic & Metabotropic Types)
o Signal-Termination:
§ Active Re-Uptake into the Axon via Na+-Dependant Transporters à Repackaged/Destroyed.
• NB: If Destroyed – Via enzymatic degradation by Mono-Amine Oxidase (MAO).
o Rate-Limiting Step?:
§ Availability of Tryptophan in the Extracellular Fluid. (Tryptophan is an Essential Amino Acid)
§ Hence, a dietary deficiency of Tryptophan à Depletion of Serotonin in the brain.

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Amino Acid Neurotransmitters:
- Glutamate:
o Roles:
§ Most common neurotransmitter in the brain.
o Synthesis:
§ Begins with conversion of Glucose à α-KetoGlutarate Via Glycolysis & TCA-Cycle.
§ Then conversion of α-KetoGlutarate à Glutamate via a Transaminase Reaction.
o Packaging:
§ Active Packaging in Vesicles
o Release:
§ Ca+ Dependant Exocytosis
o Receptors:
§ Ionotropic:
• NMDA Receptor
• Kainate Receptor
• AMPA Receptor
§ Metabotropic:
• mGluR Receptor
o Signal-Termination:
§ K+ Dependant Re-Uptake into Pre-Synaptic Neuron à Repackaged into Vesicles.

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 - GABA (Gamma Amino Butyric Acid):
o Roles:
§ Inhibitory Neurotransmitter in Brain
o Synthesis:
§ Begins with conversion of Glucose à α-KetoGlutarate Via Glycolysis & TCA-Cycle.
§ Then conversion of α-KetoGlutarate à Glutamate via a Transaminase Reaction.
§ Then conversion of Glutamate à GABA by Glutamic-Acid-Decarboxylase (+ VitB6).
o Packaging:
§ Packaged into vesicles by the Vesicular GABA Transporter (VGAT)
o Release:
§ Ca+ Dependant Exocytosis
o Receptors:
§ GABAA: - Ligand Gated Cl- Channels (Ionotropic)...Stimulation à Cl- Influx à Hyperpolarises.
§ GABAB: - G-Protein Linked (Metabotropic)...Stimulation à K+ Efflux à Hyperpolarises.
o Signal-Termination:
§ K+ Dependant Re-Uptake into Pre-Synaptic Neuron à Destruction by GABA-Transaminase.

- Glycine:
o Roles:
§ Inhibitory Neurotransmitter in the Fore-Brain, Brain-Stem & Spinal Cord
• Motor Functions
• Sensory Functions
o Synthesis:
§ Begins with Glucose à 3-Phospho Glycerate à Serine à Glycine
o Packaging:
§ Vesicles
o Release:
§ Ca+ Dependant Release
o Receptors:
§ Ionotropic Cl- Receptors à Cl- Influx à Hyperpolarisation.
o Signal-Termination:
§ Re-Uptake of Glycine into Pre-Synaptic Neuron

See SS Materials for Introductions to Myasthenia Gravis, Glaucoma & Parkinsons Disease.

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 Week 4
Neuroscience Notes
Memories

NB: We still don’t know where exactly long-term memory is stored.

- Believed that memory is stored throughout the brain.

However: We DO know that in creating memories, cells of the brain Change!!

- Eg. New Synapses: An Architectural Change in the brain
- Eg. Strengthening of Synapses: Functional Changes (Ie. LTP)

Process of Memory Creation:

1. External Stimuli:
a. Sensory input bombards the brain & is sent to Cerebral Cortex.
2. Temporary Storage (Cerebral Cortex):
a. Sorts & Evaluates the Information.
b. Depending which inputs you focus on, determines what info is sent to Short Term Memory.
i. Input not focussed on is Forgotten.
3. Short Term Memory:
a. In Medial Temporal Lobe (Hippocampus, Amygdala & Surrounding Cortical Areas).
b. Excitement/Rehearsal/Association/Emotion à Transfer to Long Term Memory.
i. Input not subjected to the above is Forgotten.
4. Long Term Memory:
a. Requires: ACh – for Declarative; or Dopamine – for Non-Declarative.
i. Declarative – Stored in ≈ Prefrontal Cortex
ii. Non-Declarative – Stored in ≈ Premotor Cortex.

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Short-Term Memory (STM):
- Based in Hippocampus.
o However, small links are established with Cortex (Visual/Auditory/Olfactory/Gustatory)
o These Links are made by Changes to Neuron Signalling that don’t require protein synthesis (Quicker)
- Lasts Seconds à Several Hours MAX. (AKA: “Crammers” Memory)
o Ie. Changes to Neurons are Transient. (Temporary)
- Limited to ≈7-8 “Chunks” of Info.
- Amnesia ≈ Damage to Connection between STM & LTM.

NB: Hippocampus sits in the Medial walls of the ‘Horns’ of the Lateral Ventricle.

Working Memory:
- NB: Often Grouped with STM.
- Temporary Retention, Integration (With other brain areas) & Manipulation of Sensory Info...
TO FACILITATE A RESPONSE.
o Eg. Crossing the Road:
§ 1. Look Left – Remember position of cars
§ 2. Look Right
§ 3. Look Left Again – Compare position of cars to the initial look à Is it safe to cross??
- Associated with Prefrontal Cortex:
o Closely tied to STM.
- Neurotransmitter:
o Dopamine

Long-Term Memory (LTM):

- Limitless Capacity:
o The amount we can remember depends on Access rather than Capacity.
- Usually Requires STM Input:
o Generally LTM-Creation requires the info to pass through STM first.
o However, some info can bypass STM by ‘hijacking’ existing LTM links
§ (Eg. Tying a fact to a Previously-Learned Fact)
- LTM Creation - Influenced by 4 Factors:
o 1. Genetics
o 2. Age
o 3. Trauma
o 4. Malnutrition
- LTM Creation – Improved by:
o Positive/Powerful Emotional State
o Rehearsal
o Association of New data with Old Data.
o The Belief that the Memory is Important
§ (Making memories is expensive & the brain must be convinced that it’s worth the expense)

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- 2 Types of Long-Term Memory:
o 1. Declarative (EXPLICIT):
§ Brain Regions:
• Hippocampus
• Para-Hippocampal Regions (Medial Temporal Lobe)
• Areas of Cerebral Cortex
• Thalamus + Hypothalamus
§ Learning “WHAT”:
• Facts/Words/Ideas/Concepts/Events

o 2. Non-Declarative (IMPLICIT):
§ Learning “HOW”: - How to do things/How to recognise things.
• Procedural:
o Walking
o Driving a car
o Doing Algebra
o How to get Home
• Priming (Anticipation): - ie. The use of a trigger to pull out a memory.
o Ache in gut if you get a letter from Tax Office – Due to Previous Association.
o Reaction to seeing your Partner.
• Classically-Conditioned:
o Emotional:
§ Eg. Fear when seeing a Shark.
§ Eg. Ringing Bell à Dog Salivates
o Motor:
§
• Non-Associative:
o Isolated events not linked to anything

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Circuit of Declarative Memory:
1. Outside Stimuli:
a. Afferent Sensory Info à Sensory Nerves à Spinal Cord à Medulla à Brain (Somatosensory Cortex)
2. Somato-Sensory Cortex:
a. Sensory Info is Sorted & Evaluated.
b. Whatever is the main focus of your attention is Prioritised à Sent to Short-Term Memory
In Medial Temporal Lobe (Hippocampus, Amygdala & Surrounding Cortical Areas).
3. Medial Temporal Lobe Areas:
a. Role: Memory Consolidation & Retrieval Via Communication with Thalamus & Prefrontal Cortex.
b. Basal Forebrain:
i. Primes the Medial-Temporal Lobe & Prefrontal Cortex with Acetylcholine à Triggers LTP in
Hippocampus
ii. à Enables Long-Term Memory Formation.
(NB: Loss of ACh input in Alzheimer’s à ↓Memory Formation & Retrieval.)
4. Feedback to Association Cortices:
a. Facilitates Retrieval of Memories.

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Circuit of Non-Declarative (Procedural) Memory:
1. Sensory & Motor Input:
a. Afferent Sensori-Motor Infoà Spinal Cord à Medulla à Brain (Association Cortices)
2. Association Cortices:
a. (Somatosensory/Visual/Auditory/etc)
b. Relay Sensori-Motor Inputs to the Basal Nuclei.
3. Basal Nuclei:
a. Relays Sensori-Motor Inputs through the Thalamus to the Premotor Cortex.
b. Substantia-Nigra:
i. Releases Dopamine onto Basal Nuclei à primes this circuit.
(NB: Loss of Dopamine Input – Ie. Parkinson’s – Interferes with Procedural Memory)
4. Premotor Cortex:
a. Plans & Organises learned Actions.

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 Long-Term Memory Formation @ the Cellular Level:

- Simply – By Remodelling the Neuron (Functionally/Structurally)

- More Specifically, Synaptic Remodelling:
o Critical to many neurological changes

Synaptic Remodelling:
- Long-Term Potentiation (LTP):
o Definition: “A Long-Lasting Post-Synaptic Depolarisation, induced through Repetitive Stimulation &
Summation of Excitatory Post-Synaptic Potentials.”
§ Simply – “A Persistent Increase in Synaptic Strength”
o Calcium, The #1 Mediator of LTP:
§ NMDA-mediated Ca+ Influx à Activation of Enzymes that cause:
• ↑Neurotransmitter Release
• Or Changes in Post-Synaptic Receptors
o The #1 Neurotransmitter:
§ Glutamate à binds to NMDA and/or AMPA Receptors.
• NMDA Receptors:
o Act as Coincidence Detectors (Simultaneous Signals)
o Ie. Detects coupling of occurrences.
o Is essentially a Ligand(Glutamate)-Gated Ca+ Channel
o Has a Voltage-Dependant Mg+-Block à Acts as a Voltage-Gate.
o Therefore, NMDA Receptor is Ligand & Voltage-Gated.

• AMPA Receptors:
o Is a Ligand-Gated Na+ Channel.
o When Glutamate Binds à Channel Opens à Depolarisation à AP.
o Action Potential ‘Kicks’ out the Mg+ Block on the NMDA Receptor.

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o 3 Phases of LTP:
§ 1. Induction - (Synaptic Plasticity)
• Alleviating of the NMDA-Receptor’s Mg+ Block.
o This may be done by:
§ AMPA-Receptor mediated Action Potential.
§ Metabotropic-Receptor linked to Ion-Channel à AP
§ 2. Expression - (Synaptic Augmentation)
• NMDA-Mediated Ca+ Influx à Activation of Enzymes that:
o 1. Modify Proteins in Post-Synaptic Terminal or ↑in Pre-Synaptic
Neurotransmitter Release à Strengthens response to subsequent Stimuli.
o 2. Activation of Genes in Post-Synaptic Neuron’s Nucleus à Synthesis of
Synaptic Proteins à ↑Synaptic Strength
§ 3. Maintenance - (Long Term Loss/Continuation of LTP)
• Rise in mRNA Levels à Augmented Synthesis of Proteins linked to Memory.
o This ↑in Protein Synthesis is regulated by a (+)Transcription Factor: “cAMP
Response Element Binding” protein (CREB).
o This perpetual ↑Protein-Synthesis à Long-Lasting ↑Synaptic Strength that
is believed to underlie memory.

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- Long Term Depression (LTD):
o Definition: “The Weakening of a Neuronal Synapse that lasts from hours-days.
o Calcium, The #1 Mediator of LTP:
§ NMDA-mediated Ca+ Influx à Activation of Phosphatases that cause:
• De-phosphorylation of AMPA-Receptors.
o à In Hippocampus à AMPA Dephosphorylation à ↓Amplitude of Post-
Synaptic Potential to the Normal Level (Prior to LTP).
o à Can also remove receptors from post-synaptic membrane & place them in
reserve.
o Results From:
§ Strong Synaptic Stimulation (Cerebellum)...Or
§ Persistent Weak Synaptic Stimulation (Hippocampus)
o Function in:
§ Overall:
• Plays a role in modulating impact of formed memories to prevent overload
§ Hippocampus:
• Thought to return LTP’d synapses back to a normal level so they will be available to
store new information.
§ Cerebellum:
• Thought to promote Motor Learning.

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 Common Memory Disorders:
- Alzheimer’s:
o What?:
§ Progressive memory loss (“Mild Cognitive Impairment”), Dementia & overwhelming
Retrograde & Anterograde Amnesia.
§ No real diagnostic tests.
o Genetic Aetiology: (Autosomal Dominant)
§ Amyloid Precursor-Protein Gene.
§ Presenilin 1 Gene
§ Presenilin 2 Gene
o Symptoms Due To:
§ Loss of ACh Innervation onto Prefrontal Cortex & Medial-Temporal Lobe (hippocampus) by
Basal Forebrain.
o Affects:
§ Basal Forebrain Cholinergic System (Ie. Loss of ACh innervation)
§ Striatum (Caudate & Putamen) – Part of Basal Ganglia.
§ Thalamus
§ Cerebellum
o Inability to:
§ Define simple words
§ Understand use of common items
§ Comprehend numbers
• Ie. A Loss in Declarative Memory.
o Emotional Disturbances:
§ Confusion
§ Agitation
§ Delusion
§ Paranoia
- Amnesia:
o Typically Declarative Memory Loss. (Therefore Hippocampal Damage)
o Commonly caused by Temporal Lobe Damage (Hippocampus and/or Thalamus)
§ NB: L-Hippocampus = Language
R-Hippocampus = Spatial Memory
o Anterograde:
§ - Inability to form new memories from time of Injury/Damage Onwards.
§ Non-Declarative Memory is Unaffected
o Retrograde:
§ - Inability to recall memories from time of Injury/Damage Backwards.
- Korsakoff:
o Anterograde & Retrograde Amnesia
o Caused by severe Thiamine Deficiency (Alcoholics & severe Malnutrition)
o àLoss of connection between Temporal Lobes (Hippocampus) & Frontal Cortex.

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 Week 5
Neuroscience Notes
Neurobiology of Emotions

Definitions: (You will not be asked for definitions in the exam) – (Not by Anna Marie Babey anyway)
- Affect:
o “The Experience of a Feeling/Emotion that’s NOT Related to Bodily Changes.”
- Emotion:
o “A Mental And Physiological reaction to stimuli, experienced as Affect plus Physiological Changes in
the Body.”
- Feelings:
o “A partly mental, partly physical response to a person, thing or situation, marked by pleasure, pain,
attraction or repulsion.”
- Arousal:
o “The Visceral (Body’s) Response to stimuli; Including Autonomic Nervous System & Neuro-
Endocrine Activity.”
- Cognition:
o “The process of knowing, including both awareness & judgement.”
- Behaviour:
o “The Active Response to Stimuli (Posture, Facial Expression, Speed, Eye Movement, Vocalisation,
etc)”

Emotion:
- Why does it Exist?
o Critical To Survival:
§ Both the ability to Experience Emotion and to Recognise Other’s Emotions
§ Gut Reactions
§ Recognising Danger, Friend/Foe
§ Vital to Decision Making
§ Important role in learning.
- Theories of Emotion:
o A link exists between Physiological Responses to Stimuli & Affect of Emotion, but which comes first?
§ Cannon-Bard Theory:
• Conscious Awareness of Emotion comes first, then the Visceral Reactions.
§ James-Lange Theory:
• Visceral Reactions comes first, then the Conscious Emotional Experience follows.

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 § Currently, the most Plausible Theory:
• Visceral Reaction (Physiological Responses) comes first, causing the Emotional
Experience (Feelings & Thoughts)
• However, the Emotional Experience can Influence and/or Perpetuate the Visceral
Response.

- 3 Phases/Components/Types of Emotion:
1. Primary Emotions:
§ “What is Felt 1st” – The 1st Instantaneous Emotion - (Usually the Simplest/Primitive Emotions)
§ Generally independent of culture (Universal)
• Joy
• Sadness
• Fear
• Anger
• Surprise
2. Secondary Emotions:
§ “What is Felt 2nd” – What the Primary Emotion Leads to – (Slightly more Complex Emotion)
§ Generally a Combination of Primary Emotions + Context.
• Affection/Love
• Lust
• Contentment
• Disgust
• Envy
• Guilt
3. Tertiary Emotions:
§ An Aggregate of Primary and/or Secondary Emotions – (The most Complex Emotions)
§ Generally the result of a Decision, taking into account Many Factors.
• Satisfaction
• Hope
• Frustration
• Gloom
• Contempt

- Physiological Context of Emotion:

o The physiological state of a person & body can influence resulting emotions & emotional reactivity.
§ Well-being
§ Depression
§ Calm
§ Tense
§ Fatigue

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Consciousness & Emotion:
- Emotional Experience is thought to underpin Consciousness. (Ie. Ability to “feel” is being “truly alive”)
- Consciousness:
o Core Consciousness:
§ Sense of ‘Here & Now’. “Feeling”
o Extended Consciousness:
§ Ability to Recall Past Experiences, Learn & Plan for the Future.

- Emotions affect the way we respond to stimuli:

o People with ‘Alexithymia’ can’t feel emotions. They experience:
§ Difficulty linking a Stimuli to an Experience
§ Serious Difficulty with Decision-Making
§ Difficulty Understanding Emotions
§ Difficulty Describing Emotions
§ Minimal Imagination
§ Feeling ‘cold’/‘alouf’

- Rational Brain Vs. Emotional Brain:

o Higher Cognitive Processing & Decision-Making relies on Co-Operation of the “Rational Brain” & the
“Emotional Brain”.
o Anatomically, the “Emotional Brain” is favoured. (Higher number & organisation of Synaptic
Connections)
o Relative Contributions of both “Rational” & “Emotional” Brains depend heavily on Context.
§ Eg. Triage – Letting someone die to save another’s life.
• Saving the one that can be saved is consistent with the “Rational Brain”
• However, letting someone die goes against the “Emotional Brain”.

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Neuroanatomy of Emotion – The Limbic System:
- The Papez Circuit:
o 1. Thalamus relays Sensory Input to Cingulate Cortex.
o 2. Cingulate Cortex - gives you the Emotional Experience
- also relays to the Neocortex, which gives Context/Colouring to the Emotion.
- also relays to the Hippocampus à
o 3. Hippocampus Relays to the Hypothalamus – Causes the Emotional Expression (Visceral Response)

- NB: No single region of the brain is responsible for Emotions. Instead, most regions involved have multiple
roles.

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Brain Regions Involved in Recognition, Induction & Regulation of Emotions:

- Thalamus:
o Funnels Sensory info to Amygdala, and the Cerebral & Cingulate Cortices.
o Important in Fact-Based (Explicit) Memory.

- Cingulate Gyrus:
o Regulates Attention
o Emotional ‘Colouring’

- Ventromedial Prefrontal Cortex:

o Conscious Recognition of Emotions

- Cerebral Hemispheres:
o R-Brain à More Associated with Negative Emotions
o L-Brain à More Associated with Positive Emotions

- Sensory Cortices & Association Areas:

o Recognition of Stimuli.
o Sensory Cortices: (Visual, Auditory, Olfactory, Gustatory, Tactile)
o Sensory Association Areas: (Novel Vs. Familiar)

- Insula:
o Involved with Recognition & Feeling of Disgust.

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- ***Amygdala***:
o #1 Structure involved in Emotion à The “Heart” of the Limbic System.
o “The Fight/Flight Centre”
o Linked to all but 8 areas of the Cortex à :. Thought to be #1 integrator of Cognitive & Emotional Info.
o Afferents (Receives Input From...):
§ Brainstem – inputs associated with Physical States (BP/HR/etc)
§ Hypothalamus - inputs associated with Physical States (BP/HR/etc)
§ Thalamus – Sensory Info
§ Hippocampus – inputs associated with Explicit Memory
§ Cortex – Sensory Inputs & Decisions related to Perceived Threats
o Efferents (Sends Output to...):
§ Brainstem – influences Visceral Fear-Driven, Fight/Flight Responses.
§ Hypothalamus – Influence on Memory & Aggression
§ Thalamus – Influences processing of new sensory info
§ Hippocampus – Fear is an important driver for learning & memory
§ Pre-Frontal Cortex – Fear is important in Decision Making & Cognition
o Regulates:
§ Fear & Aggression
§ Vigilance & Attention
§ Recognition of Emotion (in Self & Others)
§ Emotional Contribution to Memory. (Emotional Implicit Memory)

- Hypothalamus:
o Visceral Responses to Emotion
o Aggression
o Sex Drive

- Brain Stem:
o Visceral Responses to Emotion

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 AfraTafreeh.com exclusive

Neurotransmitters & Emotion:

- *Noradrenaline:
o Activated By:
§ Novel, Unexpected Stimuli
o Released By:
§ Locus Coeruleus (A Nucleus
In the Pons involved with
physiological responses to
stress & panic.)
o Regulates:
§ Mood/Arousal
§ Anxiety
§ Pain
§ Sleep/Wake Cycles
§ Motor Activity

- *Serotonin: What we target in treating Depression.

o Activated By:
§ General activity/arousal
o Released By:
§ Raphe Nuclei (A group of
Nuclei In the brainstem)
o Regulates:
§ Mood
§ Emotions
§ Sleep/Wake Cycles
§ Dominance/Aggression
§ Anxiety

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 - *Dopamine:
o Activated By:
§ Pleasurable Activities
o Released By:
§ Ventral Tegmental Area (VTA)
§ Substantia Nigra
o Regulates:
§ Somehow plays a role in Regulation of Perception of Emotion
§ Involved in Reward Centre

- Glutamate & GABA:

o Reduces Anxiety

- Acetylcholine:
o Released By:
§ Basal & Septal Nuclei of Meynert
o Regulates:
§ Cognitive Processing
§ Arousal & Attention

Panic Disorder:
- Overwhelming wave of Fear & Anxiety:
o Not necessarily associated with apparent trigger (Can be spontaneous)
- NB: Direct administration of CCK (Cholecystokinin) to brain can cause Panic-Attack Symptoms

Aggression:
- Affective Aggression Vs Predatory Aggression:
o Predatory aggression is related to feeding behaviour & isn’t accompanied by sympathetic
physiological response with which affective aggression is associated.
- Associated Structures:
o Cerebral Cortex
o Amygdala
o Hypothalamus
o Periaqueductal Grey-Matter (PAG)
o Ventral Tegmental Area (VTA)
IE. “Aggression is controlled by a neural pathway from the Amygdala through the Hypothalamus, PAG &
VTA.
- Neurotransmitter:
o Serotonin
- Possible Hormonal Link:
o Adenosine.

Pleasure & Reward: The ‘Reward Circuit’:

- Brain Structures Involved:
o *Ventral Tegmental Area (VTA)
o *Nucleus Accumbens
o Amygdala
o Pre-Frontal Cortex
o Thalamus
- Neurotransmitters Involved:
o *Dopamine - VTA & Nucleus Accumbens

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Fear:
- Brain Structures Involved:
o Thalamus à
§ Amygdala
o Thalamus à
§ Primary Sensory Cortex
§ Association Cortices
- Long & Short Pathways:
o Long:
§ Info processed by higher brain centres & Hppocampus.
§ Results in a more complex response
o Short:
§ Info sent straight to Amygdala
§ Results in a basic response (Recoil from stimulus/Freeze)
§ Advantage = No cortical processing means quicker reaction times à ↑Survival.
- Process of Fear:
o 1.Sensory Info enters brain à Thalamus
o 2.Thalamus Sends info to Amygdala (Via Long/Short Route)
o 3.Amygdala activates Visceral Responses through Hypothalamus
o 4.Amygdala Activates Ventromedial Pre-Frontal Cortex (Allows conscious recognition of the Emotion)
o 5.Visual Cortex also inform Prefrontal Cortex about the Threat.

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 Week 6
Neuroscience Notes
Somatosensory Processing

Sensation Types: NB: Sensations are initiated by RECEPTOR ACTIVATION.

- Tactile:
o Touch
o Vibration
o Stretch
o Pressure
o Itches
- Temperature:
o Hot/Cold
- Pain:
o AKA: ‘Nociception’
- Proprioception:
o Sensing the position of the body in space.
- Visceral:
o Blood Pressure
o pH
o O2
o CO2

Sensory Receptors:
What Are They?
- Specialized Nerve Endings that monitor & respond to the Environment.
Classification – Based on 3 Things:
- 1. Physical Location:
o Exteroceptors - Located in Skin (Respond to External Stimuli)
o Interoceptors - Located Viscerally (Respond to Internal Stimuli)
o Proprioceptors - Located in Muscle/Bone/Tendon
- 2. Type of Stimulus:
o Mechanoreceptors - Respond to Physical Forces
o Thermoreceptors - Respond to Temperature
o Nociceptors - Respond to Damaging Stimulus
o Chemoreceptors - Respond to Chemicals (Smell/Taste OR Blood O2/CO2/H+)
o Photoreceptors - Respond to Light (Eyes)
- 3. Receptor Structure
o Simple - Naked (“Free”) Nerve Endings (Pain & Temperature)
o Complex - Structurally Elaborate Nerve Endings (Pressure,Vibration, Stretch)
(Enhances Specificity)
NB: Q – Why are Pain Receptors ‘Simple’?
A – Pain, a basic survival mechanism would have been first to evolve and its receptors have been sufficient
since. Hence there has been no need for pain receptors to evolve further.

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Receptor Types:

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Receptor Transduction:
- Receptors respond to Stimuli by Transducing them into Electrical Signals
- These ‘Electrical Signals’ = Ion Movements across the Membrane à Changes Membrane Potential
o These Changes in Membrane Potential are Graded – IE. Stimulatory or Inhibitory (Depol/Hyperpol)
o These Graded Potentials at the Receptor Level = “Receptor Potentials”

- “Receptor Potentials” may summate to Threshold à Initiating an Action Potential

o These Action Potentials at the Receptor Level = “Generator Potentials”

Receptors: Nature of Activity:

- When Are They Active?
o Tonic Receptors:
§ Continually Firing
§ – Eg. Proprioceptors
o Phasic Receptors:
§ Fire only with a Change in the Environment.
§ – Eg. Thermoreceptors
- When Do They Inactivate? (How Quickly do they “Adapt”?):
o NB: “Adaptation” = Time Taken for receptor to Stop Firing during Sustained Stimulation
§ RARs – Rapidly Adapting Receptors:
• Receptor quickly stops firing under continuous stimulus
• - Eg. Touch Receptors (Can’t feel clothes after a while)
§ SARs – Slowly Adapting Receptors:
• Receptor maintains firing under continuous stimulus
• - Eg. Muscle Stretch Receptors (Proprioceptors)

Receptive Fields:
- A Receptive Field: The Area Monitored by 1x Receptor.
o Ie. Touch anywhere in that field, the sensation will come from the entire receptive field.

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 - Large Receptive Fields:
o Low Receptor Density
o Poor Localisation
o – Eg. Skin on your Back

- Small Receptive Fields:

o High Receptor Density
o Good Localisation
o – Eg. Skin on your Fingertips
o NB: 2 Point Discrimination is best with Small, Dense Receptor Areas

Somatosensory Pathways:
- First Order Neurons (Peripheral Afferent Nerves):
o (Eg. Dorsal Root of Spinal Nerves & Sensory Cranial Nerves)
o Sensory info is “Frequency Coded”.
o Enter Spinal Cord via Dorsal Nerve Root à Terminate in Dorsal Horn.
o NB: Cell-Bodies of the Pseudounipolar-Neuron Receptors culminate in the Dorsal Root Ganglion

o Vary by Diameter & Myelination – Affects Speeds of Conduction & Therefore type of Sensory Info:
§ Larger + Myelinated = Fastest
§ Smaller + Non-Myelinated = Slowest

NB: Proprioceptors are FAST to Ensure FINE MOTOR CONTROL.

NB: There are 2 Types of Pain Receptors – The Fastest is responsible for the Initial (Sharp) Pain
– The Slowest is responsible for the Dull Ache that follows.

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- Second Order Neurons (Ascending Pathways of Spinal Cord):
o Once inside the Spinal Cord, 1st-Order Neurons à Synapse with 2nd-Order Neurons
o 2nd-Order Neurons:
§ Often responsible for Decussation (Crossing of Fibre-Tracts to the Other Side of the Body)
§ Different 1st-Order Neurons à Synapse with different 2nd-Order Neurons.....
• Therefore, Different Sensory Info takes Different Ascending Pathways to the Brain.

- Third Order Neurons:

o NB: 3rd-Order Neurons are only Relevant to the Posterior Column & The SpinoThalamic Pathways.
§ The SpinoCerebellar Pathway terminates in the Cerebellum with 2nd-Order Neurons.
o Carry Sensory Info from Thalamus à to Primary Somatosensory Cortex in Parietal Lobe.
§ Thalamus – Sorts incoming Sensory Info à Sends it to Cortex.

(The Dark Blue Area)

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The 3 Ascending Pathways:
- Posterior Column Pathway:
o Synapses with 2nd-Order Neurons in
Medulla
o Decussate in the Medulla
o Neurons Are:
§ Large & Myelinated
§ Rapidly Adapting
o Sensory Info:
§ Touch
§ Vibration
§ 2-Point Discrimination
§ Proprioception

- SpinoThalamic Pathway:
o Synapses with 2nd-Order Neurons in
Spinal Cord @ Level of Spinal Root
o Decussate in Spinal Cord @ Level of
Spinal Root.
o Neurons Are:
§ Small & Myelinated
§ Slowly Adapting
o Sensory Info:
§ Crude Touch & Pressure
§ Pain
§ Temperature

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 - SpinoCerebellar Pathway:
o Synapse with 2nd-Order Neurons in Spinal Cord
o Doesn’t Decussate – Remains Ipsilateral
§ (“On the Same Side of the Body”)
o Neurons Are:
§ Large & Myelinated
§ Slowly Adapting
o Sensory Info:
§ Proprioception from:
• Muscle Spindles
• Golgi Tendon Organs
• Joint Capsules
§ à Coordinate Skeletal Muscle Activity

Somatosensory Processing:
- Somatosensory Cortex:
o Roles:
§ Detection of Sensation & Conscious Awareness of Sensation
§ Feature/Quality Recognition (ie. Texture/Size/Shape)
o Exhibits ‘Somatotopy’ (Body Mapping)
§ – ie. Specific Cortical Areas responsible for Particular Body Regions
o Receptor Density in a Body Region determines the Size of the respective Cortical Area. – See Below:

- Somatosensory Association Area:

o The Somatosensory Cortex has Connections to the Somatosensory Association Areas
o Role:
§ Compares Received Stimulus to Past Experiences.

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 Week 7
Neuroscience Notes
Motor Processing

Motor Processing Hierarchy - The Levels of Motor Control:

- 1. Ready (Strategy) – Deciding ‘What to do’:
o Prefrontal Cortex
o Somatosensory Association Cortex (5 & 7)
o Basal Ganglia (NB: Basal Ganglia are
the interface between ‘Strategy’ &
‘Tactics’.)
- 2. Set (Tactics) – Deciding ‘How to do it’:
o Basal Ganglia
o Pre-Motor Area (PMA)
o Supplementary Motor Area (SMA)
- 3. Go (Execution) – ‘Action’:
o Primary Motor Cortex (M1)
o Cerebellum
o Brainstem
o Descending Tracts
o Spinal Nerves
o Peripheral Motor Neurons

Brain Regions involved in Voluntary Motor Movement:

- Cortical Regions:
o Pre-Frontal Cortex (Frontal Lobe)
o Somatosensory Association Areas (Parietal Lobe)
o Pre-Motor Area (Frontal Lobe)
o Supplementary-Motor Area (Frontal Lobe)
o Primary Motor Cortex (M1) (Frontal Lobe)
§ Broca’s Area (Frontal Lobe)
- Sub-Cortical Regions:
o Basal Ganglia
o Cerebellum

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Roles of these Brain Regions (In Motor Processing):
- Pre-Frontal Cortex:
o Consciously Decides ‘what movement’ is required for the desired outcome. (Managerial Function)

- Somatosensory Association Areas:

o Tells the brain where the body is in space (Proprioception)

- Pre-Motor Area & Supplementary-Motor Areas:

o Plans ‘how to do the movement’.
o Is also the memory bank of Complex, Patterned & Highly Skilled Learned Movements.

- Primary Motor Cortex (M1):

o ‘Initiates the movement’ (Typically precise or skilled voluntary movement)
o NB: M1 also exhibits Somatotopy – The Bigger the Cortical Area, The More Precise the Movements
o Receives Direct & Indirect Inputs:
§ Direct – From: Prefrontal Cortex, SMA/PMA, Somatosensory Areas
§ Indirect – From: Cerebellum (Via Thalamus)
o Broca’s Area – Area of M1 that controls the Muscles responsible for speech (Tongue/Jaw/Lips/Face)

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- Basal Ganglia:
o Involved in Action-Selection & Initiation of Voluntary & Patterned Movements (Eg. Walking)
§ Motor Control & Motor Learning
• NB: Also has a role in Cognition & Memory
o A Loop Exists between the Cortex à Basal Ganglia à Thalamus à Pre-Motor Cortex à Cortex
§ Receives inputs from the Entire Cortex. (SMA/Prefrontal Cortex/Sensory Cortex/M1)
• Info travels through Basal Ganglia in This Order: StriatumàGlobus Pallidus.
§ Sends info to the PMA & *SMA via the (Ventro-Lateral Nucleus of the) Thalamus (VLo)

NB: The GLOBUS PALLIDUS is Spontaneously Active:

Globus Pallidus à Thalamus (Inhibits Thalamic-SMA Activity à Keeps the SMA ‘Quiet’)

o Consists of:
§ Striatum:
• Caudate Nucleus: Cognition & Behaviour
• Putamen: Motor (Automatic performance of previously learned movements.)
§ Globus Pallidus
o & Other Associated Structures:
§ Subthalamic Nuclei
§ Substantia Nigra: Eye Movement, Motor Planning, (Reward Seeking, Learning, & Addiction)

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- Cerebellum:
o A Loop exists between the Cortex à Pons à Cerebellum à Thalamus à M1 à Cortex.
§ Receives inputs from the Cerebral Cortex (M1, PMA, *Somatosensory Areas) via the Pons.
• Also receives Proprioceptive Feedback
§ Sends info to the Primary Motor Cortex (M1) via the VentroLateral Nucleus of the Thalamus.
• Informs Primary Motor Cortex (M1) about Direction, Force & Timing of Movements.

o Functions:
§ Precise Timing & Appropriate Patterns of Skeletal Muscle Contraction – Required for Smooth,
Coordinated movements & agility needed for daily living (Driving/Typing/Playing Music/etc)
§ Involved in the Correct Sequencing & Coordination of Muscle Contractions.
§ Involved in Motor Learning – Compares intention with result & corrects for next time.
§ Balance & Posture
o NB: Cerebellar Activity is Subconscious (Ie. We have no awareness of its functioning.)
o Output into Descending Pathways:
§ Vermis à Ventromedial Pathways
§ Hemispheres à Lateral Pathways

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o Cerebellar Processing:
§ 1. Cortical Motor Areas Notify the Cerebellum (via ‘relay nuclei’ in the brainstem) of their
intent to initiate voluntary muscle contractions.
§ 2. Constant Proprioceptive Input (Muscle/Tendon Tension, Joint Position, etc) enables the
cerebellum to evaluate the body’s position & momentum.
§ 3. Cerebellum calculates optimum Force, Direction & Extent of Muscle Contraction to ensure
Smooth, Accurate & Coordinated Movements.
§ 4. Cerebellum sends its “Blueprint” for coordinating movement to the Cerebral Motor Cortex
via the Superior Peduncles. It also sends info to Brainstem Nuclei à Influences Motor
Neurons of the Spinal Cord.
o Analogy:
§ Just as an ‘Autopilot’ compares a plane’s instruments with its planned course, the
Cerebellum continually compares the higher brain’s intention with the body’s performance
& makes appropriate corrections.

NB: The Cerebellar Peduncles

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Descending Tracts Involved in Motor Function:
- Descending Motor Pathways:
o Lateral Pathways:
§ 2 Divisions:
• #1 Corticospinal Tract:
• Rubrospinal Tract:
§ Roles:
• Both Tracts – Voluntary Movement of Distal Extremities (Particularly Hands & Feet)
§ Corticospinal Tract Receives Input From:
• Primary Motor Cortex (M1) – The Main Origin
• Pre-Motor Area
• Supplementary Motor Area
• Somatosensory Areas
§ Rubrospinal Tract Receives Input From:
• Primary Motor Area (M1)
• Pre-Motor Area
• Supplementary Motor Area
• Cerebellum
§ Efferent Pathway of Upper Motor Neurons:
• Corticospinal Tract:
o Originates in Primary Motor Cortex
o Run through the Internal Capsule to the Brainstem.
o Decussate in Medullary Pyramids (Medulla)
• Rubrospinal Tract:
o Originates in Red Nucleus of Midbrain.
o Decussate immediately below Red Nucleus (In the Pons)
àà
o Continue down the spinal cord in the Lateral White Matter.
o Terminate in Ventral Horn of Spinal Grey Matter

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o Ventromedial (Indirect/Extrapyramidal) Pathways:
§ 4 Divisions:
• Tectospinal (AKA: Colliculospinal) Tract
• Vestibulospinal Tract
• Pontine Reticulospinal Tract
• Medullary Reticulospinal Tract
§ General Roles – Reflexively Maintains:
• Head & Eye Coordination (“Visual Tracking”)
• Balance
• Muscle Tone Ie. Proximal & Axial Muscle Groups (Trunk/Hip/Neck/Back/etc)
• Body Posture
§ Specific Functions:
• Tectospinal/Colliculospinal: Visual Tracking (Head/Eye Coordination)
• Vestibulospinal: Maintain Balance During Standing & Moving
• Pontine Reticulospinal: Maintains Muscle Tone & Visceral Motor Functions
• Medullary Reticulospinal: Maintains Muscle Tone & Visceral Motor Functions
§ Origins:
• Tectospinal/Colliculospinal: Superior Colliculus of Midbrain (in Brain Stem)
• Vestibulospinal: Vestibular Nuclei in Medulla (in Brain Stem)
• Pontine Reticulospinal: Pontine part of Reticular Formation of Brainstem
• Medullary Reticulospinal: Medullary part of Reticular Formation of Brainstem
§ All Divisions Receive Some Input From:
• The Corticospinal (Pyramidal) Pathways – Project into & Influence the Activity of
these Brainstem Motor Nuclei (From which these tracts originate)

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- NB: These Descending ‘Upper Motor Neurons’ Terminate in the Ventral Grey Horns of the Spinal Cord Grey
Matter by Synapsing with either:
o Spinal Interneurons – Enabling info to be sent to multiple outputs.
§ Some Interneurons are ‘Central Pattern Generators’ à generate timing for patterned
movements (Eg. Walking)
o Or Lower Motor Neurons – That directly innervate skeletal muscle.

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Marieb’s Version of Descending Motor Pathways & Spinal Cord Tracts:

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 Week 8
Neuroscience Notes
The Peripheral Nervous System

Composition of PNS:
- Spinal Nerves
- Cranial Nerves
- Peripheral Branch of Autonomic NS:
o Sympathetic Trunks & Ganglia
o Enteric Nervous System (Alimentary
Tract)

Functional Divisions of PNS:

- Afferent (Sensory)
- Efferent (Motor):
o Somatic/Voluntary (Skeletal Muscle)
o Autonomic:
§ Sympathetic
§ Parasympathetic

This Week’s Focus = The Autonomic Nervous System:

- Effectors:
o Cardiac Muscle
o Smooth Muscle
o Glands
o (As opposed to the Somatic-NS & Skeletal Muscle)

- Efferent Pathways & Ganglia:

o As opposed to the Somatic-NS which uses a mono-synaptic
system (& Hence Lacks Ganglia), the Autonomic-NS uses a
2-Neuron-Chain system.

o 1. The Pre-Ganglionic Neuron:

§ The Cell-Body of the first neuron
§ Resides in the Brain or Spinal Cord
o 2. The Pre-Ganglionic Axon:
§ Synapses with a Ganglionic Neuron.
§ (Thin, Lightly Myelinated Fibres)
o 3. The Ganglionic Neuron:
§ Resides in an ‘Autonomic Ganglion’ outside the CNS.
o 4. The Post-Ganglionic Axon:
§ Extends from the Ganglion to the Effector Organ.
§ (Fibres are even Thinner & Totally Unmyelinated)

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Divisions of the Autonomic NS:
- The 2 Divisions of the ANS (Sympathetic & Parasympathetic) serve the same visceral organs, but cause
Opposite Effects. This Dual Innervation counterbalances each division’s activities à Maintains Homeostasis.
- Sympathetic:
o “Fight/Flight”
o Mobilizes the body during activity
o Effects are Widespread
- Parasympathetic:
o “Rest/Digest”
o Conserves Body Energy & Promotes Maintenance Functions.
o Has relatively Short-Lived Effects (Due to short-acting nature of Acetylcholine)
o Effects are relatively Localised

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 Anatomy of the Autonomic NS:

Sympathetic & Parasympathetic Divisions Differ Anatomically in 3 Ways:

- 1. Site of Origin
- 2. Fibre Lengths
- 3. Location of Ganglia

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Anatomy: The Parasympathetic (Craniosacral) Division:
- Fibres originate from:
o Brain Stem
o Sacral Region of Spinal Cord
- Fibre Lengths:
o Preganglionic Fibres – Extend nearly all the way to the structures to be innervated.
o Postganglionic Fibres – Very Short; Extend from the Terminal Ganglia & synapse with Effector Cells.
- Ganglia Location:
o The ‘Terminal Ganglia’ are located Very Close To or Within the Target Organs.

- The Cranial Outflow:

o Fibres Originate From Cranial-Nerve Nuclei in the Brain Stem.
o Fibres Extend to their Terminal Ganglia via 4 of the paired Cranial Nerves:
§ III – Oculomotor Nerves à Pupil Constriction & Lens Accommodation (close sight)
§ VII – Facial Nerves à Stimulate large Glands in the head
(Nasal/Lacrimal/Submandibular & Sublingual Salivary)
§ IX – Glossopharyngeal Nerves à Stimulate Parotid Salivary Glands
§ X – Vagus Nerves à Serves virtually all organs of the thoracic & abdominal
Cavities (Except Distal Large Intestine)
- The Sacral Outflow:
o Fibres Originate from Neurons in the Lateral Gray Matter of Spinal Cord Segments S2-S4.
o Fibres Extend to their Terminal Ganglia via Splanchnic Nerves of the Pelvic Plexus.
o Serve Distal Large Intestine & the Pelvic Organs (Bladder, Ureters, Repro. Organs)

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Anatomy: The Sympathetic (Thoraco-Lumbar) Division:
- NB: Sympathetic-NS innervates more organs than the Parasympathetic, and its effects are longer-lasting.
- Fibres originate from:
o Cell bodies of Preganglionic Neurons in the Lateral Horns Spinal Cord Segments T1 à L2.
- Fibre Lengths:
o Preganglionic Fibres – Exit the Spinal Cord via the Ventral Root à Then pass through a White Ramus
Communicans à Synapse adjoining Sympathetic Trunk (Chain) Ganglion.
(NB: These fibres are short)
o Postganglionic Fibres – Exit the Sympathetic Ganglion at/below/above their spinal level via a Gray
Ramus Communicans à Then enters the Ventral Spinal Nerve at that level à
Effector Organs.

NB: The Colour of the Rami Communicans reveals whether or not their fibres are myelinated.
Preganglionic Fibres = Myelinated Postganglionic Fibres = Unmyelinated

- Ganglia Location:
o Sympathetic Trunks (Chains of Ganglia) Flank each side of the Vertebral Column from the Neck to
Pelvis.

NB: Although the Sympathetic Trunks exist along the length of the spinal cord, the Fibres arise only
from Thoracic & Lumbar cord segments.

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Visceral Reflexes:
- Similar to the Somatic-NS, the ANS also has reflex arcs;
- Visceral Reflex Arcs Components:
o Visceral Sensory Neurons (Chemical Changes/Stretch/Irritation of Viscera)
Neurons originate in Sensory Ganglia of Cranial Nerves or Dorsal
Root Ganglia.
o Integration Centre
o Motor Neuron
o Effector

- This Explains the Phenomenon of ‘Referred Pain’:

o Visceral pain afferents enter the spinal cord via the Dorsal Root Ganglion, the same pathway as
somatic pain fibres. Hence pain stimuli arising in the Viscera can be confused as Somatic in origin.

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 Physiology of the Autonomic NS:

Neurotransmitters of the PNS:

- Afferent (Sensory): *Glutamate*/Calcitonin-Gene-Related Peptide/Substance P
- Efferent (Motor):
o Somatic/Voluntary (Skeletal Muscle): Acetylcholine (ACh)
o Autonomic:
§ Sympathetic:
• Preganglionic: Acetylcholine (ACh) àStimulates Ganglia & Adrenal Medulla
• Postganglionic: Norepinephrine
• àAdrenal Medulla: Stim. by Acetylcholine (ACh) to release Epinephrine & NE
into Blood.
§ Parasympathetic:
• Preganglionic: Acetylcholine (ACh)
• Postganglionic: Acetylcholine (ACh)

Somatic Division: Axons extend from CNS to their Effectors (Skeletal Muscle). They are typically Thick & Heavily
Myelinated and have a High Conduction Speed.
Their Neurotransmitter is Acetylcholine, and its effect is always Stimulatory.

Autonomic Division: Pre-Ganglionic Axons extend from CNS & synapse with either: (1) Peripheral Autonomic Ganglia,
or (2) Cells of the Adrenal Medulla; and release Acetylcholine.
(1) Post-Ganglionic Axons extend from Ganglia to Effectors & Release Either:
ACh (Parasympathetic)
or NE (Sympathetic)
(2) Adrenal Medullary Cells Release NE & Epinephrine into the Blood.

(NB: Pre-Ganglionic Fibres are Thin & Lightly Myelinated & Post-Ganglionic Fibres are Thinner & Unmyelinated.
Hence Conduction Speed within the Autonomic Neurons is Slow – Much slower than Somatic NS)

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 AfraTafreeh.com exclusive

Receptors of the ANS:

- Parasympathetic - Cholinergic (ACh) Receptors:
o Nicotinic:
§ Found on:
• (Motor End-Plates of Skeletal Muscle - Somatic)
• Receptive Regions of All Ganglionic Neurons (Both Sympathetic & Parasympathetic)
• Hormone-Producing Cells of the Adrenal Medulla
§ Action:
• Binding of ACh à Directly Opens Ion Channels (:.Ionotropic) à Depolarises the
Postsynaptic Cell à Stimulatory.
o Muscarinic:
§ Found on:
• All Effector Cells stimulated by Postganglionic Cholinergic Fibres
(Ie. All Parasympathetic target organs & some Sympathetic Targets [eccrine sweat
glands & some skeletal-muscle blood vessels])
§ Action:
• Binding of ACh à Activates the receptor’s G-Protein, which detaches from the
receptor à Causes an intra-cellular signalling cascade (:.Metabotropic).
à May be Stimulatory OR Inhibitory Depending on the Subclass of Muscarinic
Receptor on the target organ.
§ Tissue-Specific Receptor Subtypes:
• M1 – Brain
• M2 – Heart
• M3 – Smooth Muscle & Glands
- Sympathetic - Adrenergic Receptors:
o – Receptors that respond to Norepinephrine/Epinephrine.
o – May be Excitatory OR Inhibitory depending on which Subclass of receptor Predominates in that
organ. (Organs responsive to NE/Epi often have more than one receptor subclass)
o Alpha:
§ α1/2
o Beta:
§ β1/2/3

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Clinical Manipulation of the Peripheral NS:
- PNS is easy to manipulate
- Aim: To Use the Nervous System to regulate Organ Function.
- Drugs: Mimic/Enhance/Block messages sent along the nerves.
- Problem: Side Effects – Because the PNS only uses 2 Neurotransmitters, Side effects can be widespread.
o Eg. Some Elicit Drugs have Sympathomimetic side effects:
§ Cocaine & Amphetamines à ↑↑Cardiovascular Stimulation (Tachycardia & Hypertension)
- Can Reduce Side Effects by:
o Topical Application
o Targeting specific receptor subtypes with more specific drugs.
o Targeting Tissue-Specific Differences in Receptor Subtypes.
- Examples of PNS Manipulation:
o Somatic NS:
§ Acetylcholinesterase Inhibitors (à↓Deactivation of ACh in Synapse à ↑ACh Action)
§ Neuromuscular Blockers (Eg. Nicotinic Antagonists)
o Autonomic NS:
§ Sympathetic:
• Agents that affect Release/Reuptake of Catecholamines (NE, Epi & Dopamine)
• Adrenergic Agonists
• Adrenergic Antagonists
§ Parasympathetic:
• Acetylcholinesterase Inhibitors (à↓Deactivation of ACh in Synapseà ↑ACh Action)
• Muscarinic Agonists
• Muscarinic Antagonists
- Ganglionic Blockers:
o Drugs which block chemical transmission at autonomic ganglia – Essentially Denervates the entire
Autonomic Nervous System. (Main effect – Vasodilation [Loss of vasomotor tone]
o Effects vary from tissue to tissue, depending on whether Sympathetic/Parasympathetic nerves are
usually dominant in that tissue:
§ If Sympathetic usually dominates, Ganglionic Blockers mimic Parasympathetic Stimulation.
§ If Parasympathetic usually dominates, Ganglionic Blockers mimic Sympathetic Stimulation.

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Sympathetic & Parasympathetic Tone:
- Sympathetic (Vasomotor) Tone:
o The continual state of Partial Constriction of the Vascular System that Maintains BP (even @ rest)
o During Activity, a Higher BP is needed à the Vasomotor Fibres fire more rapidly à Vasoconstriction.
o NB: Alpha-Blockers dull the effects of the Sympathetic/Vasomotor Tone à Control Hypertension.
- Parasympathetic Tone:
o Slows the heart, sets the Normal activity levels of the Digestive & Urinary Systems, & Stimulates
Glandular Secretion (Except Adrenal Glands & Skin Glands)
o NB: The Sympathetic division an override this during times of stress.
o NB: Drugs that block Parasympathetic Responses à ↑HR, Faecal/Urinary Retention & ↓Glandular
Secretion.

Unique Roles of the Sympathetic NS:

- NB: The Sympathetic Division is more Wide-Spread than the Parasympathetic Division – Because it
innervates more organs.
o Eg. Adrenal Medulla, Sweat Glands, Hair-Follicle Muscles of the Skin, the Kidneys & Most Blood
Vessels Only Receive Sympathetic Fibres.
- There are other Uniquely Sympathetic Functions:
o Thermoregulatory Response to Heat:
§ Cutaneous vasodilation.
§ Activation of sweat glands.
o Thermoregulatory Response to Cold:
§ Cutaneous vasoconstriction.
o Release of Renin from the Kidneys:
§ Sympathetic impulses Stimulate Renin Release à Promotes ↑BP
o Metabolic Effects:
§ Sympathetic Stimulation à Release of Adrenal Medullary Hormones à
• ↑metabolic Rate of body cells
• ↑Blood Glucose Levels
• Mobilises fats for use as fuels.
• Puts skeletal muscle on ‘red alert’ – Contract more strongly & quickly.

Central Control of the Autonomic NS:

- ANS Activity is regulated by a hierarchy of CNS controls:
o Hypothalamus
o Brain Stem
o Spinal Cord
- NB: Subconscious Cerebral inputs via Limbic Lobe influences Hypothalamic Functioning.

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Disorders of the Peripheral Nervous System:
- Categories:
o Inflammation (Eg. Guillain Barre Syndrome – Immune mediated demyelinating neuropathy)
(Eg. Myasthenia Gravis – Antibody attack on Nicotinic ACh Receptor in NMJ)
o Trauma (Eg. Spinal Injuries)
o Metabolic (Eg. Diabetic Neuropathies – Macro/Micro-vascular)
(Eg. Vitamin Deficiencies – B12, B6 & E)
o Toxicity (Eg. Urea/Alcohol/etc.)
o Genetics
o Infection (Eg. Shingles / Diphtheria / Leprosy)

Examples of Homeostatic Imbalances of The ANS:

- Hypertension – Results from overactive sympathetic vasoconstriction promoted by chronic stress.
Can be treated with β-Blockers / other Adrenergic Antagonist.
- Raynaud’s Disease – Characterised by intermittent attacks of peripheral cyanosis, provoked by exposure to
cold or emotional stress. It is an exaggerated vasoconstriction response.
- Autonomic Dysreflexia – Uncontrolled activation of Autonomic Neurons (Mechanism Unclear) in patients
with quadriplegia à ↑Arterial BP, Headache, Flushed Face, Sweating.
- Is Life Threatening.

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 Week 9
Neuroscience Notes
The Cranial Nerves & Their Pathways

Similarities Between Spinal Nerves & Cranial Nerves:

- Cranial Nerves develop similar to Spinal Nerves, & hence have a similar structural Organisation:
o Sensory:
§ Similar to Afferent Spinal Nerves – Sensory Cranial Nerves’ Dendrites are associated with
peripheral sensory receptors & their Cell Bodies are located in a Sensory Ganglia (Similar to
the Dorsal Root Ganglion in the spinal cord). Their axons then terminate in the Sensory
Nuclei of the Brainstem (Similar to Dorsal Horn of Spinal Cord), and synapse with one of the
Ascending Pathways (Depending on the type of stimulus):
• Touch à Posterior Pathway
• Pain à Spinothalamic
• Proprioception à Spinocerebellar
o Somatic Motor:
§ Similar to Efferent Spinal Nerves – Motor Cranial Nerves (Both Somatic & Branchial) have
their Cell Bodies in grey-matter Motor Nuclei in the Brainstem (Similar to Ventral Horn of
Spinal Cord). Their axons leave the brainstem & directly innervate the Skeletal Muscles.
o Visceral Motor:
§ Similar to Autonomic Spinal Nerves – Visceral-Motor Cranial Nerves have their cell bodies in
the Grey-Matter Visceral Nuclei in the Brainstem (Similar to Lateral Horn of Spinal Cord).
Their axons then synapse with a 2nd-Order Neuron in an Autonomic Ganglion, where the 2nd
neuron innervates the smooth muscle.

o Eg. Just as spinal nerves grow in association with their Somites, some Cranial Nerves grow in
association with The 6 Pharyngeal Arches: (See Next Page)

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The Pharyngeal (Branchial) Arches:
- NB: There are 6 pharyngeal arches, but the 5th only exists transiently during embryonic growth
- (No structures result from the 5th arch)
- Appear ≈4-5 weeks of development

Pharyngeal Arch Nerve Muscular Contributions

1st – “Mandibular” Trigeminal (V) Muscles of Mastication:
- Ant. Digastric
- Mylohyoid
- Tensor Tympani
- Tensor Veli Palatini
2nd – “Hyoid Arch” Facial (VII) - Muscles of Facial Expression
- Post. Digastric
- Stylohyoid
- Buccinator
3rd Glossopharyngeal (IX) - Stylopharyngeus
4th Vagus (X) - Cricothyroid Muscle
- Soft Palate Muscles
6th Vagus (X) - Intrinsic Laryngeal Muscles

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The 12 Cranial Nerves & Respective Branches:

Nerve Branches Functional Components

I Olfactory nerve Special Sensory

II Optic nerve Special Sensory
III Oculomotor nerve Somatic Motor
Visceral Motor
(parasympathetic)
IV Trochlear nerve Somatic Motor
V Trigeminal nerve - V1 Ophthalmic Division General Sensory
- V2 Maxillary Division
- V3 Mandibular Division
Branchial Motor
VI Abducent nerve Somatic Motor
VII Facial nerve Branchial Motor
Special Sensory
Visceral Motor
(Parasympathetic)
VIII Vestibulocochlear - Vestibular Division Special Sensory
- Cochlear Division Special Sensory
IX Glossopharyngeal Branchial Motor
Visceral Motor
Visceral Sensory
Special Sensory
General Sensory
X Vagus Branchial Motor
Visceral Motor
Visceral Sensory
Special Sensory
General Sensory
XI Spinal Accessory Somatic Motor
XII Hypoglossal Somatic Motor

- NB: Cranial Nerves are Numbered Systematically according to their attachment to the brain. (Rostral-Caudal)
- NB: Cranial Nerves are Named based on their Distribution or Function.
- NB: Other than the Vagus (Which extends to the abdomen), Cranial Nerves serve Only the Head & Neck.

Mnemonics:
- Oh Oh Oh, Try Try Again, Four Very Good Virgins Are Hot.
- Oh Oh Oh, To Touch And Feel Virgin Girl’s Vaginas And Hymens

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Cranial Nerve Nuclei:
- Location:
o CN I (Olfactory) & II (Optic) = Are both extensions of the Forebrain.
o CN III – XII (All others) = They originate from Nuclei located in the Brainstem.
- Organisation:
o Nuclei of similar Functional Components (Ie. General Somatic/Visceral Motor or General
Somatic/Visceral Sensory) are generally aligned into functional columns in the brainstem.

Sensory Ganglia of Cranial Nerves:

Cranial Nerve: Receptor Types: Sensory Ganglia:

Olfactory Olfactory (Smell) Olfactory Epithelium
Optic Retinal (Vision) Retina of the Eye
Trigeminal Somatosensory Trigeminal Ganglion
Facial Somatosensory Geniculate Ganglion
Vestibulocochlear Equilibrium Vestibular Ganglion
& Hearing & Spiral Ganglion
Glossopharyngeal Somatosensory, Visceral & Taste Inferior Ganglion
Vagus Somatosensory, Visceral & Taste Superior & Inferior Ganglion

Parasympathetic Ganglia of Cranial Nerves:

Cranial Nerve Ganglion Location Main Distribution

Oculomotor Ciliary Between the Optic Nerve & the Lateral Ciliary Muscle & Pupillary
Rectus Muscle of Eye Sphincter of Eyes
Facial Pterygopalatine In Pterygopalatine Fossa; Just anterior to Lacrimal (Tear) Gland
the opening of the Pterygopalatine Canal.
Submandibular Just inferior to Submandibular Salivary Sublingual & Submandibular
Duct Salivary Glands
Glossopharyngeal Otic Between Tensor Veli Palatini & Parotid Salivary Gland.
Mandibular Nerve (Just anterior to
Foramen Ovale of Sphenoid Bone)

NB: Sympathetic Input is important for the Dual Innervation setup of the Autonomic NS. The Sympathetic Fibres
ascending from the Superior Cervical Sympathetic Ganglion hitch a ride with the Parasympathetic Cranial Nerves and
follow them to their targets.

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Functional Components of Cranial Nerves:
- Cranial Nerves carry one/more of the following 5 Functional Components:
o Efferent:
1. Voluntary (Somatic) Motor:
a. Somatic Motor: “General Somatic Efferents” (GSE)
i. Innervate striated skeletal muscle derived from embryonic somites, not
pharyngeal arches. (Incl. Ocular Muscles, Tongue, External Neck Muscles –
Sternocleidomastoid & Trapezius)
b. Branchial Motor: “Special Visceral Efferents” (SVE)
i. Innervate striated skeletal muscle derived from embryonic pharyngeal arches.
(Incl. Muscles of the Face, Palate, Pharynx, Larynx & Mastication)

(Oculomotor, Trochlear, Trigeminal, Abducens, Facial,

Glossopharyngeal, Vagus, Accessory & Hypoglossal)

2. Involuntary (Visceral) Motor: “General Visceral Efferents” (GVE)

i. Innervate Smooth Muscle in vessels/glands/etc. Via a 2-neuron approach;
(Presynaptic fibres emerge from the brain as cranial nerves, which then synapse
in a parasympathetic ganglion. The postsynaptic neurons then innervate the
smooth muscles & glands etc.)
ii. Constitute the Cranial Outflow of the Parasympathetic Nervous System.

(Oculomotor, Facial, Glossopharyngeal, Vagus)

o Afferent:
3. Somatic Sensation: “General Somatic Afferents” (GSA)
i. (Touch, Pressure, Heat, Cold, etc)

(Trigeminal, Facial, Glossopharyngeal & Vagus)

4. Visceral Sensation: “General Visceral Afferents” (GVA)

i. (Blood Pressure & Blood-O2/CO2 from Carotid Sinus & Body, plus Visceral
Sensation from Pharynx, Larynx Trachea, Bronchi, Lungs, Heart & GI Tract.)

(Oculomotor, Trigeminal, Facial, Glossopharyngeal, Vagus)

5. Special Sensation: “Special Somatic/Visceral Afferents” (SSA/SVA)

i. (Vision, Taste, Smell, Hearing & Balance)

(Olfactory, Optic, Facial, Vestibulocochlear, Vagus)

- NB: YOU NEED TO KNOW WHICH NERVES CARRY EACH TYPE OF INFORMATION – See Table Overleaf:

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Nerve Functional Location of Nerve Cranial Exit Functions (major)
Components Cell Bodies Point

I Olfactory nerve Special Sensory Olfactory Epithelium Cribriform Plate Smell

of The Ethmoid
Bone
II Optic nerve Special Sensory Retinal Ganglion Optic Canal Vision and associated reflexes
III Oculomotor Somatic Motor Midbrain Movements of eyes (Superiorly,
nerve Superior Orbital Inferiorly & Medially)
Visceral Motor Presynaptic: Fissure Pupillary constriction and lens
(parasympathetic) Midbrain accommodation
Postsynaptic: (parasympathetic)
Ciliary Ganglion
IV Trochlear nerve Somatic Motor Midbrain Superior Orbital Movements of eyes
Fissure (Inferolaterally)
V Trigeminal nerve
- V1 Opthalmic General Sensory Trigeminal Ganglion Superior Orbital Sensation from Cornea, & V1
Division Fissure Dermatome

- V2 Maxillary Foramen Sensation from Maxillary Teeth,

Division Rotundum Nasal Mucosa, Maxillary
Sinuses, Palate, & V2
Dermatome

- V3 Foramen Ovale Sensation from Mandibular

Mandibular Teeth, Mucosa of Mouth,
Division Tongue & V3 Dermatome

Branchial Motor Pons Muscles of Mastication &

Swallowing

VI Abducent nerve Somatic Motor Pons Superior Orbital Lateral Rectus Muscle -
Fissure Abduction (Lateral Rotation) of
the Eye
VII Facial nerve Branchial Motor Pons Internal Acoustic Facial Muscles + Some Muscles
Meatus; Facial of Mastication
Special Sensory Geniculate Ganglion Canal; Taste (Anterior 2/3 of Tongue)
Visceral Motor Presynaptic: Stylomastoid Stimulation of Submandibular
(Parasympathetic) Pons Foramen & Sublingual Salivary Glands, &
Postsynaptic: Lacrimal Glands.
Pterygopalatine
Ganglion;
Submandibular
Ganglion

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VIII Vestibulocochlear
- Vestibular Special Sensory Vestibular Ganglion Internal Acoustic Position of the Head & Balance
Division Meatus (The body’s Gyro)
- Cochlear Special Sensory Spiral Ganglion Hearing (Via Spiral Organ)
Division
IX Branchial Motor Medulla Jugular Foramen Stylopharyngeus Muscle
Glossopharyngeal (Assists with swallowing)
Visceral Motor Presynaptic: Stimulates Parotid Salivary
Medulla Gland
Postsynaptic:
Otic Ganglion
Visceral Sensory Superior Ganglion Visceral Sensation from Parotid
Gland, Carotid Sinus, Pharynx &
Middle Ear
Special Sensory Inferior Ganglion Taste(Posterior 1/3 of Tongue)
General Sensory Inferior Ganglion Cutaneous Sensation of
External Ear
X Vagus Branchial Motor Medulla Jugular Foramen Constrictor Muscles of Pharynx,
Muscles of Larynx, Palate &
Upper 2/3 Esophagus
Visceral Motor Presynaptic: Maintains Smooth Muscle Tone
Medulla in Trachea & Bronchi, Peristalsis
Postsynaptic: in GIT & ↓HR.
Viscera
Visceral Sensory Superior Ganglion Visceral Sensation from Base of
Tongue, Pharynx, Larynx
Trachea, Bronchi, Heart,
Esophagus, Stomach &
Intestine à L-Colic Flexure.
Special Sensory Inferior Ganglion Taste (Epiglottis & Palate)
General Sensory Superior Ganglion Sensation from the External
Ear.
XI Spinal Somatic Motor Spinal Cord Jugular Foramen Sternocleidomastoid &
Accessory Trapezius Muscles
XII Hypoglossal Somatic Motor Medulla Hypoglossal Intrinsic & Extrinsic Muscles of
Canal the Tongue.

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More Detail: NB: YOU WILL NEED TO KNOW WHERE EACH CN. ENTERS/EXITS THE CRANIUM
I. Olfactory:
a. Function:
i. Purely Special Sensory; Carry Afferent Impulses of Smell (Olfaction)
b. Origin & Course:
i. Olfactory Nerves arise from Olfactory Receptors in the Olfactory Epithelium. They pass up
through the Cribriform Plate of the Ethmoid Bone & synapse with the Olfactory Bulb.
ii. Olfactory Bulb Neurons run posteriorly as the Olfactory Tract & terminates in Primary
Olfactory Cortex.

II. Optic:
a. Function:
i. Purely Special Sensory; Carry Afferent Impulses of Vision
b. Origin & Course:
i. Fibres arise from the Retina and form the Optic Nerve.
ii. The Optic Nerve passes through the Optic Canal of the Orbit.
iii. The Optic Nerves converge to form the Optic Chiasma where half of each nerve’s fibres cross
over & continue on as Optic Tracts.
iv. The Optic Tracts synapse in the Thalamus, & Thalamic fibres extend to the Visual Cortex.

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III. Oculomotor:
a. Function:
i. Somatic Motor– Voluntary Movement of 4 of the 6 of the Extrinsic Eye Muscles
(Inf. Oblique, Sup. Rectus, Inf. Rectus, Med. Rectus & Upper-Eyelid Muscle)
NB: Proprioceptive Afferents exist for each muscle.
ii. Visceral Motor – Parasympathetic control of Pupillary Sphincter (Constriction) & Ciliary
Muscle (Lens Accommodation)
b. Origin & Course:
i. Fibres arise from the Midbrain and pass through the Superior Orbital Fissure to the eye.

IV. Trochlear:
a. Function:
i. Purely Somatic Motor – Voluntary Movement of 1 of the 6 Extrinsic Eye Muscles
(The Superior Oblique)
b. Origin & Course:
i. Fibres arise from the Midbrain and pass through the Superior Orbital Fissure to the Eye.

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V. Trigeminal:
NB: Has 3 Divisions (Ophthalmic, Maxillary & Mandibular), each with different specific functions &
courses through the skull.
a. Function:
i. Mostly Somatosensory (From Face)
ii. Some Branchial Motor
b. Origin & Course:
i. Ophthalmic – Fibres run from Face à Through Superior Orbital Fissure à Pons.
ii. Maxillary – Fibres run from face à Through the Foramen Rotundum à Pons.
iii. Mandibular – Fibres pass through the Foramen Ovale

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VI. Abducents:
a. Function:
i. Purely Somatic Motor – Voluntary Movement of the Lateral Rectus Muscle of the Eye.
(Abducts the eye – hence the name)
NB: Proprioceptive Afferents exist as well.
b. Origin & Course:
i. Fibres arise from the Pons and pass through the Superior Orbital Fissure to the Eye.

VII. Facial:
a. Function:
i. Branchial Motor – Voluntary Movement of Muscles of Facial Expression
1. Has 5 Branches (See Picture) – KNOW THESE & Their Myotomes.
ii. Special Sensory – Taste Buds of Anterior 2/3 of Tongue
iii. Visceral Motor – Parasympathetic control of Lacrimal (Tear) Glands, Nasal & Palatine Glands,
& Submandibular & Sublngual Salivary Glands.
b. Origin & Course:
i. Fibres arise from the Pons & enter the Temporal Bone via the Internal Acoustic Meatus and
emerge through the Stylomastoid Foramen to run through lateral face.

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VIII. Vestibulocochlear:
a. Function:
i. Special Sensory:
1. Vestibular Branch – Sense of Equilibrium/Balance.
2. Cochlear Branch – Sense of Hearing.
b. Origin & Course:
i. Fibres arise from the Vestibule & the Cochlear of the Inner Ear of the Temporal Bone & pass
through the Internal Acoustic Meatus and enter the brainstem @ the Pons-Medulla Border.

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IX. Glossopharyngeal:
a. Function:
i. Somatic Motor – Voluntary Movement of the Stylopharyngeus
(Elevates the Pharynx in Swallowing)
ii. Visceral Motor – Parasympathetic control of Parotid Salivary Glands
(Nerve Cell Bodies locate in the Otic Ganglion)
iii. Special Sensory – Taste Buds of Posterior 1/3 of Tongue
iv. SomatoSensory – Touch/Pressure/Pain from Pharynx, Posterior Tongue & External Ear
v. Visceral Sensory – Chemoreceptors in Carotid Body (Blood O2 / CO2) & Baroreceptors in
Carotid Sinus (BP)
b. Origin & Course:
i. Fibres arise from Medulla, leave skull via the Jugular Foramen & run to the Throat.

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X. Vagus:
a. Function:
i. Visceral Motor – Parasympathetic Control of:
1. Heart (HR)
2. Lungs (Breathing)
3. Abdominal Organs (GI Activity)
ii. Visceral Sensory – Visceral Sensation from:
1. Thoracic Viscera
2. Abdominal Viscera
3. Aortic Arch Baroreceptors (BP)
4. Carotid & Aortic Bodies (Chemoreceptors)
iii. Special Sensory – Taste Buds from Posterior Tongue
iv. Somatic Motor – Voluntary control of Muscles of Pharynx & Larynx involved in swallowing.
b. Origin & Course:
NB: Vagus – the only cranial nerve to extend beyond the head & neck.
i. Fibres arise from Medulla, pass through the skull via the Jugular Foramen & descend
through the Neck into the Thorax & Abdomen.

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XI. Accessory:
a. Function:
i. Somatic Motor – Voluntary Movement of Sternocleidomastoid & Trapezius Muscles
b. Origin & Course:
i. Unique in that it is formed by union of a Cranial Root & a Spinal Root.
1. Cranial Root – Arises from Medulla of Brainstem
2. Spinal Root – Arises from Cervical Region of Spinal Cord (C1-C5) & Enters the Skull via
the Foramen Magnum where it joins with the Cranial Root.
ii. The Resulting Accessory Nerve exits the skull through the Jugular Foramen, where it
bifurcates to either 1) Join the Vagus Nerve; or 2) Run down to the Neck Muscles.

XII. Hypoglossal:
a. Function:
i. Somatic Motor – Voluntary Movement of the Tongue (Food Mixing/Manipulation, Speech &
Swallowing)
b. Origin & Course:
i. Fibres arise from the Medulla & exit the skull via the Hypoglossal Canal to travel to the
underside of the Tongue.

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Cranial Foramina That Carry Cranial Nerves:

Cranial Foramina Cranial Nerves

Cribriform Foramina in Cribriform Plate Olfactory Nerves
Optic Canals Optic Nerves
Superior Orbital Fissure Oculomotor
Trochlear
Abducens
Trigeminal (Ophthalmic Division)
Foramen Rotundum (“Round Foramen”) Trigeminal (Maxillary Division)
Foramen Ovale (“Oval Foramen”) Trigeminal (Mandibular Division)
Groove of the Greater Petrosal Nerve Petrosal Nerve (Branch of the Facial Nerve)
Internal Acoustic Meatus Facial (And exits the skull via the Stylomastoid Foramen)
Vestibulocochlear
Jugular Foramen Glossopharyngeal
Vagus
Accessory (Both Roots Exit the Skull Here)
Hypoglossal Canal Hypoglossal
Foramen Magnum Accessory (Spinal Root Enters the Skull Here)

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Ie. Know which cranial nerves exit through which foramina.

Ie. Know which nerves are associated with each pharyngeal arch.

Ie. Know the major branches of each cranial nerve.

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 BASIC ANATOMY & PHYSIOLOGY
Special Senses

Vision:
Accessory Structures of the Eye:
- Eyebrows:
o Shade the eyes from sunlight
- E elid Palpeb ae
o Protect the eye when threatened by foreign objects
- Conj nc i a Joined Toge he
o Transparent mucus memb ane lining he e elid Pal eb al C nj nc i a he an e i e eball
face B lba C nj nc i a
- Lacrimal Apparatus:
o Consists of:
Lacrimal Gland (Tear Gland):
Located in the orbit above the eye.
Lacrimal Canaliculi:
2 openings on medial margin of each eyelid.
- Eyelid Muscles:
o Levator Palpebrae Superioris Muscle:
Elevates & Retracts Upper Eyelid (Opens Eye)
o Orbicularis Oculi Muscle:
(A Sphincter Muscle) - Closes Eye
- Extrinsic Eye Muscles:
o Eyeball movement is controlled by 6 muscles
o The 4x Rectus Muscles originate from a common tendinous ring (Annular Ring) at the back of the
eye.
o The 2x Oblique Muscles take different paths through the orbit. They are required to cancel the
medial pull of the superior & inferior recti to allow purely vertical eye movement.

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Eye Anatomy:
- 3-Layered Wall (Tunics):
o 1. Fibrous Layer:
2 Regions:
Cornea:
o The Clear, Anterior part of the eye that lets light in.
Sclera:
o The white/opaque, Posterior part of the eye.
o 2. Vascular Layer:
Middle Layer
2 Parts:
Choroid:
o Highly vascular, dark membrane (Posterior 5/6 of eye).
Supplies nutrition to all eye layers
Absorbs light, preventing it from scattering/reflecting within the
eye.
I i Rainbo
o The Anterior, coloured portion of the Vascular Layer
o Lies between the Cornea & the Lens.
o 3. Retinal Layer:
Innermost Layer
2 Sub-Layers:
Pigmented Layer:
o Outer Retinal Layer
o Dark, Single-cell-thick lining adjacent to the Choroid.
Neural Layer:
o Inner Retinal Layer
o Transparent layer of Photoreceptors/Neurons/ & Glia
o Composed of 3 Types of Neurons:
Photoreceptors:
2 Types:
o Rods Light Detectors (Dim & Fuzzy)
o Cones Colour Detectors (Bright & Sharp)
Bipolar Neurons:
Connect Photoreceptors to Ganglion Cells
Ganglion Cells:
Generate & Conduct the Action Potentials Brain

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- The E e x Segments & Fluids:
o The Lens & Suspensory Ligaments (Ciliary Zonule) Divide the eye into 2 segments. (Ant/Post).
o 1. Anterior Segment (In front of the lens):
Filled i h A eo H mo
Clear, plasma-like substance
Has the same refractive index as the Cornea
Continually formed by capillaries of the Ciliary Processes (in the Posterior
Chamber).
o Flows from the Posterior Chamber to the Anterior Chamber
o Drains from Ant. Chamber through the Scleral Venous Sinus (Canal of
Schlemm) which encircles the Limbus.
Functions:
o Its pressure supports the eyeball internally.
o Supplies Nutrients & Oxygen to the Lens & Cornea
Subdivided by the Iris into 2 Chambers:
Anterior Chamber:
o Between the Cornea & the Iris
Posterior Chamber:
o Between the Iris & the Lens.

o 2. Posterior Segment (Behind the lens):

Filled i h Vi eo H mo Gla Fl id
A clear Gel
Has the same refractive index as the cornea
Formed in the Embryo & Lasts a Lifetime
Functions:
o Supports the posterior surface of the lens
o Holds the Neural Retina firmly against the Pigmented Layer
o Contributes to Intraocular Pressure

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- The E e Len
o Features:
Responsible for 1/3 of the Po er of the Eye. (Cornea is other 2/3)
Biconvex
Held in place by the Ciliary Zonule (Suspensory Ligaments)
o Lens Physics:
A len f a ce ain e ha a ce ain Focal Point. The distance between the lens & the
focal point is the Focal Distance.
NB: The eye has a fixed Focal Distance, therefore the Lens Po e m be a iable.
o Function:
Focuses light rays onto the retina.
Accommodation: Change ha e hence len P e main ain F cal Di ance

- 3 Prerequesites to Near-Vision
o 1. Accommodation of the Lenses:
Achieved by contraction of the ciliary muscles Thickens lens More power.
o 2. Constriction of The Pupils:
Achieved by contraction of the Constrictor Muscles of the Iris.
Allows increased clarity
o 3. Convergence of The Eyeballs:
Keeps the object being looked at focussed on the Retinal Fovea

- Photoreceptors:
o The cells that transduce light. (Rods & Cones)
o Contain an array of Visual Pigments (Photopigments) that change shape as they absorb light:
o Differences (Rods Vs. Cones):
Have different thresholds for activation.
Contain different visual pigments - absorb different wavelengths of light.
A e i ed diffe en l
o Rods:
High Sensitivity (Respond well to dim light)
C n ain nl e f Ph igmen The ef e nl end a m n ch me ignal
o Cones:
Low Sensitivity (Requires bright light for activation)
Have 1 of 3 different pigments that respond to different colours. (Allow you to see colour)

- Phototransduction:
o The light-ab bing m lec le i called Retinal A de i a i e f Vi amin-A)
o Retinal c mbine i h ein called Opsins f m -types of Photopigments.

- Light/Dark Adaptation:
o Light Adaptation:
Occurs when we move from Darkness into Bright Light.
To Compensate, the Rod system quickly desensitises and essentially turns off. The Cone
system rapidly adapts, and takes over. Hence, overall the retina Desensitises.
o Dark Adaptation:

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 Occurs when we move from Brightness to Darkness. Initially we see nothing but black
because:
1. Cones stop functioning in low light. &
Beca e R d ha e been bleached b he b igh ligh a e ill ned ff
Once rhodopsin accumulates in the Rods, their function slowly increases.

- Pathways to the Brain:

o Ganglion Cell axons become the Optic Nerve.
o Some of the Optic Nerve Fibres cross @ the Optic Chiasm.
o After the Optic Chiasm, Optic Nerves become the Op ic T ac .
o Optic Tract fibres synapse in the:
Superior Colliculi of the Midbrain (Blue Circles):
- Visual Reflex Centres controlling Extrinsic Eye Muscles
Lateral Geniculate Nucleus of the Thalamus (Red Circle):
- Sorts/Relays info Via the Optic Radiation to the Primary Visual Cortex. (Pink
Circle)
Primary Visual Cortex (Pink Circle):
Topographical map of the Retina (Similar to Homunculus)
o Sends Info to Visual Association Areas regarding Form, Colour & Motion.

o Information Route/Pathway: Photoreceptor Bipolar Cell Ganglion Cell Optic Nerve

Optic Chiasm Optic Tract Superior Colliculus / Lateral Geniculate Nucleus of the Thalamus
Primary Visual Cortex Visual Association Area Perception.

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 Taste/Smell:

Gustation (Taste):
- Structure of Taste Buds:
o Each taste bud consists of 50-100 epithelial cells. (3 Types of associated epithelial cells):
Supporting Cells:
Form the bulk of the taste bud.
Receptor Cells:
Have Long Microvilli that project from their tips, through a taste pore to the
surface.
These Long Microvilli (Gustatory Hairs) are the sensitive portions of these cells.
Taste fibres of the Facial/Glossopharyngeal/Vagus Cranial Nerves coil around the
Receptor Cells.

- Basic Taste Sensations:

o Sweet - Sugars, some Amino Acids, Lead Salts
o Sour - Acids
o Salt - Metal Ions (Particularly Sodium)
o Bitter - Alkaloids (Quinine, Caffeine, and Nicotine) NB: Dislike for bitter is Protective.
o Umami - Delici - Glutamate (Steak, Cheese) & MSG.
- Physiology of Taste:
o Tasting requires a chemical to dissolve in the saliva, then diffuse through a Taste Pore, and contact
Gustatory Hairs.
o Binding of chemical induces a depolarising potential Release of Neurotransmitter.
o Neurotransmitter Triggers dendrites of sensory nerves Action Potentials.
- Taste Transduction:
o Basic Overview:
Stimulation of Gustatory Cell lead an in in acell la Ca+] Causes NT Release
Stimulates sensory nerves.
o Each taste-quality has its own way of stimulating the receptor cells:
Salty due to Na+ influx directly depolarises the Gustatory Cell.
Sour due to H+ either: 1) Entering the cell, 2) Opening Ion Channels, or 3) Blocking K +
Channels.
Bitter, Sweet & Umami G-Protein Linked Receptors that produce depolarisation.
- Gustatory Pathway:
o Afferent fibres from taste buds run in 3 Cranial Nerves:
Facial (first 2/3 of tongue)
Glossopharyngeal (last 1/3 of tongue)
Vagus (Epiglottis & Lower Pharynx)
o Afferent Fibres synapse in the Solitary Nucleus of the Medulla Thalamus Gustatory Cortex in
Parietal Lobes.

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 AfraTafreeh.com exclusive

Olfaction (Smell):
- Location of Olfactory Receptors:
o L ca ed in he Olfac E i heli m a 5cm2 patch of Pseudostratified Columnar Epithelium in the
roof of the Nasal Cavity.
- Structure of Olfactory Receptor Cells:
o They are Modified Bipolar Neurons
o Have a thin apical dendrite, terminating in the olfactory mucus as Olfactory Cilia. S face A ea
o Have thin, Unmyelinated Axons that collect to form the Olfactory Nerve (CN-I)
Filaments of the Olfactory Nerves project superiorly through the Cribriform Plate.
Axons Synapse in the Olfactory Bulbs.

- Physiology of Olfactory Receptors:

o For an odorant to be smelt, it must dissolve in the olfactory mucus.
o Once dissolved, odorants:
Stimulate the olfactory receptors by binding to Odorant Binding Proteins in the membranes
of the Olfactory Cilia
Depolarisation Action potential Stimulates the Olfactory Bulb.
- The Olfactory Pathway:
o Olfactory Receptors Mi al Cell in Gl me li Each glomerulus receives only 1 type of odour)
Mitral Cell Axons (Olfactory Tracts) Either:
1) The Thalamus Olfactory Cortex & Frontal Lobe (conscious
interpretation/identification).
2) The Hypothalamus, Amygdala & other Limbic System regions Elicit emotional
responses to odours.

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 Special Senses II: Hearing & Equilibrium

Functional Overview of the Ear:

- Ear is Responsible for 2 Special Senses:
o Hearing Associated with Outer, Middle & Inner Ear (Cochlear) Structures.
o Equilibrium - Associated with just the Inner Ear (Vestibular Apparatus)
- NB: Receptors for both = Hair Cells (NB: their functional differences are due to specialised anatomy)
o How they Work:
Hai Cell ha e Cilia projecting from their apical surface into gelatinous masses:
The e Cilia a e di ed b m emen in he gela in ma e Change in Membrane
Potential (:. Hair Cells are Mechanoreceptors)
o How Distortion of Cilia causes the Change in Membrane Potential:
At the top of each cilia, there are Mechano-Gated K+ Channels j ined ge he b Tip
Links
At Rest: Half of the K+ Channels are open, maintaining RMP.
If Distorted & Tip Links are Stretched: All K+ Channels open Depolarisation
If Distorted & Tip Links are Compressed: All K+ Channels are closed Repolarisation

Ear Anatomy:
- Outer Ear:
o Pinna (Auricle):
The Outermost part of the ear
o External Auditory Canal:
The canal that conducts the soundwaves waves into the Tympanic Membrane (Eardrum)
- Middle Ear:
o Tympanic Membrane (Eardrum):
Thin, translucent, connective Tissue Membrane (Skin on outside, mucosa on inside)
Connect to the 3 Auditory Ossicles
o The 3 Auditory Ossicles:
Malleus Hamme Malle
Incus An il
Stapes S i
NB: 2 Skeletal Muscles (Tensor Tympani & Stapedius) Reflexively contract when ears are
assaulted by loud sounds Reduces Sound Conduction.
o Oval Window of the Cochlea:
Transfers Vibration of the Stapes Into the Cochlea.
o Eustachian (Pharyngotympanic) Tube:
Equalizes pressure between the Outer & Middle Ear

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- Inner Ear (Cochlea & Vestibular Apparatus):
o Cochlea - HEARING:
The Spiral-Shaped Organ
Begins @ the Oval Window:
The Entry Point of the Cochlea.
Ends @ the Round Window:
The Exit-Point of the Cochlea
Consists of 3 Coiled Ducts Separated by 2 Membranes:
Scala Vestibuli (Vestibular Duct):
o Begins @ the Oval Window
o Ends @ the apex of the Cochlea
o Filled with Perilymph.
o Separated from the Scala Media by the Vestibular Membrane.
Scala Media (Cochlear Duct):
o Runs through the middle of the Cochlea.
o Separates the Vestibular Duct & Tympanic Duct.
o Filled with Endolymph.
o Separated from the Scala Tympani by the Basilar Membrane.
o Contains the Spiral Organ of Corti: (See Next Page)
Scala Tympani (Tympanic Duct):
o Begins @ the apex of the Cochlea
o Ends @ the Round Window
o Filled with Perilymph.

The Spiral Organ of Corti:

Sits inside the Scala Media & runs along the Basilar Membrane.
Composed of:
o The Tectorial Membrane (Overlying the Hair Cells)
o Hair Cells (Receptors for hearing) Associated with cochlear nerve fibres:
1x Row of Inner Hair Cells Has several inputs to the Spiral
Ganglion
3x Rows of Outer Hair Cells Has Only 1 input to the Spiral
Ganglion
o Supporting Cells
o The Basilar Membrane
Cochlear Branch of the Vestibulocochlear Nerve Originates Here.

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 Audiotransduction:
Waves exit the Scala Media by Penetrating the Basilar Membrane & enter the
Scala Tympani:
o The waves penetrating the Basilar Membrane cause it to Vibrate.
o Vibration of the Basilar Membrane pushes the Hair Cells in the Organ of
Corti up into the Tectorial Membrane, Distorting the Cilia & Initiating
Graded Potentials in the Cochlear Nerve.

Waves continue down the Scala Tympani & leave the Cochlea via the Round
Window This prevents echoing of the sound waves within the Cochlea.

Pitch & Volume:

Pitch is coded in the point along the basilar membrane which is distorted by the
wave.
Volume is coded by the degree of distortion of the hair cells by the wave.

Pathway From the Cochlea to the Brain:

- Hair Cells Cochlear Branch of the Vestibulocochlear Nerve Cochlear Nuclei of the Medulla Superior
Olivary Nucleus Lateral Lemniscal Tract Inferior Colliculus Medial Geniculate Nucleus of the
Thalamus
o Primary Auditory Cortex (Conscious Sound)
o Superior Colliculus (Auditory Reflexes Startle, Turning Head, etc.)

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o Vestibular Apparatus - EQUILIBRIUM:
Vestibular Branch of the Vestibulocochlear Nerve Originates Here.
Consists of:
A Vestibule, Containing:
o 1x Utricle:
o 1x Saccule:
& 3 Semicircular Canals.

The Vestibule: NB: Both the Utricle & Saccule have a Maculae:
Maculae = Receptor Organs for Linear Acceleration (Static Equilibrium)
o Provides Info about Orientation of the Head with respect to Gravity, Linear
Acceleration & Angular Acceleration.
Composed of:
o Hair Cells (Cilia Project into the Otolithic Membrane)
o Supporting Cells
o Otolithic Membrane - Gela in Ma i h O li h Ea S ne of
Calcium Carbonate Crys al e ing n The e O li h ide he
inertia required to move the Otolithic Membrane during head movement)

The 3 Semicircular Canals: NB A he end of each Canal i a S elling Crista Ampularis :

Crista Ampularis = Receptors for Rotation (Dynamic Equilibrium).
Composed of:
o Hair Cells (Cilia Project into the Cupula)
o Supporting Cells
o Cupula (Gelatinous Mass encircling the entryway of each Crista
Ampularis. Rotation of the head in the plane of the canal causes fluid
movement over the Cupula, distorting the Hair Cells)

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 NB: There are 2 Semi-Circular Canals for each Plane of Movement:
o One on each side of the head
o This allows you to determine the Direction of head motion.

NB: Each Semi-Circular Canal is Responsible for a different Plane:

o Anterior Ea -to-Sh lde M i n
o Posterior- N dding M i n
o Lateral - Shaking n M i n

Equilibrium Pathways To the Brain:

- Equilibrium is Subconscious
- Info goes straight to the reflex centres in the Brainstem & Cerebellum:
o Vestibular Nuclei:
Integrates Balance + Receive some Visual & Somatic Inputs
Sends commands to Brainstem Motor Centres controlling Eyes & Neck/Limb/Trunk
Reflexes.

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 Week 10
Neuroscience Notes
Special Senses I: Vision, Taste/Smell

The Special Senses:

- There are 5 Special Senses:
o Vision
o Taste
o Smell
o Hearing
o Equilibrium
- They allow us to respond to:
o Photons (Light)
o Chemicals
o Vapours
o Air-Waves
o Gravity & Body Movement
- ALL Sensory Receptor Cells are confined to the Head Region.
o NB: In contrast to general receptors (which are just modified nerve-endings), sensory receptors of
the special senses are distinct Receptor Cells, & are housed in complex sensory organs. (eg. Eye)
o NB: All Receptor Cells are CILIATED.

Vision:
Accessory Structures of the Eye:
- Eyebrows:
o Shade the eyes from sunlight
o Prevent water/perspiration trickling down the forehead into the eyes.
- Eyelids (‘Palpebrae’):
o Protect the eye when threatened by foreign objects
o Blinking prevents drying of the eyes
- Conjunctiva (“Joined Together”):
o Transparent mucus membrane lining the eyelids (‘Palpebral Conjunctiva’) & the anterior eyeball
surface (‘Bulbar Conjunctiva’).
o Produces lubricating mucus – Prevents drying out.

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- Lacrimal Apparatus:
o Consists of:
§ Lacrimal Gland (Tear Gland):
• Located in the orbit above the eye.
• - Secretes dilute saline (Lacrimal secretion/tears)
§ Lacrimal Canaliculi:
• 2 openings on medial margin of each eyelid.
• - Drains tears into the Lacrimal Sac à Nasolacrimal Duct à Nose.
o NB: Lacrimal fluid contains Mucus, Antibodies & Lysozyme (an antibacterial)

- Extrinsic Eye Muscles:

o Eyeball movement is controlled by 6 muscles
o The 4x Rectus Muscles originate from a common tendinous ring (Annular Ring) at the back of the
eye.
o The 2x Oblique Muscles take different paths through the orbit. They are required to cancel the
medial pull of the superior & inferior recti to allow purely vertical eye movement.

Lateral View of R-Eye Superior View of R-Eye

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Eye Anatomy:
- 3-Layered Wall (Tunics):

o 1. Fibrous Layer:
§ Outermost layer
§ Made of Dense Connective Tissue
§ 2 Regions:
• Cornea:
o The Clear, Anterior part of the eye that lets light in.
o Major role in the refractive apparatus of the eye.
• Sclera:
o The white/opaque, Posterior part of the eye.
o Protects & shapes the eyeball.
o It is continuous with the Dura Mater of the brain via the optic nerve sheath.
o 2. Vascular Layer:
§ Middle Layer
§ 2 Parts:
• Choroid:
o Highly vascular, dark membrane (Posterior 5/6 of eye).
§ Supplies nutrition to all eye layers
§ Absorbs light, preventing it from scattering/reflecting within the eye.
o Anteriorly, it becomes the Ciliary Body:
§ A thickened ring of smooth muscle around the lens.
§ These Ciliary Muscles control lens shape.
§ The Ciliary Zonule (Suspensory ligaments) connects the Ciliary
Muscles to the lens.
• Iris (“Rainbow”):
o The Anterior, coloured portion of the Vascular Layer
o Lies between the Cornea & the Lens.
o Its round, central opening (The Pupil) allows light in.
o Consists of 2 Smooth Muscle Layers:
§ Sphincter Pupillae (Circular) à Pupil Constriction
§ Dilator Pupillae (Radial) à Pupil Dilation

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o 3. Retinal Layer:
§ Innermost Layer
§ 2 Sub-Layers:
• Pigmented Layer:
o Outer Retinal Layer
o Dark, Single-cell-thick lining adjacent to the Choroid.
o Absorbs light, prevents scattering/reflection within the eye.
o Also function as phagocytes, removing dead/damaged photoreceptor cells.
o Store Vitamin-A (needed by photoreceptor cells)
• Neural Layer:
o Inner Retinal Layer
o Transparent layer of Photoreceptors/Neurons/ & Glia
o Direct Role in Vision (Light Transduction)
o Composed of 3 Types of Neurons:
§ Photoreceptors:
• Light Transduction
• Blood Supply = The Choroid
• 2 Types:
o Rods – Light Detectors (Dim & Fuzzy)
o Cones – Colour Detectors (Bright & Sharp)
§ Bipolar Neurons:
• Connect Photoreceptors to Ganglion Cells
• Blood Supply = The Central Artery/Vein of the Retina.
§ Ganglion Cells:
• Generate & Conduct the Action Potentials à Brain
• Blood Supply = The Central Artery/Vein of the Retina.
o NB: Also contains other types of neurons (Amacrine Cells & Horizontal Cells)
which play a role in visual processing.
o The Optic Disc - Where the Ganglion Cells’ Axons exit the eye to form the
optic nerve. (Aka: Blind Spot)
o The Macula Lutea (“Yellow Spot”):
§ Oval region directly at the eye’s Posterior Pole.
§ Contains mostly Cones
§ The Fovea Centralis – a tiny pit in the centre of the Macula Lutea –
Contains ONLY Cones.
o NB: Cone density decreases toward the retinal periphery.
o NB: Rod density increases toward the retinal periphery.

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- The Eye’s 2 Segments & Fluids:
o The Lens & its Ciliary Zonule (Suspensory Ligaments) Divide the eye into 2 segments:
o 1. Anterior Segment:
§ In front of the lens.
§ Filled with ‘Aqueous Humour’ – a clear, plasma-like substance:
• Features:
o Continually formed by capillaries of the Ciliary Processes in the posterior
chamber.
o Flows from the Posterior Chamber to the Anterior Chamber
o Drains from Ant. Chamber into venous blood via the Scleral Venous Sinus
(Canal of Schlemm) which encircles the Sclera-Cornea Junction
o Has the same refractive index as the Cornea
• Functions:
o Its pressure supports the eyeball internally.
o Supplies Nutrients & Oxygen to the Lens & Cornea
§ Subdivided by the Iris into 2 Chambers:
• Anterior Chamber:
o Between the Cornea & the Iris
• Posterior Chamber:
o Between the Iris & the Lens.
§ Contains:
• Cornea
• Iris
• Lens
• Ciliary Muscles (Lens accommodation)
• Ciliary Processes (Aqueous humour production)
• Aqueous Humour
• Ciliary Zonule (Suspensory Ligaments)
• Scleral Venous Sinuses (Canal Of Schlemm)

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o 2. Posterior Segment:
§ Behind the lens.
§ Filled with a clear gel called ‘Vitreous Humour’ (“Glassy Fluid”):
• Features:
o Formed in the Embryo & Lasts a Lifetime
o Has the same refractive index as the cornea
• Functions:
o Transmits light
o Supports the posterior surface of the lens
o Holds the Neural Retina firmly against the Pigmented Layer
o Contributes to Intraocular Pressure
§ Contains:
• Vitreous Humour
• Retina
• Choroid
• Sclera
• Macula Lutea & Fovea Centralis
• Optic Disc
• Optic Nerve

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- The Eye’s Lens:
o Features:
§ Biconvex
§ Transparent
§ Flexible
§ Enclosed in a thin, elastic capsule
§ Held in place by the Ciliary Zonule (Suspensory Ligaments)
§ 2 Parts:
• Lens Epithelium:
o On the Anterior Lens Surface
o Cuboidal Cells
• Lens Fibres:
o Form the bulk of the lens
o Arranged in layers (like an onion)
o Lens Physics:
§ A lens of a certain ‘power’ has a certain Focal Point. The distance between the lens & the
focal point is the Focal Distance.
§ NB: The eye has a fixed Focal Distance, therefore the Lens ‘Power’ must be variable.
o Function:
§ Focuses light rays onto the retina.
§ Accommodation: Changes shape (& hence, lens ‘Power’) to maintain Focal Distance.

o Focal Disorders:
§ Emmetropia (Normal Vision)
§ Myopia (Short Sighted) – Eye is too long
§ Hyperopia (Far Sighted) – Eye is too short

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- Photoreceptors:
o The cells that transduce light. (Rods & Cones)
o Contain an array of Visual Pigments (Photopigments) that change shape as they absorb light:
o These Photopigments are imbedded in areas of the Photoreceptor Membranes that form discs.
§ NB: Folding the PM into discs magnifies the surface area available for trapping light.
o Photoreceptor Anatomy:
§ Outer Segment:
• Contains the Membranous Discs embedded with Photopigments
§ Connecting Cilia:
• Joins the Outer & Inner Segments
§ Inner Segment:
• Contains the Photoreceptor Cell Bodies
o Differences (Rods Vs. Cones):
§ Have different thresholds for activation.
§ Contain different visual pigments - absorb different wavelengths of light.
§ Are “wired” differently.
o Rods:
§ High Sensitivity (Respond well to dim light)
§ Contain only 1 type of Photopigment (Therefore only send a ‘monochrome’ signal)
• Hence why things have no ‘colour’ in very dim light.
§ As many as 100 Rods may feed into a single Ganglion Cell à Fuzzy, indistinct vision.
o Cones:
§ Low Sensitivity (Requires bright light for activation)
§ Have 1 of 3 different pigments that respond to different colours. (Allow you to see colour)
§ Each Cone has its OWN Private Ganglion Cell à Detailed, High-Res vision.

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- Phototransduction:
o Transforming light waves into electrical impulses.
o The light-absorbing molecule is called ‘Retinal’. (A derivative of Vitamin-A)
o Retinal combines with proteins called ‘Opsins’, to form 4-types of Photopigments.
o The wavelengths absorbed by the different Photopigments depend on the Type of Opsin contained.
o The Underlying Process:
§ In the Dark:
• Cyclic-GMP holds Na+ Channels open in the Outer-Segment Membrane (Na Influx)
• Na+ Flows from the Outer-Segment, through the Connecting Cilia, and into the cell
body. Na/K-ATPases pump Na+ out of the cell body. (This constant flow of current is
around -40mV, and is termed “Dark Current”)
• -40mV is a Depolarisation Potential (RMP ≈ -70mV) à Cell is Active
• Active Photoreceptors constantly release Glutamate.
• Glutamate Directly Inhibits the Bipolar Neurons à Indirectly inhibit Ganglion Cells.

§ When Light Strikes:

• Light strikes the inactive isomer of Retinal (“11-cis”), converting it to its active
isomer.

• The Active Retinal Isomer (“all-trans” Isomer) causes Opsin to change shape to its
activated form.
• The Retinal-Opsin combination breaks down, allowing Retinal & Opsin to separate.
• The “All-Trans”-Retinal activates an enzyme cascade à ↓cGMP levels à Closure of
Na+ Channels in Outer-Segment.
• Current Flow Ceases à “Dark Current” disappears à Cell is repolarised to ≈-70mV
• Cell is Inhibited à Stops releasing Glutamate à Removes Bipolar Cell Inhibition.
• Active Bipolar Cell à Stimulates Ganglion Cell à Action Potential along Optic Nerve.

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- Light/Dark Adaptation:
o Light Adaptation:
§ Occurs when we move from Darkness into Bright Light. We are momentarily dazzled – as the
retina is still “set” for dim light. At this point, both Rods & Cones are strongly stimulated,
causing large amounts of Photopigment to be broken down à Floods the brain with signals
à Glare.
§ To Compensate, the Rod system quickly desensitises and essentially turns off. The Cone
system rapidly adapts, and takes over. Hence, overall the retina Desensitises.
§ Can take up to 60sec.
o Dark Adaptation:
§ Occurs when we move from Brightness to Darkness. Initially we see nothing but black
because:
• 1. Cones stop functioning in low light. &
• 2. Because Rods have been ‘bleached’ out by the bright light & are still turned off.
§ Once rhodopsin accumulates in the Rods, their function slowly increases.
§ Can take more than 30mins.
- Retinal Processing:
o Most Direct Route of Info – Photoreceptor à Bipolar Cell à Ganglion Cell.
o However, Lateral Inputs (Horizontal & Amacrine Cells) – Provide a level of Processing @ the Retina.
- Pathways to the Brain:
o Ganglion Cell axons become the Optic Nerve.
o Some of the Optic Nerve Fibres cross @ the Optic Chiasm.
o After the Optic Chiasm, Optic Nerves become the ‘Optic Tracts’.

o Optic Tract fibres synapse in the:

§ Superior Colliculi of the Midbrain (Blue Circles):
• - Visual Reflex Centres controlling Extrinsic Eye Muscles
§ Lateral Geniculate Nucleus of the Thalamus (Red Circle):
• - Sorts/Relays info Via the Optic Radiation to the Primary Visual Cortex. (Pink Circle)
• Emphasis on Cone input
• Sharpens Contrast
§ Primary Visual Cortex (Pink Circle):
• Topographical map of the Retina (Similar to Homunculus)
• Basic Processing Tasks:
o Light Vs. Dark
o Orientation of Object
o Sends Info to Visual Association Areas – regarding Form, Colour & Motion.
§ More Complex Processing occurs elsewhere: (Temporal, Parietal & Frontal Lobes)

o Information Route/Pathway: Photoreceptor à Bipolar Cell à Ganglion Cell à Optic Nerve à Optic
Chiasm à Optic Tract à Superior Colliculus / Lateral Geniculate Nucleus of the Thalamus à Primary
Visual Cortex à Visual Association Area à Perception.

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 Taste/Smell:
Overview:
- Function: To alert us to whether stuff nearby/in our mouth is to be savoured or avoided.
- Receptor Type: Chemoreceptors (Respond to chemicals dissolved in solution)

Gustation (Taste):
- Location of Taste Buds:
o Located primarily in the oral cavity:
§ Mainly on the Papillae of the Tongue
§ Also on Soft Palate
§ Inner surface of Cheeks
§ Pharynx
§ Epiglottis
o Most taste buds are found on the Papillae of the Tongue:
§ On the tops of the Fungiform Papillae
§ On the side-walls of the Circumvallate Papillae
- Structure of Taste Buds:
o Each taste bud consists of 50-100 epithelial cells. (3 Types of associated epithelial cells):
§ Supporting Cells:
• Form the bulk of the taste bud.
• Insulate the Receptor Cells from each other
§ Receptor Cells:
• Have Long Microvilli that project from their tips, through a taste pore to the surface.
• These Long Microvilli (Gustatory Hairs) are the sensitive portions of these cells.
• Taste fibres of the Facial/Glossopharyngeal/Vagus Cranial Nerves coil around the
Receptor Cells.
§ Basal Cells:
• Act as stem cells
• Divide & differentiate to replace the Receptor Cells every 7-10 Days

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- Basic Taste Sensations:
o Sweet - Sugars, some Amino Acids, Lead Salts
o Sour - Acids
o Salt - Metal Ions (Particularly Sodium)
o Bitter - Alkaloids (Quinine, Caffeine, and Nicotine) – NB: Dislike for bitter is Protective.
o Umami - “Delicious” - Glutamate (Steak, Cheese) & MSG.
o NB: Most ‘tastes’ are a mixture of these basic taste sensations.
o NB: Taste ‘likes/dislikes’ have homeostatic values –
§ Umami à leads to intake of Proteins
§ Sweet à leads to carbohydrate & mineral intake
§ Salt à leads to electrolyte intake
§ Sour à many sour (naturally acidic foods) are a rich source of Vit.C
§ Bitter à Many natural poisons & ‘off’ foods are bitter – hence a natural dislike is protective.
- Physiology of Taste:
o Tasting requires a chemical to dissolve in the saliva, then diffuse through a Taste Pore, and contact
Gustatory Hairs.
o Binding of chemical induces a depolarising potential à Release of Neurotransmitter.
o Neurotransmitter à Triggers dendrites of sensory nerves à Action Potentials.
o NB: Different receptor cells have different thresholds (Eg. Bitter cells are very sensitive)
- Taste Transduction:
o Basic Overview:
§ Stimulation of Gustatory Cell à leads to an ↑in intracellular [Ca+] à Causes NT Release à
Stimulates sensory nerves.
o Each taste-quality has its own way of stimulating the receptor cells:
§ Salty – due to Na+ influx à directly depolarises the Gustatory Cell.
§ Sour – due to H+ either: 1) Entering the cell, 2) Opening Ion Channels, or 3) Blocking K+
Channels.
§ Bitter, Sweet & Umami – G-Protein Linked Receptors that produce depolarisation.
- Gustatory Pathway:
o Afferent fibres from taste buds run in 3 Cranial Nerves:
§ Facial (first 2/3 of tongue)
§ Glossopharyngeal (last 1/3 of tongue)
§ Vagus (Epiglottis & Lower Pharynx)
o Afferent Fibres synapse in the Solitary Nucleus of the Medulla à Thalamus à Gustatory Cortex in
Parietal Lobes.

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Olfaction (Smell):
- NB: ≈80% of taste is in fact smell.
- Location of Olfactory Receptors:
o Located in the ‘Olfactory Epithelium’ – a 5cm2 patch of Pseudostratified Columnar Epithelium in the
roof of the Nasal Cavity.
o Between the olfactory epithelial cells are the Olfactory Receptor Cells.
- Olfactory Receptor Regeneration:
o Basal Cells in the basal side of the olfactory epithelium differentiate & replace Olfactory Receptor
Cells every ≈60 days.
- Structure of Olfactory Receptor Cells:
o They are Modified Bipolar Neurons
o Have a thin apical dendrite, terminating in the olfactory mucus as Olfactory Cilia. (↑Surface Area)
o Have thin, Unmyelinated Axons that collect to form the Olfactory Nerve (CN-I)
§ Filaments of the Olfactory Nerves project superiorly through the Cribriform Plate.
§ Axons Synapse in the Olfactory Bulbs.

- Specificity of the Olfactory Receptors:

o Humans can distinguish ≈10,000 odours, but smell can’t be classified like taste can.
o Receptors are stimulated by different combinations of chemicals.
o There are thought to be ≈1000 “smell” genes that code for special “Odorant binding proteins”
(Special Receptor Proteins).
o It is though that each receptor cell has only 1 type of receptor protein à Specificity.

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- Physiology of Olfactory Receptors:
o For an odorant to be smelt, it must dissolve in the olfactory mucus.
o Once dissolved, odorants:
§ Stimulate the olfactory receptors by binding to Odorant Binding Proteins in the membranes
of the Olfactory Cilia
§ Stimulated Odorant Binding Proteins à Activate G-Proteins à Activate Adenylate Cyclase
§ Active Adenylate Cyclase synthesises Cyclic AMP
§ cAMP à Opening Cation Channels à Depolarisation.
§ Depolarisation à Action potential à Stimulates the Olfactory Bulb.

- The Olfactory Pathway:

o Olfactory Receptors à Mitral Cells (in ‘Glomeruli’ – Each glomerulus receives only 1 type of odour)
à Mitral Cell Axons (Olfactory Tracts) à Either:
§ 1) The Thalamus à Olfactory Cortex & Frontal Lobe (conscious interpretation/identification).
§ 2) The Hypothalamus, Amygdala & other Limbic System regions – Elicit emotional responses
to odours.
- Desensitisation:
o In the Olfactory Bulbs, there are Granule Cells that release GABA (Inhibitory NT) à Inhibits Mitral
Cells.
o This inhibition of Mitral Cells ensures that only highly excitatory impulses are transmitted.
o This enables us to ‘shut out’ constant smells.

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 Week 11
Neuroscience Notes
Special Senses II: Hearing & Equilibrium

Functional Overview of the Ear:

- Ear is Responsible for 2 Special Senses:
o Hearing – Associated with Outer, Middle & Inner Ear (Cochlear) Structures.
o Equilibrium - Associated with just the Inner Ear (Vestibular Apparatus)
- NB: Receptors for both = “Hair Cells”: (NB: their functional differences are due to specialised anatomy)
o How they Work:
§ Hair Cells have ‘Cilia’ projecting from their apical surface into gelatinous masses:
• Ie. Otolithic Membrane (in the Maculae of the Cochlea)
• Ie. The Cupulae (in the Crista Ampullaris of the Vestibular Apparatus)
§ These ‘Cilia’ are distorted by movements in the gelatinous masses à Change in Membrane
Potential (:. Hair Cells are Mechanoreceptors)
• The Greater the distortion, the greater the change in Membrane Potential.
• NB: The Polarity of the Change in Membrane Potential is determined by the
Direction of the distortion.
o How Distortion of Cilia causes the Change in Membrane Potential:
§ At the top of each cilia, there are Mechano-Gated K+ Channels, joined together by ‘Tip Links’
§ At Rest: Half of the K+ Channels are open, maintaining RMP.
§ If Distorted & Tip Links are Stretched: All K+ Channels open à Depolarisation
§ If Distorted & Tip Links are Compressed: All K+ Channels are closed à Repolarisation
o NB: Neurotransmission from Hair Cells à Cochlear Nerve Dendrites is via Ca+-Mediated Exocytosis.

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Ear Anatomy:
- Outer Ear:
(Air-Filled)
o Pinna (Auricle):
§ The Outermost part of the ear
§ The bit that funnels sound waves into the External Auditory Canal
o External Auditory Canal:
§ The canal that conducts the soundwaves waves into the Tympanic Membrane (Eardrum)
§ Contains Ceruminous Glands – Secrete Cerumin (Earwax)
§ Abuts the Middle ear @ the Tympanic Membrane (Ear-Drum)

- Middle Ear:
(Air-Filled Cavity within the Temporal Bone)
o Tympanic Membrane (Eardrum):
§ Thin, translucent, connective Tissue Membrane (Skin on outside, mucosa on inside)
§ Connect to the 3 Auditory Ossicles
§ Soundwaves cause it to vibrate à Causes the Auditory Ossicles to Vibrate.
o The 3 Auditory Ossicles:
§ Malleus (“Hammer”/“Mallet”)
§ Incus (“Anvil”)
§ Stapes (“Stirrup”)
§ NB: 2 Skeletal Muscles (Tensor Tympani & Stapedius) Reflexively contract when ears are
assaulted by loud sounds – Reduces Sound Conduction.
o Oval Window of the Cochlea:
§ Transfers Vibration of the Stapes à Into the Cochlea.
o Eustachian (Pharyngotympanic) Tube:
§ Equalizes pressure between the Outer & Middle Ear

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- Inner Ear – (Cochlea & Vestibular Apparatus):
(Fluid-Filled Bony & Membranous Labyrinths)

o Cochlea - HEARING:
§ The Spiral-Shaped Organ
§ Begins @ the Oval Window:
• The Entry Point of the Cochlea.
• The hole covered by membrane
• Separates the air-filled middle ear from the fluid-filled inner ear.
§ Ends @ the Round Window:
• The Exit-Point of the Cochlea
• Also covered by membrane
• Also separates the air-filled middle ear from the fluid-filled inner ear.
§ Consists of 3 Coiled Ducts – Separated by 2 Membranes:
• Scala Vestibuli (Vestibular Duct):
o Begins @ the Oval Window
o Ends @ the apex of the Cochlea
o Filled with Perilymph.
o Separated from the Scala Media by the Vestibular Membrane.
• Scala Media (Cochlear Duct):
o Runs through the middle of the Cochlea.
o Separates the Vestibular Duct & Tympanic Duct.
o Filled with Endolymph.
o Separated from the Scala Tympani by the Basilar Membrane.
o Contains the Spiral Organ of Corti: (See Next Page)
• Scala Tympani (Tympanic Duct):
o Begins @ the apex of the Cochlea
o Ends @ the Round Window
o Filled with Perilymph.

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 § The Spiral Organ of Corti:
• Sits inside the Scala Media & runs along the Basilar Membrane.

• Composed of:
o The Tectorial Membrane (Overlying the Hair Cells)
o Hair Cells (Receptors for hearing) – Associated with cochlear nerve fibres:
§ 1x Row of Inner Hair Cells – Has several inputs to the Spiral Ganglion
- Sends most of the auditory info.
§ 3x Rows of Outer Hair Cells – Has Only 1 input to the Spiral Ganglion
- Plays a role in Signal Amplification
o Supporting Cells
o The Basilar Membrane
• Cochlear Branch of the Vestibulocochlear Nerve Originates Here.

Cochlear Nerve

Scala Vestibuli

Scala Media

Scala Tympani

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§ Audiotransduction:
• Soundwaves are funnelled by the Auricle of the ear into the External Auditory Canal.
• à Soundwaves vibrate the Tympanic Membrane (Eardrum)
• à Eardrum vibration is passed through the Auditory Ossicles to the Oval Window.
o NB: This transfer of vibration from the EardrumàOval Window AMPLIFIES it
by ≈20x (As the eardrum surface area is ≈20x that of the Oval Window)

• à Oval Window vibration is transmitted into the Perilymph of the Scala Vestibuli.
• à Waves travelling through the Scala Vestibuli penetrate the Vestibular Membrane
at different points relative its Resonant Frequency & enter the Scala Media:
o High sounds resonate the Vestibular Membrane closer to the oval window
o Low sounds resonate the Vestibular Membrane away from the oval window

• à Waves exit the Scala Media by Penetrating the Basilar Membrane & enter the
Scala Tympani:
o The waves penetrating the Basilar Membrane cause it to Vibrate.
o Vibration of the Basilar Membrane pushes the Hair Cells in the Organ of Corti
up into the Tectorial Membrane, Distorting the Cilia & Initiating Graded
Potentials in the Cochlear Nerve.

• à Waves continue down the Scala Tympani & leave the Cochlea via the Round
Window – This prevents echoing of the sound waves within the Cochlea.

§ Pitch & Volume:

• Pitch – is coded in the area of the basilar membrane which is distorted by the wave.
• Volume – is coded by the degree of distortion of the hair cells by the wave.

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Pathway From the Cochlea to the Brain:
- Hair Cells à Cochlear Nerve (Incl. Spiral Ganglia) à Cochlear Branch of the Vestibulocochlear Nerve à
Cochlear Nuclei of the Medulla à

- à Superior Olivary Nucleus à Lateral Lemniscal Tract à Inferior Colliculus à Medial Geniculate Nucleus of
the Thalamus à
o Primary Auditory Cortex – (Conscious Sound)
o Superior Colliculus – (Auditory Reflexes – Startle, Turning Head, etc.)

§ Deafness:
• Conduction Deafness:
o Problem with Soundwave Conduction (Ie. Mechanical Structures)
§ Eg. Earwax
§ Eg. Perforated Ear Drum
§ Eg. Fused Ossicles
• Sensorineural Deafness:
o Problem with Soundwave Transduction (Ie. Neural Structures)
§ Eg. Damaged Hair Cells
§ Eg. Damaged Cochlear Nerve
§ Eg. Damaged Auditory Cortex

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o Vestibular Apparatus - EQUILIBRIUM:
§ Vestibular Branch of the Vestibulocochlear Nerve Originates Here.
§ Consists of:
• A Vestibule, Containing:
o 1x Utricle:
o 1x Saccule:
• & 3 Semicircular Canals.

§ The Vestibule: NB: Both the Utricle & Saccule have a Maculae:
• Maculae = Receptor Organs for Linear Acceleration (Static Equilibrium)
o Provides Info about Orientation of the Head with respect to Gravity, Linear
Acceleration & Angular Acceleration.
• Composed of:
o Hair Cells (Cilia Project into the Otolithic Membrane)
o Supporting Cells
o Otolithic Membrane - (Gelatinous Mass with ‘Otoliths’ – “Ear Stones” – of
Calcium Carbonate Crystals resting on top. These ‘Otoliths’ provide the
inertia required to move the Otolithic Membrane during head movement)

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§ The 3 Semicircular Canals: NB: At the end of each Canal is a Swelling = “Crista Ampularis”:
• Crista Ampularis = Receptors for Rotation (Dynamic Equilibrium).
• Composed of:
o Hair Cells (Cilia Project into the Cupula)
o Supporting Cells
o Cupula – (Gelatinous Mass encircling the entryway of each Crista Ampularis.
Rotation of the head in the plane of the canal causes fluid movement over
the Cupula, distorting the Hair Cells)

• NB: There are 2 Semi-Circular Canals for each ‘Plane’ of Movement:

o One on each side of the head
o This allows you to determine the Direction of head motion.

• NB: Each Semi-Circular Canal is Responsible for a different Plane:

o Anterior – (‘Ear-to-Shoulder’ Motion)
o Posterior- (‘Nodding’ Motion)
o Lateral - (‘Shaking’ (‘no’) Motion)

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Equilibrium Pathways To the Brain:
- Equilibrium is Subconscious
- Info goes straight to the reflex centres in the Brainstem & Cerebellum:
o Vestibular Nuclei:
§ Integrates Balance + Receive some Visual & Somatic Inputs
§ Sends commands to Brainstem Motor Centres controlling Eyes & Neck/Limb/Trunk Reflexes.

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 Week 12
Neuroscience Notes
Pain & Nociception

Overview of Nociceptive Nerves:

- = Sensory nerves that carry “Pain” information (Nociception)
o à Tells the brain that tissues have been injured – Important for survival.
- 2 Types of Nociceptive Nerves:
o Type-C Fibres:
§ Very Thin, Un-Myelinated Fibres :. Slow Conduction :. Dull, Achy, Burning Pain
§ Poorly-Localised
o Type-Aδ Fibres:
§ Relatively Thin, Myelinated Fibres :. Faster (-than C-Fibres) :. Sharp (Acute), Searing Pain
§ Well-Localised
- NB: Conduction Speed increases with ↑Myelination & ↑Diameter.
- NB: Both Fibres are sensitive to the same stimuli.
- NB: Both Fibres Respond to the Multiple Stimuli – Ie. Are Polymodal

- Nociceptors Are Polymodal:

o Ie. Respond to a wide variety of stimuli:
§ Eg. Mechanical
§ Eg. Chemical
§ Eg. Thermal
o However, the stimulus must be sufficiently intense to stimulate Nociception. (Due to High Threshold)
§ Nociception is stimulated by Opening of cation channels à Brings nerve to threshold à
Voltage-Gated Na+ Channels open à Depolarisation (Action Potential).
o NB: Much of this polymodality is due to the TRPV1-Receptor’s ability to respond to various stimuli.
(Explained Later)

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- Organisation of Nociceptors:
o 1. Nociceptive Nerve:
§ Distal Nerve Terminals = Simple, Un-encapsulated Nerve-Endings in Viscera/Periphery.
§ Cell Body is in Dorsal Root Ganglia

o 2. Dorsal Horn of Spinal Cord:

§ Proximal (Central) Nerve Terminal Synapses in Dorsal Horn of Spinal Cord.
§ The Substantia Gelatinosa Modulates Nociceptive Transmission – A whitish gelatinous mass
at the apex of the dorsal horn – Plays a role in inhibiting the communication between
Nociceptive Nerves & Ascending Pathways à Suppress Pain.
o 3. Ascending Spinal Pathways:
§ Nociceptive Nerves synapse with 1 of 2 Ascending Pathways transmits to the Brain:
• Spinothalamic Pathways
o Neospinothalamic
o Palaeospinothalamc
• Reticulospinal Pathway

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- Neurotransmitters:
o Predominantly Peptide NT’s (Neuropeptides):
§ *Substance-P
§ Neurokinin-A (NKA)
§ CGRP (Calcitonin-Gene Related Peptide)
§ – and the Amino Acid: *Glutamate
o Synthesised in Cell Bodies:
§ Peptides = Proteins :. Requires DNA for Synthesis :. Synthesis occurs close to the Nucleus.
§ NB: Neuropeptides are stored & transported in Vesicles.
o Bilateral NT Transport & Release:
§ Released @ Dorsal Horn à Nociceptive Transmission
§ Released @ Distal-Terminal à ‘Neurogenic Component of Inflammation’ à Lowers
Threshold à Ie. Makes the Nociceptor Hypersensitive à Potentiates Further Nociception.

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Process of Nociception:
- 1. Noxious Stimulus @ Distal Nerve Terminal:
o A Potentially Damaging Stimulus (Or summation of multiple different potentially damaging stimuli)
brings the Nerve to Threshold à Action Potential, leading toà
§ 1. NT release in Dorsal Horn (Glutamate & Substance P)à Transmits to Ascending Pathways
§ 2. Bilateral Neuropeptide Transport to Central & Peripheral Nerve Terminals.
o “PRODUCTIVE PAIN” – Pain Associated with Initial Activation of Nociceptive Nerves :
§ Via opening of Cation Channel Receptors in Distal Nerve Terminals à Depolarisation.
§ Examples of Receptors & Their Stimulators That Stimulate/Modulate Nociception:
• *TRPV1-Receptor (Ca+ Channel)(“TRP Vanilloid Receptor1”). Opened by:
o Capsaicin (from hot chillies)
o H+ (Acid)(Often a result of inflammation)
o Heat Hence, Polymodal.
o Mechanical (Mechanism unclear) àNociception
o Eicosanoids (Lipid mediators of inflammation)
• Bradykinin Receptors:
o Sensitive to Bradykinin.
o Bradykinin Activates TRPV1-Receptor à Depolarisation à Nociception.
• Prostanoid Receptors:
o Sensitive to Prostaglandins.
o Open Na+ Channels à
o Inhibit K+ Channels à à ↑MP à :. Lowers Threshold à ↑Sensitivity
o Open TRPV1-Receptors à
• Opiate/Cannabinoid Receptors:
o Sensitive to Opioid Peptides Cannabinoids.
o Open K+ Channels à K+-Efflux à ↓MP (Hyperpolarises Cell) à ↓Sensitivity
o NB: This is one of the targets of Opioid Analgesics.
• ASIC – (“Acid Sensitive (gated) Ion Channel”):
o Sensitive to H+ Ions
o Stimulation à Depolarisation of Cell à Nociception
• Also Exhibits Receptors for a Wide Range of Mediators (Most not shown):
o Glutamate
o GABA
o ACh
o Serotonin
o ATP
o Noradrenaline
o Histamine
o Somatostatin

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- 2. Bilateral Neuropeptide Transport:
o The Nociceptor Releases Neuropeptides (Substance-P, Glutamate, Neurokinin-A & CGRP) at both
ends:
§ Release @ Dorsal Horn à Nociceptive Transmission
§ Distal-Terminal Release à ‘Neurogenic Component of Inflammation’ à Lowers Threshold à
Ie. Makes the Nociceptor Hypersensitive à Potentiates Further Nociception.

o “NON-PRODUCTIVE PAIN” – Pain Associated with Ongoing Chemical Stimulation (Potentiation):

§ (Pain persists long after the initial noxious stimulus – particularly with Inflammation/Injury)
• NB: Non-Productive Pain should dissipate as the injury heals.
§ Chemical Factors Responsible:
• *Nociceptor Neuropeptides (Potentiators):
o *Substance-P
o Neurokinin-A (NKA)
o CGRP
o – And *Glutamate (Amino Acid)
• *Prostaglandins (Potent Pain-Enhancing Substances)
o Released during Inflammation & Ischaemia à Enhance the actions of other
mediators (Esp. Bradykinin & Serotonin) à Hyper-sensitising Distal
Nociceptive Nerve Terminals.
o How? – By 1) Inhibiting K+ Ion Channels,
And 2) Hypersensitising TRPV1-Receptors to noxious stimuli.
• Kinins (Potent Pain-Producing Substances):
o *Bradykinin
§ 1. Produces Pain - Triggers Action Potential in Nociceptive Neuron by
activating TRPV1R Receptors (Ca+ Influx à Depolarisation)
§ 2. Triggers Prostaglandin & Bradykinin Release à enhances its own
action on the Nerve Terminal
o Kallidin
• Neurotransmitters (Mediators):
o Serotonin
o Histamine
o ACh
• Metabolites:
o Lactic Acid (eg. Ischaemic pain if stimulus damaged the tissue’s blood supply)
o K+
o H+
o ATP Released by damaged/lysed cells
o ADP
§ Non-Chemical Factor:
• Primary Nociceptive Afferents inhibit the Substantia Gelatinosa à Inhibit Pain
Suppression à Potentiate Pain.
§ NB: NSAIDs (Non-Steroidal Anti Inflammatory Drugs) – eg. Ibuprofen & Aspirin, elicit their
effect by Reducing Prostaglandin Synthesis à Therefore preventing Sensitisation of
Nociceptive Terminals.

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- 3. Synaptic Transmission @ Dorsal Horn (Nociceptors Synapse with Ascending Fibre-Tracts in Spinal Cord):
o The 2 Primary Neurotransmitters:
§ *Substance-P
§ *Glutamate
o Other less-important NT’s:
§ VIP
§ Somatostatin
§ Serotonin
§ CCK
§ GABA
§ Opioids

o Nociceptive Nerves synapse with 1 of 2 Ascending Pathways that transmit to the Brain:
§ 1. Spinothalamic Pathways (Spine à Thalamus):
• Neospinothalamic (Lateral):
o Somatotopical
o Small Receptive Fields à Good Localisation
o Aδ-Fibres = Main Afferents
o Function = Localizing & Discrimination of Pain.
o Projections from the Thalamus Lead to:
§ *Primary Somatosensory Cortex
• Palaeospinothalamic (Medial):
o Not Somatotopical
o Broad Receptive Fields à Poor Localisation
o C-Fibres = Main Afferents
o Function = ‘Alerting’ – “We’ve been Injured”
o Projections from the Thalamus lead to:
§ *Primary Somatosensory Cortex
§ Somatosensory Association Areas
§ Prefrontal Cortex
§ Cingulate Cortex
§ 2. Spinoreticular Pathway (Spine à Reticular Formation [RAS] in Brainstem) :
• Lacks Somatotopy.
• Broad Receptive Fields à Poor Localisation
• Function = ‘Alerting’ – “We’ve been Injured”
• RAS Function:
o Arousal/motivation/consciousness/circadian rhythms/HR/Respiration/etc.
o Is also the FILTER between the Conscious & Unconscious mind, ignoring
background ‘Noise’ & only bringing the ‘Important’ stimuli to Consciousness.
• RAS Projects to many brain regions:
o Including Thalamus & Hypothalamus à Changes body state
§ NB: Both decussate at the spinal cord level & ascend on the Contralateral side.
§ NB: Thalamus receives ALL SENSORY INPUTS – only ≈10% is Nociceptive.
§ (3.) Trigeminal Nerve:
• Responsible for Nociceptive Info from Head & Face
• Projects to Thalamus (Similar to Spinothalamic)

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o Regulating Nociceptive Transmission - “The Pain-Gate Mechanism” & “Descending Inhibitory
Pathways”:
§ The Substantia Gelatinosa (Spinal Regulation of Nociceptive Transmission):
• A whitish gelatinous group of neurons at the apex of the dorsal horn
• When Active à Suppresses Pain.
• Pain-Modulation @ the level of the Spinal Cord:
o àInhibiting Nociceptive Transmission à Suppressing Pain:
§ Afferent Mechanoreceptors (Aβ-Fibres) & Descending Inhibitory
Pathways à Stimulates the SG à Decreases Nociceptive
Transmission à Decreases Pain.
§ NB: Exploited in Narcotic Analgesics
o àPotentiating Nociceptive Transmission à Potentiating Pain:
§ Afferent Nociceptive Signals (C & Aδ-Fibres) à Inhibiting the SG à
Increased Nociceptive Transmission à Increased Pain

§ Descending Inhibitory Pathways (Central Regulation of Nociceptive Transmission):

• Pathway: A Neuronal chain from the PAG (Midbrain) à NRM (Rostro-Ventral
Medulla) à Substantia-Gelatinosa & Dorsal Horn of the Spinal Cord.
• Functions to Temporarily Inhibit Nociceptive Transmission between Nociceptors &
Spinal Cord (A few hours max).
• CNS Regions Involved:
o PAG – Periaqueductal Grey matter (Midbrain):
§ Receives Inputs from:
• *Locus Coeruleus*
• Reticular Formation (Aka: Reticular Activating System – RAS)
• Amygdala
• Hypothalamus
• Prefrontal Cortex
• Insula
§ Projects to – ‘Nucleus Raphe Magnus’ (Raphe Nuclei) in the Rostro-
Ventral Medulla.
§ NB: It is Disinhibited (Activated) by Opioids & GABA-Antagonists à
Activates NRM à Inhibits Dorsal Horn Synapse.
o NRM – Nucleus Raphe Magnus (Rostro-Ventral Medulla):
§ Projects to Dorsal Horn of Spinal Cord & acts in 2 Places:
• 1. Directly Inhibits Nociceptive Transmission @ the Synapse.
• 2. Stimulates Substantia Gelatinosa à Inhibits Nociceptive
Transmission.
o Substantia Gelatinosa (Dorsal Horn of Spinal Cord):
§ When activated, it directly suppresses Nociceptive Transmission @
the Synapse.

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• Neurotransmitters Involved:
o *OPIOIDS*:
§ 1. Remove Inhibition of PAG (Activates PAG) à Stimulate NRM à
Inhibits Dorsal Horn Synapse
§ 2. Directly Inhibit Dorsal-Horn Synapse
§ – Hence, opioid analgesics work by activating Descending Inhibitory
Pathways & Direct inhibition of Dorsal Horn Synapse.
o *Noradrenaline – (From Locus Coeruleus – Directly Inhibits Dorsal-Horn
Synapse)
o *Serotonin (5-HT) – (From NRM – Directly Inhibits Dorsal-Horn Synapse)
o *Enkephalins – (From NRM – Directly Inhibits Dorsal-Horn Synapse)
o Adenosine ?
o NB: Low-Dose Tri-Cyclic Anti-Depressants can treat Neuropathic pain by
blocking re-uptake of NE, 5-HT, & Enkephalins in Dorsal Horn Synapse.

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o “Wind-Up”:
§ = Potentiation @ Synapses between C-Fibres & Dorsal Horn Nerves (Spinal Cord).
§ Afferent Nociception à Release of Substance-P & Glutamate into Dorsal Horn Synapse à
Remodelling of the synapse à ↓Threshold à Super-Sensitivity (↑Excitability).
• NB: Temporary(Normal)/Permanent(Abnormal)
§ Remodelling Events:
• Presynaptic:
o ↑Presynaptic NT Release
o ↓Presynaptic Inhibition
• Postsynaptic:
o ↑Postsynaptic Facilitation (Lowered Threshold)
o ↓Postsynaptic Inhibition
§ NB: This ‘Remodelling’ is mediated by both:
• Phosphorylation of Proteins/Receptors à Changes Function.
• ↑Transcription due to Prolonged action of Second-Messengers (eg. cAMP)
triggering Transcription Factors à ↑Number of proteins/New Proteins.
§ NB: Very Similar To Long-Term Potentiation (LTP):
• A Long-Lasting Post-Synaptic Depolarisation, induced through Repetitive Stimulation
& Summation of Excitatory Post-Synaptic Potentials.”
• Simply – “A Persistent Increase in Synaptic Strength & Excitability”
§ Termination of “Wind-Up”:
• Phosphorylated receptors/enzymes will be de-phosphorylated by Phosphatases.
• The excess synaptic proteins will degrade (due to half-life) and be replaced by the
correct number & type of proteins by normal transcription.

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 AfraTafreeh.com exclusive

- 4. Processing of Nociceptive Signals by the Brain:

o We Don’t know much about Central Nociceptive Processing.
o We Do Know:
§ -that Thalamic neurons project to Limbic Structures & Hypothalamus (As well as Sens.Cortex)
§ -Incoming Nociceptive Signals are “Weighted” in terms of importance.
§ -The brain’s “Response” depends entirely on comparison between the “Weight” of the signal
and all other sensory input
§ -Expectation/Anticipation of a painful event heightens the pain sensation after stimulus.
§ -Distraction is often effective in reducing pain.
o Pain = a decision made by the brain – Based on more than just Nociception:
§ Other Sensory Input
§ Context (Memory/Emotional/Danger (Survival)/Body Status/etc)

o There is no simple relationship between Nociception & Pain.

§ Nociception without Pain = eg. Firewalkers
§ Pain without Nociception = eg. Phantom Limb Pain/Neuropathic Pain

o Therefore Pain is SUBJECTIVE:

§ 2 equal injuries will affect 2 people differently.
§ 2 equal injuries @ different times affect the Same Person differently.
• Therefore, pain cannot be directly measured. Instead, a patient’s rating of pain is the
only measurement to go by (even if it is subjective).
o Q: How does the brain distinguish between ‘Fast’ (Aδ-Fibre) & ‘Slow’ (C-Fibre) input given that
both fibres terminate in the dorsal horn?
§ A: Hypothesis = 2 Ways:
• 1. Although the different fibre types synapse in the same ‘place’ (Dorsal Horn), they
synapse on different ascending neurons – Therefore, their individual info is carried to
the brain along separate pathways.
• 2. The brain uses the delay in the signals coming from the 2 fibre types (as they
conduct at different speeds) to determine fibre-type origin.

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 Clinical Relevance:
Neural Regeneration:
- Body’s attempt to re-connect severed/damaged nerves:
o Mediated by Schwann Cells
o Growth Factors are essential
o Aim – to extend a new segment of Axon àTarget.
o Rate – 1.5mm/day
- Process:
o 1. Axon is severed
o 2. Axon end seals & swells (as substances normally transported along the axon accumulate)
o 3. Axon distal to injury degenerates due to lack of nutrients & fragments are phagocytosed.
o 4. However, the Neurilemma in the Endoneurium remains Intact.
o 5. Schwann Cells Proliferate around site of injury, release growth factors & form a Regeneration-Tube
§ A) Growth Factors encourage Axonal Regrowth – “Sprouting”
§ B) Regeneration Tube guides these ‘Lamellopodia’ (Sprouts) to their original contacts.
o 6. Schwann Cells protect, support, and Re-Myelinate the Regenerating Axons.
o 7. Excess ‘sprouts’ are culled once a connection is re-established.
- Result:
o Never the same, but restores adequate sensitivity of sensory inputs
o NB: The CNS isn’t capable of Neural Regeneration.

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- NB: Neural Regeneration can become Corrupted:
o Disrupted Neural Regeneration 1 – Neuromas:
§ Sprout may overshoot the target, or the path forward may be blocked.
§ If no connection is made, sprouts can turn back on themselves à Forms a “Neuroma”.
• This can cause Sprout-ends to remodelà changing subtypes of ion channels &
receptors à Changing Sensitivity to stimulation.
o Voltage-gated Na+ channels go from high to low-threshold à ↑Sensitivity.
• NB: Neuromas can be a source of Spontaneous Ectopic Discharge (Similar to Heart)
§ NB: Thought to be a major cause of Phantom Limb Pain:
• Shooting/Stabbing/Pricking/Squeezing/Burning pains in distal portion of missing limb

o Disrupted Neural Regeneration 2 – Wrong Connection:

§ Relevant to Damaged Sensory Afferents close to DRG or Spinal Cord...
§ If Sprouts overshoot their target in the dorsal horn à they can synapse on the wrong
ascending fibres à Changes the Nature of the Innervation à Signals are misinterpreted by
the brain.
• Eg. A Damaged Aδ-Fibre (Mechano-afferent) synapses onto an Ascending Neuron
that is normally associated with C-Fibres.
• Result: Mechanical Sensory Input is now interpreted as Pain.

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Types/Features of Pain:
- Altered Pain Sensitivity:
o Increased pain sensitivity to noxious/non-noxious stimuli à ↑Non-Productive Pain.
§ Hyperalgesia:
• Where a mild noxious stimulus results in a heightened sense of pain.
• Ie. Something that should only hurt a little, hurts a lot.
§ Allodynia:
• Where pain is provoked by a non-noxious stimulus.
• Ie. Something that shouldn’t hurt, does.
o NB: Both can be Associated with Either:
§ A Healing Injury (Normal):
• Potentiation @ distal nerve terminals – Substance-P, Neurokinin-A & CGRP.
• Pain Amplifiers – Prostaglandins & Bradykinin
• “Wind-Up”: Potentiation @ central nerve terminals – Substance-P & Glutamate –
Temporary Remodelling of the synapse à ↓Threshold.
§ Neuropathic Origin (Abnormal):
• “Wind-Up”: Potentiation @ central nerve terminals – Substance-P & Glutamate –
Permanent Remodelling of the synapse à ↓Threshold.
• Other potential causes of Permanent Nociceptive Synapse Remodelling:
o Injury (Mech. Damage)
o Stroke (Ischaemic Damage)
o Multiple Sclerosis
o Diabetic Neuropathy
o Shingles

- Altered Pain Sensation:

o Dysthesia:
§ Unpleasant, abnormal sensation – Burning/Wetness/Itching/Electric Shock/Incl.Paresthesia.
§ May be Spontaneous Or Evoked
o Paresthesia:
§ Abnormal Tingling/Pricking/Numbness in Skin.
§ Eg. ‘Pins & Needles’

- Neuropathic Pain:
o Severe, Chronic Pain that isn’t associated with any current peripheral tissue damage. Rather, it is
caused by a primary lesion/dysfunction of the Nervous System that is often impossible to identify.
o Often results from Corrupted Neural Regeneration secondary to a past injury.
o Simply – Pain that doesn’t have an exogenous trigger.
o A Result of Permanent Synaptic Remodelling à Hypersensitisation:
§ Anatomical Malformations – Eg. Neuromas (Tangle of Nerves) due to mechanical nerve
injury & subsequent failed Neural Regeneration.
§ Molecular Alterations – Eg. Damaged nerve terminals begin to express α-Adrenergic
Receptors (NB: Abnormal) àBecome sensitive to Adrenaline.
• Therefore, Sympathetic Activity à Systemic Adrenaline Release à Pain.
§ Cellular Alterations – Eg. Spontaneous Neuronal Discharges due to a change in
number/type/& Sensitivity of Na+ Channels.
§ Physiological Alterations – Eg. Permanent “Wind-Up” à ↓Threshold.
§ Other potential causes of Permanent Nociceptive Synapse Remodelling:
• Injury (Mech. Damage)
• Stroke (Ischaemic Damage)
• Multiple Sclerosis
• Diabetic Neuropathy
• Shingles
o NB: Low-Dose Tri-Cyclic Anti-Depressants can treat Neuropathic pain by blocking re-uptake of NE,
5-HT, & Enkephalins in Dorsal Horn Synapse à Maintained Inhibition of Nociceptive Transmission.

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- Chronic Pain:
o On-going pain associated with a Progressive Disorder or Non-Healing Injury.
§ Includes ‘Neuropathic Pain’
o Is often insensitive to Narcotic Analgesics (Opioids)
o NB: There is often Discordance between Pain-Experience & Self-Report of Pain.

- Visceral & Parietal Pain:

o Visceral Pain:
§ NB: Visceral Sensory Inputs are Primarily Nociceptive.
§ NB: Primarily Associated with C-Fibres (Dull, Aching Pain)
§ Main Causes of Visceral Pain:
• Ischaemia
• Chemical Stimuli (Eg. Gastric/Duodenal Ulcer Rupture)
• Muscle Spasms in Hollow Organ
• Over-Distension of Hollow Organ
§ Most Sensitive to Diffuse Organ Damage rather than Localised Organ Damage.
• Ie. Diffuse organ damage à causes severe pain.
§ Nature of Visceral Pain:
• Dull
• Achy
• Poorly Localised
o Parietal Pain:
§ NB: Primarily Associated with Aδ-Fibres (Sharp, stabbing pain)
§ Main Cause of Parietal Pain:
• Severely Diseased Organ à Spreads to Parietal Membranes:
o Peritoneum
o Pleura
o Pericardium
o Meninges (NB: Brain is impervious to pain, but Meninges & Vessels aren’t)
§ NB: Meningitis is one of the most severe headaches known.
o Etc
• These Parietal Membranes have large numbers of Nociceptors.
§ Nature of Parietal Pain:
• Sharp
• Well-Localised

- Referred Pain:
o = Pain experienced as being associated with a tissue/body part that isn’t the actual site of injury:
§ Typically, Visceral Pain is felt in the Dermatomes of the Spinal Roots that also receive the
Visceral Afferents.
o Occurs due to Convergence of Visceral & Cutaneous Nociceptive signals @ the Spinal Cord:
§ Visceral C-Fibres synapse onto (and activate) the same Ascending Neurons as
Cutaneous/Muscular Aδ-Fibres.
§ Therefore, Noxious Visceral Stimuli are felt as pain in the tissues covered by the Aδ-Fibres
synapsing on the same Dorsal Horn Neuron.

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Reporting Pain:
- Paediatrics:
o Children experiencing pain may not be able to accurately report on that pain for many reasons:
§ May be Neonatal
§ May be unwilling to cooperate
§ May be incapable of understanding what you are asking when inquiring about their pain.
§ May be unable to describe their experience
§ They are afraid that if they report pain, they will get a needle (which they fear more)
§ May want to please Parents/Authority Figures (Docs/Nurses)
§ May be mentally/physically disabled
o This inability to accurately report on pain leads to “Discordance”, a feature of Paediatric Pain:
§ Where a child reports a certain degree (or lack) of pain that conflicts with observed
behaviour and activities.
§ The temptation is to attribute this to attention-seeking, malingering or psychological
problems.
§ However, discordance is simply a sign of a problem in pain evaluation
(measurement/assessment) and indicates the need to pursue further investigations.
o Measuring Pain in Children:
§ Neonates/Very Young Children/Disabled Children:
• Reports by Parents/Care-Givers
• ‘The Oucher’ Pain Scale – A ‘Visual Analogue Scale’ - Uses ethnically-specific photos
of young children in various stages of distress.

§ Children 8 Yrs+:
• Variation of McGill Pain Questionnaire – Uses 56 Adjectives graded on a scale of 0-5.

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- Older Children & Adults:
o Self-Report Scales – Eg. The McGill Pain Questionnaire – Uses 78 Adjectives graded on a scale of 0-5.

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Treatment & Pain Management:
- Effective Management ALWAYS STARTS with an Evaluation of the Pain Report:
o The Analgesic/Combination of Analgesics is Matched to the Pain Report.
- 3 Locations to Consider when Targeting Pain:
o 1. Peripheral Targets:
§ TRPV1R Receptors (Vanilloid Receptors – Sensitive to H+/Capsaicin/Heat/Mech):
• Capsaicin:
o Activates TRPV1R Receptors on C-Fibres à Causes Substance-P release
§ à Depletes the terminal of Substance-P (A Peptide)
§ à There will be a period of Analgesia while Sub-P is re-synthesised.
o Useful For:
§ Topical Arthritis Cream
§ Some Neuropathic Pain
§ Prostanoid Receptors (Sensitive to Prostaglandins):
• Non-Steroidal Anti-Inflammatory Drugs (NSAIDs) – (Aspirin/Ibuprofen)
o Mild Analgesic
o Anti-Inflammatory:
§ ↓Prostaglandin Production by inhibiting the enzyme Cyclo-
Oxygenase [COX]) à ↓Prostaglandin-Mediated Hypersensitivity of
Nociceptive Neurons.
o Useful For:
§ Mild-Moderate pain
§ Hyperalgesia
§ Allodynia
• COX-2 Inhibitors – (Celebrex)
o Mild Anti-Inflammatory Analgesic:
§ More specific than NSAID’s – Target COX-2 Enzyme – Less Side-
Effects)
§ ↓Prostaglandin Production by inhibiting the enzyme Cyclo-
Oxygenase-2 [COX-2]) à ↓Prostaglandin-Mediated Hypersensitivity
of Nociceptive Neurons.
o Useful For:
§ Mild-Moderate pain
§ Hyperalgesia
§ Allodynia
§ Opioid Receptors:
• Opioid Drugs – (Codeine, Morphine, Fentanyl):
o Strong Analgesics - Act at all 3 levels (Periphery, Spinal Cord, Brain)
o Activated Opioid Receptors on:
§ Distal Nerve Ending – (Periphery):
• Opens K+ Channels à K+-Efflux à Hyperpolarisation.
o May be used for Acute & Chronic Pain.
§ If used Acutely, a “Step-Down” Plan (to less potent agents) must be
used to prevent addiction.
§ Unknown:
• Paracetamol – (Panadol)
o Mild Analgesic:
§ Mechanism is unknown.
o WEAK Anti-Inflammatory:
§ Weak inhibit of Prostaglandin Synthesis
o Useful For Analgesia when Inflammation isn’t an issue.

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o 2. Spinal Cord Targets:
§ Substantia Gelatinosa
§ Dorsal Horn Synapse
§ Effective Analgesics:
• Opioids – (Codeine, Morphine, Fentanyl):
o Strong Analgesics - Act at all 3 levels (Periphery, Spinal Cord, Brain)
o Activated Opioid Receptors on:
§ Distal Nerve Ending – (Periphery):
• Opens K+ Channels à K+-Efflux à Hyperpolarisation.
§ Proximal Nerve Ending – (Spinal Cord):
• Mimic Autoreceptors à Closure of Ca+ Channels à ↓Ca+-
Mediated NT Release.
§ Periaqueductal Grey Matter (PAG) – (Brain):
• Remove Inhibition of PAG (Activates PAG) à Activates NRM
à Inhibits Dorsal Horn Synapse.
o May be used for Acute & Chronic Pain.
§ If used Acutely, a “Step-Down” Plan (to less potent agents) must be
used to prevent addiction.
• Tri-Cyclic Antidepressants:
o Low-Dose Tri-Cyclic Anti-Depressants can treat Neuropathic pain by blocking
re-uptake of NE, 5-HT, & Enkephalins in Dorsal Horn Synapse à Maintained
Inhibition of Nociceptive Transmission.
• Massage Therapy:
o Aβ-Fibre Mechano-Afferents directly activate the Substantia Gelatinosa à
Inhibit Nociceptive Transmission @ Dorsal Horn Synapse.

o 3. Brain Targets:
§ Periaqueductal Grey Matter (PAG)
§ Whole Brain
§ Effective Analgesics:
• Opioids – (Codeine, Morphine, Fentanyl):
o Strong Analgesics - Act at all 3 levels (Periphery, Spinal Cord, Brain)
o Activated Opioid Receptors on:
§ Distal Nerve Ending – (Periphery):
• Opens K+ Channels à K+-Efflux à Hyperpolarisation.
§ Proximal Nerve Ending – (Spinal Cord):
• Mimic Autoreceptors à Closure of Ca+ Channels à ↓Ca+-
Mediated NT Release.
§ Periaqueductal Grey Matter (PAG) – (Brain):
• Remove Inhibition of PAG (Activates PAG) à Activates NRM
à Inhibits Dorsal Horn Synapse.
o May be used for Acute & Chronic Pain.
§ If used Acutely, a “Step-Down” Plan (to less potent agents) must be
used to prevent addiction.
• General Anaesthesia:
o Knocks out the entire conscious NS.

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 Important Clinical Neurological Things:

Pattern-Recognition of Common Neuro Symptoms & Signs:

Headaches:
Pattern: Probable Diagnoses:
Isolated SEVERE Headache History: Acute Onset ?Subarachnoid Haemorrhage (Arterial)
S Th nderclap Headache
Pain 10/10, Vomiting,
Meningism, ALOC.
Headache Following Head Injury History: Acute Onset ?Extradural Haemorrhage (Arterial)
Syx: Acute LOC Following
Severe Head Trauma Lucid
Interval Rapid
Deterioration + Vomiting +
Seizures
History: Days-Weeks-Months ?Subdural Haematoma (Venous)
Syx: Worsening Headache
following Mild Head Trauma.
Subacute Onset Headaches History: Days ?Infective:
Syx: Headache + - ?Meningitis
Constitutional Syx (Fever, - ?Encephalitis
Rash, N/V/D, Fatigue), +
Meningism/Photophobia.
Chronic or Recurrent Headaches History: Months-Years ?Tension Headache (Muscular)
Duration: Hours-Days ?Migraine (Functional)
Syx: Vague Muscle Tension/ ?Sinusitis (Inflammatory/Pressure)
Migraine/Sinus.
Pressure Headaches History: Months-Years ?Intracranial Space-Occupying Lesion
Syx: Pain worse Lying Down, ICP
Coughing, Straining or
Sneezing. + Vomiting
Headaches with Scalp Tenderness History: Older Patient ?Temporal Arteritis (Giant Cell
Syx: Headache + Extreme Arteritis)
Tenderness over Scalp Vessels.

Dizziness, Vertigo & Blackouts

Pattern: Probable Diagnoses:
Dizziness Vague Unsteadiness, Light- ?Postural/Orthostatic Hypotension
Headedness. ?Panic/Anxiety
?Palpitations (Eg. Atrial Fibrillation)
?Anaemia
Vertigo The Illusion of Movement, ?Otolith
Sensation or Rotating/Tipping. ?Vestibulocochlear Disease
+ Nausea & Vomiting (Eg. Acoustic Neuroma)
Blackout Implies ALOC, Visual ?Syncope
Disturbance, or Falling ?Epilepsy
?Hypoglycaemia
?Anaemia

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Difficulty Walking & Falls:
Pattern: Probable Diagnoses:
Spacticity Stiff, Jerky Walking ?Spastic Diplegia (Neonatal Asphyxia)
Toe-Scuffing and Catching ?Multiple Sclerosis
Maintained Narrow Base ?Cerebral Palsy
?Bilateral Spinal Cord Injury
Hemiparesis Unilateral Spacticity (See ?Stroke (ACA)
Above) + Circumduction of ?Unilateral Spinal Cord Injury
Spastic Leg to prevent Toe
Dragging.
Pa kin n Di ea e Short Rapid Steps, Shuffling, Parkinson s Disease
Shuffling Gait Maintained Narrow Base,
Stooping, Difficulty Turning
Quickly
Cerebellar Ataxia: Broad-Based Ataxia, Unstable, ?Lateral Cerebellar Lobe Disease
Broad-Based Gait Tremulous
Truncal Ataxia (Unsteady ?Midline Cerebellar (Vermis) Disease
Trunk without Limb Ataxia) +
Tendency to fall (*Remember Cpt. Jack Sparrow)
Back/Sideways
Sensory Ataxia: Broad-Based, High-Stepping, ?Polyneuropathy & Loss of
Stamping Gait Stamping Gait. Proprioception
(Worse with Eyes Closed)
Romberg s Tes Posi i e
Lower Limb Weakness: Slapping Gait: Audible Sole- ?Distal Leg Weakness (Eg. Common
Slapping & Waddling Gaits Slap when returned to Ground Peroneal nerve Palsy)
Waddling Gaits: Difficulty ?Proximal Leg Weakness (Eg.
Rising from Sitting + Waddling Polyomyelitis, Muscular Dystrophy)

(*Remember Maggie Grant)

Gait Apraxia Failure to Initiate/Organize ?Frontal Lobe Disease
Walking, Shuffling Small Steps, (Tumour, Hydrocephalus, Infarction)
Undue Hesitancy.
(But Normal Leg Mvts when
Sitting/Lying)

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Visual Field Defects + Causes:

Lesion Location Visual Field Defect

1 Retinal Lesion (Eg. Retinal Haemorrhage) Paracentral Scotoma (Focal Visual Field Defect)
2 Unilateral Optic Nerve Lesion Mononuclear Field Loss
3 Optic Chiasm Lesion Bitemporal Hemianopsia
4 Unilateral Optic Tract Lesion Contralateral Homonynous Hemaniopsia
5 Temporal Optic Radiation Lesion Contralateral Homonynous Lower Quadrantanopsia
(Upper Retinae; Lower Visual Field)
6 Parietal Optic Radiation Lesion Contralateral Homonynous Upper Quadrantanopsia
(Lower Retinae; Upper Visual Field)
7 Full-Thickness Optic Radiation Lesion Contralateral Homonynous Hemaniopsia
8 Occipital Pole Lesion (Visual Cortex Lesion) Contralateral Homonynous Hemiscotoma

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Pupillary Defects + Causes:

Afferent Pupillary Defect:

- (Ie. An Optic Nv/Optic Chiasm/Optic Tract Lesion)
- Eg. A Blind Left Eye:
o L-Pupil Unreactive to Light
o Present Consensual Reflex in L-Pupil
o R-Pupil Reactive to Light
o Absent Consensual Reflex in R-Pupil
Efferent Pupillary Defect:
- (Ie. Occulomotor Nv/Ciliary Nv Lesion)
- Eg. Left 3rd Nerve Palsy:
o L-Pupil Unreactive to Light
o Absent Consensual Reflex in L-Pupil
o R-Pupil Reactive to Light
o Present Consensual Reflex in R-Pupil

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 Revision
Functional Areas of the Brain:

Frontal Lobe Functions:

- High level Cognition. (Reasoning, Abstraction, Concentration)
- Motor Control:
o Contralateral Side (Motor Cortex)
o Voluntary Eye Movement
o Urinary Continence
- Expressive Speech Cen re Broca s Area in Dominant Hemisphere.
- Memory
- Emotion and Personality (Limbic System)

Parietal Lobe Functions:

- Contralateral Sensation (Sensory Cortex)
- Contralateral Proprioception (Dorsal Column Medial-Lemniscal Pathway)
- Non-Dominant Visuospatial Processing
- Dominant - Learned Motor Tasks

Temporal Lobe Functions:

- Smell (Olfactory Cortex)
- Hearing (Primary Auditory Cortex)
- In Dominant Receptive Speech (Wernicke s
- Memory
- Fear (Amygdala)

Occipital Lobe Functions:

- Vision (Primary Visual Cortex)
- Visual Perception (Visual Association Areas)

Brain Stem:
- Midbrain, Pons & Medulla
- 10 of the 12 cranial nerves arise from the brainstem Ipsilateral signs
- Cortical pathway decussation Contralateral Signs.
- Major Functions: Eye Movement, Swallowing, Breathing, Blood Pressure, Heart Rate, Consciousness

Cerebellum:
- Movement Balance Coordination

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 Clinical Features of Focal Brain Lesions:

Principal Features of Destructive Cortical Lesions:

Effects of Irritative Cortical Lesions:

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 Patterns of Motor Neuron Lesions:
Upper Motor Neuron Lesions:
- = Lesions of the Neural Pathway ABOVE the Anterior Horn of the Spinal Cord (Or the Motor Nuclei of the
Cranial Nerves)
- Causes:
o Stroke
o Traumatic Brain Injury
o Cerebral Palsy
- General Symptoms of UMN Syndrome:
o M scle Weakness P ramidal Weakness
o H perrefle ia D e o CNS Inhibi ion
o Spasticity
o Babinski Sign (Extension of Big Toe rather than Flexion)
o Pronator Drift (Pt Flexes Arms to 90o, Supnates Forearms & Closes Eyes; Inability to maintain this
position = Pronator Drift) (SideNB: Drifting Upwards is a Sign of a Cerebellar Lesion)
- Specific UMN Lesion Locations & Their Consequences:
Unilateral Motor Cortex Lesion (Eg. Stroke) Contralateral Hemiplegia
Unilateral Internal Capsule Lesion (Eg. Tumour) Contralateral Hemiplegia
Laceration of Spinal Cord Between Medulla & Brachial Plexus Quadriplegia
Laceration of Spinal Cord Between Brachial Plexus & Sacral Plexus Paraplegia

Lower Motor Neuron Lesions:

- = Lesions of the Neural Pathways BELOW the Anterior Horn of the Spinal Cord (Or the Motor Nuclei of the
Cranial nerves)
- Causes:
o Injuries/Trauma to Peripheral Nerves
o Poliomyelitis (Virus Selectively Attacks the Anterior Horns of the Spinal Cords)
o Guillain-Barre Syndrome
o Botulism
- General Symptoms of UMN Syndrome:
o Flaccid Paralysis of the Affected Muscle
o Muscle Wasting of the Affected Muscle
o Fasciculations
o Areflexia

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 Patterns of Loss of Sensation:

Background:
- 3 Conscious Sensory Pathways:
o Dorsal Column Medial-Lemniscal Pathway:
Vibration, Proprioception, 2-Point
Discrimination
Ascends Ipsilaterally Decussates in
Medulla Thalamus Sensory Cortex
o Spinothalamic Pathway:
Pain & Temperature
Decussates @ Spinal Level Ascends
Contralaterally Thalamus Sensory
Cortex
o Trigeminal Nerve:
All Facial Sensation
Decussates in Medulla Thalamus
Sensory Cortex
- 1 Unconscious Sensory Pathway:
o Spinocerebellar:
Role in Proprioception & Balance.

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MMSE Assessing Dementia:

-
- Interpretation:
o No Cogni i e Impairmen -30MMSE
o Mild Cogni i e Impairmen -24MMSE Relevant precursor sign to Dementia in early stages
o Modera e Cogni i e Impairmen -20
o Se ere Cogni i e Impairmen MMSE

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 NEUROLOGICAL Pathology:
BRAIN TUMOURS

Common CNS Tumours:

- General Features:
o Adults – Most are Cerebral/Supratentorial
o Children – Most are Infratentorial (Cerebellum & Brainstem)
o NB: CNS tumours NEVER Metastasise to Outside the CNS.
o Aetiologies:
Typically Secondary (Ie. Mets Breast, Lung, GIT, Melanoma)
Some are Primary (Gliomas are the Most Common) – NOT from Neurons!
o Types of Primary CNS Tumours Only Covering 3 Types:
Adults (NB: Most are Supratentorial Cerebral):
1. Meningioma
o From the Arachnoid Layer
2. Gliomas (Astrocytoma [& Glioblastoma Multiforme], Oligodendroglioma)
Children (NB: Most are Infratentorial Cerebellum & Brainstem):
2. Gliomas (Specifically Pilocytic Astrocytomas)
3. Medulloblastoma (Germ Cells)

o Clinical Features:
Slow, Progressive
Crescendo, Chronic, Morning Headache
Local Damage Nerve & Tract deficits, Paralysis, Blindness, Anosmia, Seizures
Raised ICP Headache, vomiting, papilodema & bradycardia.
Irritation Seizures
o Clinical Features Depend on Tumour Location Focal Deficits:
Brain stem Compression Drowsiness, Obtundation
Frontal Lobe Personality, Memory, Executive, Intelligence
Temporal Lobe Speech, Language & Hearing
Motor Cortex Limb weakness
Cerebellum Balance/Stumbling
Occipital Vision, Eye Movements

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 Primary CNS Tumours:

Adult CNS Tumours:

- MENINGIOMAS:
Cell of Origin: - Meningothelial Cells (Cells of the Arachnoid Granulations)
Morphology Macro: - Well Demarcated
- Attached to the Dura
- Hard, Fibrous Tumour with Calcification
Clinical Features: - Very Common, But Clinically Benign
- Non-Invasive, but Compresses the Brain Symptoms (Headache)
- Chronic, Gradually Increasing Morning Headache (Years).
- Oestrogen-Responsive :. Worse in Pregnancy/Menstruation.
Treatment: - Surgical Removal
Prognosis: - Benign
- Good Survival with Surgery

- Adulthood Gliomas LOW-GRADE ASTROCYTOMA & GLIOBLASTOMA MULTIFORME:

o ASTROCYTOMAS:
Cell of Origin: - Astrocytes
- Low-Grade ASTROCYTOMA:
Morphology Macro: - Usually Cerebral (Supratentorial)
- Solid Tumour
Clinical Features: - Space-Occupying Syx – Chronic Worsening Morning Headache,
Vomiting, Altered Mental Status, Personality Change, ALOC.
- + Focal Neurology depending on Location in the Brain.
Treatment: - Surgical Resection of Tumour
Prognosis: - Benign
- Good – 90% 5yr Survival

- High-Grade Astrocytoma GLIOBLASTOMA MULTIFORME

Morphology Macro: - Usually Cerebral (Supratentorial)
- Solid Tumour – May see some Cystic Degeneration
- Grows so fast, it looks encapsulated, but it is not.
Clinical Features: - Morning Headache, Nausea/Vomiting, Seizures, Hemiparesis
- + Memory Loss & Personality Changes.
- + Focal Neurology (Language & Executive Fx)
Treatment: - Palliative: Surgery + Chemo/Radiotherapy
- + Anticonvulsants – To Seizures
- + Corticosteroids – To Peri-Tumoural Oedema ICP
- (NB: Total Surgical Resection Impossible due to diffuse Infiltration.)
Prognosis: - Malignant – (Fast-Growing & Infiltrative)
- Poor Prognosis - <1yr Survival Rate

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Childhood CNS Tumours:
- Childhood Glioma PILOCYTIC ASTROCYTOMAS:
Morphology Macro: - Usually Cerebellar (Infratentorial) – (Rather than Cerebral in Adults)
- Cystic Tumour full of Mucoid FLuid- (Rather than Solid in Adults).
- Well-Circumscribed
Clinical Features: - Gait Abnormality (Wide Gait), Uncoordination, & Nystagmus
- Nausea, Vomiting, Irritability
- Failure to Thrive - Anorexia
- (NB: Associated with Neurofibromatosis)
Treatment: - Surgical Resection
Prognosis: - Benign – (Low-Grade, Slow-Growing)
- Good: >90% 10yr Survival Rate.

- MEDULLOBLASTOMA:
Cell of Origin: - Neuroblast Cells (Ectoderm Cells of Neural Crest = Neuroectoderm)
Morphology Macro: - Cerebellar (Infratentorial)
- Usually Form in the 4th Ventricle
Clinical Features: - Initial: Hydrocephalus (& ICP) due to 4th Ventricle Obstruction
Listlessness, Morning Headache, Vomiting.
- Later: Cerebellar Stumbling Gait, Falls, Diplopia, Nystagmus
Treatment: - Maximal Surgical Excision + Radiation + Chemotherapy
Prognosis: - High-Grade, Malignant Tumour CSF Seeding (Unique to
Medulloblastom) & Infiltration through Meninges is Common.
- Poor: 70% 5yr Survival, 50% 20yr Survival

Other CNS Tumours:

- Acoustic Neuroma (AKA: Vestib lar Sch annoma :
Cell of Origin: - Schwann Cells
Morphology Macro: - Schwannoma of the Vestibular Nerve (Part of CN8).
- Usually in the Internal Auditory Canal
- May Cerebellopontine Angle CN 5,7,9 & 10 Compression
Morphology Micro: - Homogenous Tumour – Only Schwann Cells
- Tumour cells always stay on outside of Nerve, but may compress it
against a bony structure Damage.
Clinical Features: - Typically 50-60yrs
- Sensorineural Hearing Loss/Deafness, Tinnitus
- Vertigo, Ataxia, Nausea & Vomiting
- Cerebellopontine Syndrome:
o CN 5 (Trigeminal) Palsy: Ipsilateral Corneal Reflex,
Trigeminal Neuralgia, Sensation
o CN 6 (Abducens) Palsy: Diplopia, Ipsilat. Inward-Facing Eye
o CN 7 (Facial) Palsy: Ipsilateral Facial Weakness
o (CN 8 (V/C): Ipsilateral Deafness, Tinnitus, Vertigo)
o Ipsilateral Cerebellar Signs: Nystagmus, Ataxia
Malignant/Benign: - Benign, Slow-Growing
Treatment: - Surgical + Radiotheraly (NB: Risk to Facial Nerve)
- Conservative Monitoring if Elderly.
Prognosis: - 100% Survival with Treatment.
- But some morbidity.
-

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- PITUITARY ADENOMAS:
Cell of Origin: - Pituitary Gland Embryonic Tissue
Morphology Macro: - Partially Cystic with Solid Areas
Clinical Features: - Compression of Optic Chiasm: 1. Bitemporal Inferior
Quadrantanopsia 2. Bitemporal Hemianopsia
- Headaches
- + Any Pituitary Endocrine Failure Symptoms
Malignant/Benign: - Benign – but hard to Treat & Compressive Neurology
Treatment: - Surgical Resection Hormone Replacement
Prognosis: - Benign but often recurrence.
- Good Survival, but Morbidity.

- NEUROFIBROMATOSIS Type 1 & 2

Cell of Origin: - Neural Fibroblasts
Morphology Macro: - Encapsulated, Solid Nodular Tumours (Neurofibromas)
Morphology Micro: - Whorls of Fibroblasts Within Nerves
- Well-Differentiated
Clinical Features: - NF1 Familial & Sporadic
- NF2 Autosomal Dominant
- Associated with Acoustic Neuromas (Vestibular Schwannomas)
o Tinnitus, Vertigo, Hearing Loss
- Also Associated with Meningiomas & Juvenile Cataracts
Malignant/Benign: - Benign
Treatment: - Surgical Resection of Individual Lesions – But Recurrence is common
Prognosis: - Benign – But can Extreme Morbidity/Disfigurement

- CNS Lymphoma:
Cell of Origin: - B-Cell Non-Hodgkin Lymphomas
Morphology Macro: - Multiple areas of tumour
Clinical Features: - Caused by EBV + Immunocompromise (Ie. HIV)
- Symptoms: Headache, Seizures, Cranial Nerve Palsies, Mental
Status, Focal Neurology.
- + Constitutional B-Syx: Fever, Night Sweats, Weight Loss
Malignant/Benign: - Malignant
Treatment: - Chemo/Radiotherapy + Corticosteroids (Surgery is Impossible)
Prognosis: - Poor – Due to High Grade + Concomitant Immunosuppression
- Median survival = 10mths

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 Wk 11
Infectious Disease Notes
CNS Infections

The blood brain barrier restricts the entry of pathogens into the brain and meninges:
- NB: Haematogenous spread of organisms requires spread through at least 2 layers to infect the brain.

Mechanisms of Entry into the CNS:

• Haematogenous Spread (Bloodborne Invasion) into the CNS:
– Growing across:
§ Microbes can grow in the endothelial cells and then into the astrocytes or choroid plexus
– Passive:
§ Transported across in intracellular vacuoles
– Carried in infected cells:
§ Infected inflammatory cells can migrate into the brain and meninges, lyse and release
the organism or the organisms may pass from cell to cell
– (Eg. Infection of brain or meninges by enteric viruses e.g. polio):

• Invasion Via Peripheral Nerves:

o Rabies and other Lyssaviruses may invade Muscle Cells @ The Bite Site àMove up the Nerves to
the Dorsal Root Ganglia à Spinal Cord àBrain
o Herpesviruses may migrate up the nerves using normal retrograde transport mechanisms

NB: The Blood Brain Barrier in Pharmacokinetics:

• The BBB Blocks access of certain chemicals to the CNS.
• :. Antimicrobial Drugs MUST be able to cross the BBB in order to fight CNS Infection.

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Eg. Invasion of the CNS by Rabies – (Via Peripheral Nerves):
1) Myocytes are Infected @ the bite site
2) Growth up the Motor Nerves àDorsal Root Ganglia
3) Growth up the Spinal Cord Nerves àBrain
4) Growth down the Cranial Nerves to the Salivary Glands
5) (Hence, CNS Invasion of the Rabies Virus is REQUIRED for transmission because it has to get from the Bite
Site à Peripheral Nerves à CNS à Salivary Glands àNext Bite)

• Rabies – Post Exposure Prophylaxis:

o Administration of Human Rabies Immunoglobulin
§ Used when there is a high risk of infection but insufficient time for the body to develop
its own immune response.
o Vaccination:
§ Rabies Vaccine à Promotes Active Humoral Immunity of the Host.

• Bat lyssavirus - viral antigens in neurones - immunoperoxidase staining:

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Definitions:
- Viral Meningitis:
o Inflammation of the Meninges of the brain due to viral aetiology.
o (Eg. By Herpes Simplex Virus)
- Bacterial Meningitis:
o Inflammation of the Meninges of the Brain due to Bacterial Aetiology.
o (Typically: Nesseria Meningitidis, Streptococcus Pneumoniae, Haemophilus Influenzae)
- Encephalitis:
o Inflammation of the Brain
o (Typically due to Viruses – eg. Herpes Simplex)
- Meningoencephalitis:
o Inflammation of the Brain & the Meninges
- Myelitis:
o Inflammation of the Spinal Cord à Disrupts CNS functions liking the brain & limbs.
o (Eg. Poliovirus (Poliomyelitis))
- Encephalomyelitis:
o Inflammation of the Brain and Spinal Cord
o Typically Immune-mediated following a viral infection.
o (Eg. Acute Disseminated Encephalomyelitis – Following Influenza, enterovirus, measles, mumps,
rubella, varicella zoster, etc.)
- Brain Abscesses:
o Encapsulated Pus or Free-Pus in the Brain after an Acute Focal Purulent Infection.
§ (Focal Infections include: Otitis Media/Sinusitis)

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 MENINGITIS:

Presentation: Meningism:
- *Neck Stiffness
- *Photophobia
- *Headache
- (Fever/Malaise)

Meningitis - CSF Examination:

• Three Successive Samples are Taken:
o To Eliminate Contamination
o NB: By the 3rd Sample, there should be NO Contamination
o NB: RBC indicates contamination
o Sample 1: Used for Serology
§ Serology
§ or PCR
o Sample 2: Used for Biochemistry
§ Glucose
§ Protein
§ Antigen Agglutination
o Sample 3: Used for Bacteriology – Most Precious
§ Gram stain
§ Culture

CSF Changes During CNS Infection:

- Septic Meningitis (Bacterial – N.Meningitidis, H.Influenzae, S.Pneumoniae)
o ↑Cells (Mainly Neutrophils & other Polymorphs)
o ↑Protein (Exudate)
o ↓Glucose (Due to Bacterial Metabolism)
o Positive Culture & Gram Stain
- “Aseptic” Meningitis (Typically Viral/Fungal)
o ↑Cells (Mainly Lymphocytes)
o ↑Protein
o Normal Glucose

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Septic/Bacterial Meningitis:
• More Severe than Viral
• Less Common than Viral
• Pathogenesis:

• The 3 Common Bacterial Implicated in Bacterial Meningitis:

o #1. Neisseria Meningitis:
§ Gram Negative Diplococci
§ Usually in Stressed/Crowded
§ Severe toxin sequlae à Tissue damage
§ Vaccine only for Serotypes A & C (Not B – Which is the most common)
• (NB: Serotype B Capsule molecules mimic Neural Tissue à Vaccine Cross Reacts)
§ NB: Capsule Switching:
• By the time the immune system has mounted an Adaptive Immune Resposne, N.
Meningitidis Changes the Immunogenicity of its Capsule.
• à Immune System has to Start Again
• à N. Meningitidis Prevails.

(Diplococci = Nesseria Meningitidis)

o 2. Haemohpilus Influenza:
§ Gram Negative Cocco-bacilli
§ Usually in Children / Babies
§ Toxin productionàTissue damage
§ Vaccine Available (HIb Vaccine)

o 3. Streptococcus Pneumoniae:
§ Gram Positive Cocci
§ Predisposed Adults
§ Neonates

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 • Other Aetiologies:
o Neonatal Meningitis:
§ Escherichia coli
§ Group B Streptococci
§ (High Mortality Rates (35% of cases))
o Tuberculous Meningitis:
§ Mycobacterium tuberculosis:
• Acid fast bacilli (Stains with zheil Nielson stain)
• Patients Typically have a Focus of Infection Elsewhere
• :. Most of cases are associated with Miliary (disseminated) Tuberculosis

Features Suggestive of Aetiology

1. Rash - erythematous, petechial / purpuric.
a. Suggests meningococcus (rarely Pneumococcus or Haemophilus influenzae type b)
2. CSF rhinorrheoa or otorrhoea - basal skull fracture:
a. Pneumococcus, H. influenzae, Haemolytic Strep.
b. (CSF Rhinorrhoea refers to the drainage of Cerebrospinal Fluid through the nose. It is a sign of
Basal Skull Fracture.)
3. Prominence of seizures or focal signs early:
a. Consider Listeria monocytogenes, Herpes simplex.

Aetiology Suggested by Age Group:

neonate Group B Streptococcus
E. coli,
Salmonella
Listeria monocytogenes
child< 6 Neisseria meningitides (meningococcus)
Streptococcus pneumonia (pneumococcus)
Haemophilus influenzae B
child >6 N. meningitidis
S. pneumonia
Healthy Adult S. pneumoniae,
N. meningitides
Immunosupressed, debilitated, L. monocytogenes,
elderly Gram negative enteric
organisms e.g. E. coli

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NB: Papilloedema < 1%:
• = Swelling of the Optic Disc secondary to the ↑Intracranial Pressure during Meningitis.
o Usually Bilateral
o May develop over hours to weeks.
• How it Occurs?
o The subarachnoid space of the brain is continuous with the optic nerve sheath.
o :. as CSF Pressure Increases à Pressure is transmitted to the optic nerve àOptic Nerve Sheath
acts as a Tourniquet around the Axon.

Meningitis Management:
1. Early Antibiotic Therapy is Essential for Good Outcome!!!
a. Even if they are Pre-Diagnosis.
2. Always Do Blood Cultures!!
3. Antibiotics must be:
a. Effective Against Likely Pathogens
b. Able to cross an Inflamed Blood Brain Barrier
c. Given Parenterally and in high dose.
4. Corticosteroids (Dexamethasone) are given prior to antibiotics à↓CNS Inflammation:
a. àImproves Neurological Outcome in all cases of suspected bacterial meningitis.
5. Prophylactic Measures in close contacts:
a. Meningitis Prophylaxis: Rifampicin, Ceftriaxone or Ciprofloxacin:
1. Prophylaxis with the above antibiotics WILL NOT abort infection in those already infected.
2. RATHER, It aims to Eliminate Nasopharyngeal Carriage àPrevent subsequent transmission.
3. Offered to Household, child care and CLOSE CONTACTS.
4. No evidence for salivary spread.

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 AfraTafreeh.com exclusive

Brain Abscesses:
• Incapsulated or free-pus in the substance of the brain after an acute focal purulent infection is known as
a brain abscess.
o Sites of Focal Infection that could lead to brain abscesses:
§ Otitis Media
§ Sinusitis
§ Penetrating trauma
§ Haematogenous dissemination
o Given the Possible Sites of Entry, Which Organisms are Most Likely to be Involved?
§ Otitis Media – Strep Pneumoniae
§ Sinusitis – Strep Pneumoniae
§ Penetrating Trauma – Probably Staph Aureus
o Diagnosis:
§ Blood culture should be performed, but often is not diagnostic
§ CT or MRI are Essential for Diagnosis.
§ Lumbar Puncture is Contraindicated (Due to ↑ICP)
§ Inflammatory Markers WBC, CRP & ESR are raised.

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Fungal Meningitis:
• Mainly Cryptococcus Neoformans
• Typically in Immunosuppressed
• Can be treated with antifungal drugs

Viral Meningitis:
• Less Severe than Bacterial
• More Common than bacterial
• Presentation:
o Usually are milder disease than bacterial meningitis
o Headache, fever and and general illness but less neck stiffness
o Generally Complete Recovery
• Examination of CSF:
o The CSF is clear and free of bacteria
o CSF Contains Mainly Lymphocytes
• Viruses Implicated in Viral Meningitis:
o Herpes Simplex
§ Uncommon; may follow congenital infection with HSV2
o Mumps
§ A quite common complication
o Poliovirus, cocsackievirus, echovirus
§ Commonly seen especially due to echoviruses
o Enterovirus 71
§ May follow hand foot and mouth disease
o Japanese encephalitis
§ India, Southeast Asia, Japan
o Eastern and Western equine encephalitis
§ Eastern and Western USA
o HIV
§ May occur early after infection

(NB: “Perivascular Cuffing” by monocytes around the vessels)

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 ENCEPHALITIS:

Encephalitis – Infection of the Brain:

• Encephalitis Is Usually Caused By Viruses:
o **Herpes Simplex Virus
§ The infection progresses back to the temporal lobe of the brain
§ 70% mortality rate in untreated patients
§ Treatment with Acyclovir à ↓Mortality rate
§ (Including Varicella Zoster, & Cytomegalovirus)
§ VZV: Encephalitis generally occurs as a sequel to reactivation
§ CMV: Either during primary infection (in utero) or reactivation due to immunodeficiency
(HIV)
o Poliovirus:
o Rabies:
• Other causes of encephalitis can include:
o Parasites such as Toxoplasma gondii and Plasmodium falciparum
o Fungi such as Cryptococcus neoformans
o Bacteria such as Treponema palidum
• Pathogenesis:
o àCharacteristically there are signs of cerebral dysfunction:
§ Abnormal Behaviour
§ Seizures
§ Altered Consciousness
§ Nausea/Vomiting
o and fever
• Pathogenesis of Viral Encephalitis:

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Poliovirus:
• Epidemiology:
o Non Existent in Aus (A single case would be an epidemic)
• Prevention:
o Vaccination Available
§ Live Attenuated (Oral Polio Vaccine):
• Advantages:
o Easy Administration - Given Orally
o Cheap
o Induces intestinal local immunity
o More Robust Immune Response
• Disadvantage:
o Rarely causes paralysis (1 in 2.5million)
§ Inactivated Polio Vaccine (IPV):
• Advantages:
o Carries NO risk of Vaccine-Associated Polio Paralysis
o Very Robust Immune Response
• Disadvantage:
o Difficult Administration - Has to be injected
o Confers little Mucosal Immunity in the Intestinal Tract.
o 5 Times more expensive than OPV.
o (NB: 1 in 2.5Mil recipients develop paralysis)
• 3x Serological Types:
o PV1, PV2, PV3.
o Have little cross-reaction :. Vaccination must contain ALL 3 Serotypes for Full Immunity.
o (NB: Serotype 1 causes most of the problems – Ie. Paralysis)
• The major lesion results in a flaccid paralysis
• Transmission:
o **Faecal Oral
o Respiratory
• Pathogenesis:
o Poliovirus Acquired Faecal-Orally or Respiratory Route.
o Virus Replicates in Lymphoid Tissue in the Pharynx and Gut.
o Viraemia follows à Extension to the Nervous System
o à Lytic Infection of Neurons à Paralysis
§ Anterior Horns of Spinal Cord are Most Affected.
• Clinical features:
o The incubation period = 7 to 14 days
o A minor illness with malaise, fever and a sore throat may occur
o Paralysis may extend from a single muscle to virtually every skeletal muscle
o There may be involvement of respiratory muscles à Lifelong Assisted Ventilation

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Rabies Encephalitis:
• Organism:
o Rhabdovirus (A Bat Virus)
• Transmission:
o by the bite of an infected animal
o The virus is present in the saliva of the infected animal (Dogs, foxes and other wild species)

Flavivirus Encephalitis:
• Japanese Encephalitis (JEV) is the most common cause of this infection:
o A vaccine is available for this virus
o This virus is common throughout Asia
o *Of particular importance in North Queensland
• Other members of the encephalitic subgroup of the flaviviruses include:
o Kunjin
o Murray Valley encephalitis
o West Nile virus
o St Louis encephalitis

Togavirus Encephalitis:
• Some of the togaviruses in the Americas (Eastern and Western encephalitis) can produce encephalitis
• These viruses usually infect various animal species and occasionally infect humans
• Vaccines are available for the animal species
• No vaccines are available for humans

Acute Flaccid Paralysis:

• While acute flaccid paralysis is a key clinical feature of polio infection, this syndrome can be produced my
several other factors:
• These include other picornaviruses such as enterovirus 71
• This virus also produces the syndrome hand foot and mouth disease
• In 1998 an outbreak in Taiwan involving 300,000 children resulted in 56 deaths
• In 1999 an outbreak in Perth resulted in six cases of acute flaccid paralysis

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PARASITIC INFECTIONS OF THE BRAIN:
• Toxoplasma Gondii:
o Life cycle:
§ à Cysts in Brain (Contained by Macrophages & Helper T-Cells)

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Helminthic & Protozoal Organisms Capable Of Causing CNS Infections:
Helminth Reservoir Neurological Method of Treatment
symptoms diagnosis
Tapeworm Eating Cysts in Brain Detectino of Albendazole or
uncooked Pork à Convulsions specific praziquantel
antibody in +
serum or CSF Corticosteroids
Visual detection
of cysts by MRI
Roundworm Cats and dogs Cysts in Brain Serum can be Antihelmentic
à Convulsions tested for therapy (But
Retinal Antibodies by not in ocular)
Detachment à ELISA
Blindness
Protozoan
Malaria People + Convulsions RDT Antigen Artemesinin
Mosquitoes Coma Test
Toxoplasma Cats and mice Hydrocephalus PCR of blood Antibiotics
Gondii Inctracerebral samples Antimalarials
calcification Immunostaining Atovaquone à
Kills Cysts
Trypanosome Kissing bug Abnormal gait Microscopy of: Melarsoprol
Abnormal Blood Smears Eflornithine
speech CSF
Mental state Lymph Node
change Aspirates
Other abnormal
movement RDT Antibody
Sleep Detection test.
Disturbance

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PRION INFECTIONS OF BRAIN:
• Scrapie like agents referred to as prions can produce infections in a range of domestic animals and in
humans
• NO DNA or RNA!! (Important for Exams)
• The disease is produced when there is a conformational change in the proteins referred to as prion
protein C
• The PrPSC protein:
o lThe two forms of the protein have different properties
§ lPrPC is anchored to the cell membrane by a glyco-phospho-inositol (GPI) anchor
§ lPrPSC accumulates in plaque deposits in the brain of affected individuals
o lThe two proteins have the same posttranslational modifications and cannot be distinguished by
monoclonal antibodies
• How the prions damage the cells:
o Accumulation in Neurons à Death of Neurons

• Human prion diseases:

o There are four human diseases classified as TSEs (Transmissible Spongiform Encephalopathies):
§ (NB: All are Progressive and Fatal.)
§ Creutzfeldt-Jacob disease (CJD) (Most Common In Humans)
• Iatrogenic (Person-Person – Eg. Transplant)
• Inherited
• Sporadic
§ Gertsmann-Straussler syndrome (GSS)
§ Fatal familial insomnia (FFI)
§ Kuru confined to one tribe in New Guinea and related to cannibalism in the past

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OTHER INFECTIOUS DISEASES AFFECTING THE CNS:
• Toxins produced by bacterial infections can affect the CNS:
o Eg. Tetanus
§ Organism:
• Clostridium tetani
• Found in Soil & Faeces of Domestic Animals
• Like Anaerobic Conditions
§ Pathogenesis:
• à Toxin à Tetanic Spasms (Acts on the nerves)
• (Acts by binding to Ganglioside Receptors à Blocking Release of Inhibitory NTs
à Convulsive Contractions of Voluntary Muscles)
§ Prevention:
• Tetanus Vaccine
o Eg. Botulism
§ Organism:
• Clostridium Botulinum
§ Pathogenesis:
• à Toxin à Flaccid Paralysis
o Most commonly absorbed in the gut.
• (Blocks Acetylcholine Release from Peripheral Nerves à Paralysis)
§ Presentation:
• Weakness and paralysis
• Dysphagia
• Diplopia
• Vomiting
• Vertigo
• Respiratory muscle failure
§ Treatment:
• Antibodies (Antitoxins)
• Respiratory Support

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 NEUROLOGICAL Pathology:
CNS INFECTIONS

MENINGITIS:
- Aetiology:
o Bacterial/Septic Meningitis Nesseria meningitides, Haemophilus influenza, Group B Streptococci.
Adults = Neisseria meningitides (NB: Vaccine preventable Meningococcal A & C)
Children = Haemophilus influenza (Vaccine Preventable HIB Vaccine)
Neonates = Group B Streptococci (or E.coli)
o Viral/Aseptic Meningitis Herpes Simplex Virus, Enteroviruses (Echo/Coxsackie), Influenza
o Chronic Meningitis Miliary Tuberculosis
- Pathogenesis:
o Meningeal Infection Inflammation & Oedema ICP Vomiting, Drowsiness.
o NB: Meningococcal Sepsis can Thrombocytopaenia Maculopapular Rash ... DIC
- Morphology:
o Bacterial Exudate within Meninges (Pus beneath the meninges)
o Viral No pus
o Engorged Meningeal Vessels
- Clinical Features:
o ***Meningism:
*1. Neck Stiffness (Due to Inflammation of the Meninges)
Br d inski s Sign Posi i e (Flex the Neck Pt bends knee)
Kernig s Sign Posi i e (Flex the hip and attempt knee extension Pain

*2. Photophobia
*3. Headache
o + Constitutional Syx:
Fever/Malaise
Nausea/Vomiting
May eventually have loss of consciousness. (Rare)
Irritability
Poor Feeding
o Features Suggestive of Aetiology
Non-Blanching Maculopapular Rash Suggests Meningococcus
CSF Rhinorrheoa/Otorrhoea - basal skull fracture Suggests Pneumococcus, HiB, Strep.
- Diagnosis:
o **Clinical Suspicion: (Meningism +/- Rash +/- Fever/Malaise/Vomiting +/- Headache/ALOC
+/- Brud inski s Sign Kernig s Sign
o Blood Cultures BEFORE IV Antibiotics!!
o L3-L5 Lumbar Puncture CSF Examination:
LP can Coning if ICP DO NOT do LP if:
1. Papilloedema
C shing s Response Triad BP HR Irregular Breathing)
3. Unresponsive Pupils
Can Cerebral Hernia ion Aka Cis ern Obli era ion Often Fatal
o CSF Samples (Take 3):
Sample 1 Serology (or PCR)
Sample 2 Biochemistry (Glucose, Protein)
Sample 3 Bacteriology Most Precious (Gram Stain + Culture)

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 o CSF Interpretation:
Normal Bacterial Meningitis Viral/Aseptic
Meningitis
(Usually Herpes
Virus)
CSF Pressure Normal Normal-Raised Normal-Raised
White Cell Count Normal Raised (Polymorphs) Raised
(Lymphocytes)
Glucose Same as Serum Lower than Serum Normal
(Hungry Bacteria)
Protein Normal Raised (produced by the Raised (produced by
organisms) the organisms)
Gram Stain None Presence of Bacteria Nothing Aseptic
Meningitis
- Treatment:
o (Bacterial Meningitis = Emergency Can be Fatal)
o (Viral Meningitis = Usually Self-Limiting & Less Fulminant Clinically)
o ***Treat on Suspicion!! (Don t wait for lab results )
o 1. Blood Cultures BEFORE IV Antibiotics!!
o 2. Early Antibiotic Therapy is Essential for Good Outcome!!!
IV Benzylpenicillin G, or IV Cephtriaxone (why? Because they can enter the BBB)
o 3. Corticosteroids (Dexamethasone) WITH the Antibiotics CNS Inflamma ion
Improves Neurological Outcome of bacterial meningitis.
o 4. Fundoscopy, Then Lumbar Puncture (Check for Papilloedema before doing LP)
CSF MCS
o (+ Prophylactic Measures for Close Contacts):
Meningitis Prophylaxis: Rifampicin, Ceftriaxone or Ciprofloxacin:
Offered to Household, child care and CLOSE CONTACTS.
- Prognosis:
o Good prognosis with Aggressive Treatment.
:. Treatment on Suspicion: Empirical Antibiotics (or Antivirals).
- Complications:
o Acute:
Encephalitis
Cerebral infarction
Oedema
Herniation
Waterhouse-Frederichson Syndrome (Acute Adrenal Infarction)
( Petechial Haemorrhages, DIC, Septic Shock)
o Late:
Abscess
Subdural Empyema
Epilepsy
Leptomeningeal Fibrosis & Consequent Hydrocephalus

(Diplococci = Nesseria Meningitidis)

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ENCEPHALITIS:
- Aetiology:
o Almost Always Viral (**Herpes Simplex Virus, VZV, CMV, Poliovirus, Rabies [Rhabdovirus], JEV)
- Pathogenesis:
o Viraemia Crosses BBB CNS Infection Cerebral Oedema ICP Neurological Signs
- Clinical Features:
o Infective Syx Fever, Nausea, Vomiting
o + Cerebral Syx Encephalopathy (Altered Mental State/Abnormal Behaviour/ALOC/Drowsiness)
+/- Seizures
- Treatment:
o Treat on Suspicion (Acyclovir + Dexamethasone)
- Prognosis:
o Poor - Once symptomatic, rapid inflammation & necrosis Brain-Death or Neurological Deficit
o 70% Mortality Untreated
- Investigations:
o FBC (Lymphocytosis)
o LP L mphoc es Normal Gl cose Pro ein Nega i e C l res

Normal Bacterial Viral Meningitis Encephalitis

Meningitis (Usually Herpes (typically viral)
Virus)
CSF Pressure Normal Normal-Raised Normal-Raised Markedly Raised
White Cell Count Normal Raised Raised Raised
(Polymorphs) (Lymphocytes) (Lymphocytes)
Glucose Same as Serum Lower than Normal Normal
Serum (Hungry
Bacteria)
Protein Normal Raised (produced Raised (produced Raised
by the organisms) by the organisms)
Gram Stain None Presence of Nothing Aseptic Nothing
Bacteria Meningitis

BRAIN ABSCESSES:
Incapsulated pus within the brain occurring after an acute focal purulent infection.
o Sites of Focal Infection that could lead to brain abscesses:
Otitis Media
Sinusitis
Penetrating trauma
Haematogenous dissemination
o Given the Possible Sites of Entry, Which Organisms are Most Likely to be Involved?
Otitis Media Strep Pneumoniae
Sinusitis Strep Pneumoniae
Penetrating Trauma Probably Staph Aureus
o Diagnosis:
Blood culture should be performed, but often is not diagnostic
CT or MRI are Essential for Diagnosis.
Lumbar Puncture is Contraindicated Due to ICP
Inflammatory Markers WBC, CRP & ESR are raised.

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 NEUROLOGICAL Pathology:
DEMENTIAS

Global Degeneration Dementias (Age-Related (Senile), Alzheimers, Lewy-Body, & Fronto-Temporal Pick’s):
- Dementia:
o = Acquired Global Impairment of Intellect, but with no ALOC.
- Epidemiology:
o 5% of >55yrs are demented
o 20% of >80yrs are demented
o Prevalence Doubles every 5yrs Beyond Age:60.
o 50% of dementia pts have clinically significant behavioural/psychological symptoms.
- Common Symptoms: (In order of prevalence):
o Early Cognitive:
**Memory loss
o Later Non Cognitive:
Apathy/Depression
Delusions (False Beliefs)
Anxiety
Agitation/Aggression
Hallucinations
- Types of Primary Dementias:
o Age-Related (Senile) Dementia
o Alzheimers Disease
o Lewy-Body Dementia
o Fronto-Tem al Deme ia Pick Di ea e
- Clinical Diagnosis:
o Timeline of Symptom Progression (Memory Loss Agitation/Aggression, Wandering, Apathy)
o Impact on ADLs (Especially Medications & Financials)
o MMSE (Mini-Mental State Examination)

- AGE-RELATED (SENILE) DEMENTIA:

o Aetiology:
Old Age
o Pathogenesis:
Old-Age Neuronal Atrophy (Particularly Cortex & Hippocampus) Progressive Neuronal
Loss with Time
B ai Ma De d i ic B a che
Neurons are replaced by glial cells
o Morphology:
Macro:
Cortical atrophy
E la gi g f e icle C m e a H d ce hal
Thickening of Leptomeninges (Pia Mater & Arachnoid Mater) (The “Thin”
Meninges)
o Clinical Features:
Dementia: All Spheres of Intellect affected

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- ALZHEIMERS DISEASE:
o Commonest Cause of Dementia
o Aetiology:
Exact Aetiology Unknown
Genetic & Environmental Components
(NB: Inevitable in Down-Syndromes)
o Pathogenesis:
Excess β-Amyloid Protein Formation (A Degradation product of Amyloid Precursors)
β-Amyloid Protein Deposition around Neurons Neuritic Plaques
β-Amyloid Protein Deposition in Blood Vessels Amyloid Angiopathy
o Morph:
Severe Cortical Atrophy (Widened Sulci, Narrow Gyri)
T icall S a a d B ca A ea F al A ea Extends to the rest of the
brain (Affecting motor and sensory areas may even have paralysis)
Secondary Ventricular Dilation (Compensatory Hydrocephalus)

o Clinical Features:
May be as young as 50yrs old
SLOW Insidious Onset (Years) (Cf. Lewy-Body Dementia)
Early Signs: (Neuronal Atrophy Starts in the Hippocampus)
Memory Loss is :. the First Sign
Progressive Signs: (Neuronal Atrophy Progresses to the Cortex)
Mild Cortical Atrophy:
o Increased Memory Loss
o Confusion, Apathy, Anxiety
o Difficulty Handling Money
Moderate Cortical Atrophy:
o Difficulty Recognising People
o Difficulty with Language
o Wandering & Disorientation
Late Signs: (Extreme Global Cortical Atrophy)
Seizures, Incontinence
Groaning/Moaning/Grunting
o Treatment:
Acetylcholine-Esterase Inhibitors
o Prognosis:
Mean Survival = 7yrs from Onset.
Death Typically From Aspiration Pneumonia or Other Infections.

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- DIFFUSE LEWY-BODY DEMENTIA:
o 3rd Most Common (Behind Alzheimers & Vascular)
o Aetiology:
Unknown But Genetic Link.
o Pathogenesis:
Development of Abnormal Proteins (Alpha-Synuclein) in Neurons throughout the Brain
Impair the Functioning of Neurons Rapid Decline in Cognition, Memory, Attention &
Motor
o Morphology:
Macro:
Significant Cortical Atrophy
T icall S a a d B ca A ea Extends to the rest of the brain
o Clinical Features:
Rapid Onset (within few months) Cf Al heime Di ea e
Early:
Fl c a i g C g i i Deme ia STMemory, Confusion, Language Problems)
Vivid Visual Hallucinations (Eg. Strange Faces, Frightening Creatures, or Children)
Impairment in Attention
Later:
Parkinsonism with shuffling gait & cog-wheel rigidity..
Delusions
T a ie ALOC
o Treatment:
Pharmacological Cholinesterase Inhibitors are promising.

- FRONTO-TEMPORAL DEMENTIAS Incl. Pick’s Disease :

o 4th most common dementia af e Al heime Va c la Le -Body
o Aetiology:
Other Fronto-Temporal Dementias = Genetic
Pick Di ea e U k
o Pathogenesis:
Selective Build-up of Tau Proteins within Frontal & Temporal Lobe Neurons
Frontal Lobe Dysfunction Executive Function, Personality, Disinhibition.
Temporal Love Dysfunction Aphasias (Expressive & Receptive)
o Morphology:
Macro:
Selective Atrophy of Frontal & Temporal lobes
Sparing of the Parietal & Occipital Lobes
o Clinical Features:
Younger Patients (40-65yr olds)
Dysexectutive Syx: Inability to Coordinate & Execute Tasks
**Behaviour Changes: Behaviour & Personality Change & Disinhibition
NB A Defi i g fea e f Pick Di ea e i ha Beha i Pe ali Cha ge
cc PRIOR Mem L Cf Al heime he e Mem L cc Fi
Language Changes: Progressive Aphasia (Expressive & Receptive)
NB: Memory is Preserved until Late Stages.

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- VASCULAR DEMENTIA (Multi-Infarct Dementia):
o Epidemiology:
2nd M C mm behi d Al heime f All Deme ia
o Aetiology:
Cumulative Ischaemic Brain Damage
(Mostly due to Hypertension & Atherosclerosis)
o Pathogenesis:
Either Sudden Onset Following a CVA
Or Gradual Deterioration after Successive (often unnoticeable) CVAs.
Generalised Intellectual Loss Dementia
o Morphology:
Macro:
May have Necrotic/Fibrotic Foci (If Multi-Infarct) Often Visible on MRI/CT
May have a single, large Necrotic/Fibrotic Focus (Single, Large Infarct)
May have Hypertensive Lacunar Lesions
o Clinical Features:
Memory Loss
C g i i eF c i
Confusion
Mood Changes (Depression/Irritability)
Language Problems
Executive Dysfunction ADL Ea i g D e i g Sh i g ec
Ra id Sh ffli g Gai S me ime called A he cle ic Pa ki im
Hx of Vascular Pathology (Past Hx of CVA, TIA, HTN & Focal Neurology)
o Treatment:
No Cure, but Preventable
o Prevention:
Control Hypertension
Reduce Cholesterol
Control Diabetes
Stop Smoking
Antiplatelet Drugs (Aspirin/Clopidogrel)

- DEMENTIA PUGILISTICA “Punch Drunk Syndrome :

o Aetiology:
Repetitive Trauma/Concussion
o Pathogenesis:
Repeated Concussive/Sub-Concussive Blows to the Head Cumulative Loss of Neurons,
Fibrosis, Hydrocephalus, Diffuse Axonal Injury & Cerebellar Damage.
o Morphology:
Hydrocephalus
Thinning of Corpus Callosum
o Clinical Features:
Slow Progression (Over Decades)
Deme ia Mem C g ii Pe ali
Pa ki i m T em C di a i
Unsteady Gait
Dysphasias

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 - WERNICKES-KORSAKOFF SYNDROME (Alcoholic Encephalopathy):
o Aetiology:
Alcohol Abuse Vit B1[Thiamine] Deficiency
o Pathology:
Alcohol Abuse Vit B1[Thiamine] Deficiency
Vit B1[Thiamine] is a cofactor for Glucose Metabolism :. Deficiency Neuronal ATP
Neuronal Atrophy (Particularly Cortex & Mamillary Bodies)
(Vit B1[Thiamine] Deficiency) Ataxia
o Morphology:
Cortical Atrophy
Mamillary Body Atrophy & Haemorrhages
Cerebellar Atrophy
o Clinical Features:
Cortical Atrophy Impaired Memory (Anterograde & Retrograde) + Confabulation
Mamillary Body Damage Vision Changes, Nystagmus, Unequal Pupils
Cerebellar Atrophy Ataxia
o Treatment:
Supplemental Thiamine + B12
(NB: B12 to prevent subacute degeneration of the cord)
o Prognosis:
By the time Amnesia & Psychosis are apparent, complete recovery is unlikely.

Amnesia:
- Typically Declarative Memory Loss. (Therefore Hippocampal Damage)
- Commonly caused by Temporal Lobe Damage (Hippocampus and/or Thalamus)
o NB: L-Hippocampus = Language
R-Hippocampus = Spatial Memory
- Anterograde:
o - Inability to form new memories from time of Injury/Damage Onwards.
o Non-Declarative Memory is Unaffected
- Retrograde:
o - Inability to recall memories from time of Injury/Damage Backwards.

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 NEUROLOGICAL Pathology:
EAR PATHOLOGY

Ear Complaints:
- Deafness:
o Conductive:
Due to a condition that blocks the conduction of sound through the Outer & Middle Ear.
Originating in the Outer Ear:
o External auditory canal obstruction. (Wax/Foreign Bodies/Infection/Pus)
Originating in the Tympanic Membrane:
o Perforation or Scarring due to Infection or Trauma.
Originating in the Middle Ear:
o Otitis Media Fills the Tympanic Cavity with pus.
o Otosclerosis Ossicles become fused together

o Sensorineural:
Due to a disorder of the inner ear, the cochlear nerve, or its central connections to the
brain.
Noise-Induced Damage to Cochlear Hair Cells.
Stroke in the Auditory Cortex causing hearing loss.
Acoustic Neuroma (tumour of CN8) causing deafness on the affected side.
Ototoxic Drugs Damage to Cochlea Nerve
Meningitis
Presb c sis Progressive age-related hearing degradation.

- Tinnitus:
o A Percieved Ringing in the ears Or buzzing hissing clicking roaring etc
o Commonly occurs immediately after Acoustic Trauma (Eg. Clubbing)
o Is a problem of the Peripheral auditory system (Not the brain)

- Vertigo:
o Sensation of Spinning Distinct from faintness
o Usually a problem of the Vestibular Apparatus or the Vestibulocochlear Nerve (CN8)
Benign Paroxysmal (sudden onset) Positional Vertigo
Vestibular Neuronitis
Drugs (Eg. Alcohol)
Brainstem Lesions, Multiple Sclerosis, Migraine.

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- Otalgia:
o Pain of the Ear
o Most often caused by some form of Otitis:
Acute Otitis Media (Acute Middle Ear Infection).
Caused by Respiratory Pathogens which enter via Eustachian Tube.
Can Present with:
o URTI; Rhinitis; Cough; Fever
o Ear ache Ear-pulling
Otoscopy may show:
o Swollen, bulging, red Ear-drum.
o Fluid behind drum (fluid in middle ear)

Chronic Otitis Media (Chronic Middle Ear Infection):

Caused by:
o Chronic Respiratory Infections
o Nasopharyngeal colonisation in early infancy.
o Eustachian tube dysfunction
Can Present with:
o Chronic ear discharge.
o Hearing loss
o Developmental delay/poor school performance.
Can result in a variety of Conditions:
o Retraction or Perforation of Eardrum.
o Loss of Eardrum Elasticity
o Fluid behind an intact eardrum.
o Scarring of ossicles.
o Erosion of the bony cavity of the middle ear.
o Cholesteatoma (Keratinizing Squamous epithelioma in mid.ear or eardrum)
Grommets can relieve middle ear pressure and allow draining of exudate.

Otitis Externa (External Ear Infection):

Caused by:
o Humidity/Swimming Bacterial/Fungal Infection.
Can Present with:
o Itch; Pain; Ear Pulling
o Fever
o Discharge

- Otorrhoea:
o Runny Ear

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 o Can be Caused by:
Otitis Media:
Acute with perforation
Chronic
Otitis Externa
Foreign Body
Cholesteatoma Chronic Infection/Erosion

Ear-Related History:
- Past Medical:
o Ear Infections?
o Ear Trauma?
o Diabetes?
o MS?
- Past Surgical:
o Ear Surgery?
- Medication?
o NB: Some are ototoxic.
- Noise Exposure:
o Occupational
o Recreational

Ear Examination:
- External Ear:
o Inspection
o Palpation (tenderness) + Cervical & Occipital Lymph Nodes.
- Otoscopy:
o Inspection of Tympanic Membrane & Middle Ear
- Hearing Tests:
o Whisper Test
o Tuning Fork Tests
o Testing for Nystagmus (Involuntary eye movement due to head movement)
o Romberg s Test standing feet together then closing eyes Loss of balance positive
o Tympanometry (tests the eardrum & ossicle mobility)
o Audiometry tests a person s responses to different pitches volumes

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 NEUROLOGICAL Pathology:
EPILEPSY

EPILEPSY:
- Terminology:
o Epileps A Recurrent Spontaneous Seizure Activity, NOT Attributable to External Cause.
(Clinical Dx Depends on the an arbitrary cutoff, usually 3/more seizures)
o Sei res Spontaneous Abnormal Electrical Activity within the Brain.
- Aetiology:
o 70% Idiopathic (Often Familial)
o Others: Post-Injury, Developmental, Tumour, Stroke, Febrile Convulsion, Trauma, Stroke, ICP,
Alcohol Withdrawal, Metabolic, Infection, Drugs.
- Common Triggers (Among Epileptics):
o **Strobe Lights are most common (Often used for Diagnosis)
- Common Triggers (Among Non-Epileptics):
o Drug/Caffeine OD
o Fever
o Alcohol Withdrawal
o Toxins
o Head Injury
o Metabolic/Electrolyte Disturbances
o NB: The above triggers have to be eliminated before Epilepsy is Diagnosed.
(Epilepsy is an ‘Innocent until proven guilty’ disease.)
o NB Sei re Epileps
- Pathogenesis:
o Hyperexcitable Neurons (Lower Threshold, Ion-Channelopathy, or Neurotransmitter Imbalance)
Inappropriate, uncontrolled, spontaneous Electrical Activity within the Brain (Seizure)
- Clinical Features:
o Prevalence: 0.5 - 1% of Adults
o Age of Onset:
Generally before 20yrs.
1st seizure before 10yrs
o Presentation:
1. Pre-Sei re Aura Eg. Deja-vu, Abdominal Discomfort, Flashing Lights, Strange Smells,
Sounds, Tastes.
2. Seizure Many Different Types
3. Post-Ictal Symptoms: Eg. Headache, Confusion, Myalgia, Temporary Weakness
- Diagnosis: a Clinical Diagnosis; Requiring:
o >2 Seizures, for which all external triggers have been eliminated.
o Positive EEG
o Seizure Induction Test
o (+ Detailed History)
o (+ Detailed Description (or video) of the Seizures)
o (No single test is enough to diagnose.)
o NB: 1x Seizure Epilepsy.
- Treatment:

(NB: Valproate “Epilim”; Carbamazepine “Tegretol”)

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Types of Seizures:
- ICES-Classified Seizures:
o Simple Par ial Sei re (Conscious & Localised):
Symptoms:
Typically – Small, Rapid Muscle Movements
May include - Focal Motor/Sensory/Autonomic/Psychic Symptoms
Duration: Very Short Duration (Less than 1min)
NB: Preservation of Consciousness & Memory is Key.
o Comple Par ial Sei re (ALOC & Localised):
Symptoms:
‘Impaired Consciousness’ Dazed/Dopey.
+ Purposeless Movements – (Hand-Wring/Pill-Rolling/Face-Washing)
Duration: Less than 2 min
NB: Impaired Consciousness Little/No Memory of Seizure.
o Par ial i h Secondar Comple -Generalised Sei re - Tonic-Clonic
Ie. Simple or Complex Partial Seizure, Progressing to Complex (Unconscious) Widespread
(Generalised) Seizure.
4 Phases:
1. Pre-Seizure Period (Aura)
2. Tonic Phase (Sustained Generalised Tonic Contraction)
3. Clonic Phase (Repetitive Generalised Synchronous Jerks)
4. Post-Ictal Coma (Sustained Post-Seizure Unconsciousness)
(May include Central Apnoea & Incontinence)
Duration:
1-2mins
However, can last for many minutes.
- Unique Seizure Types:
o M oclonic
Symptoms:
Brief, Marked Contraction of Muscles (Ie. A “Shock-Like Jerk” or a “Startle”)
Typically Upper Body
Typically Bilateral
(May be in a specific muscle group/s)
Duration:
Typically 1-5sec
o Temporal Lobe Epileps
Symptoms: Typically Behavioural Alteration:
- Automatic Activity but Without Consciousness or Memory
- Sexually Inappropriate Behaviour
- Religiosity
- Aggression
- Relived Experiences
Duration:
Can last for hours
Treatment:
Carbamazepine (Tegretol)
o Absence Sei res - (The Classic Pe i Mal
Symptom:
Abrupt Onset of Impaired Consciousness + Amnesia
Pt appears to “Zone Out”
May Purposeless Movements (Eg. Lip Smacking, Eye Blinking)
Then Pt resumes Exactly where they left off (unaware of time lapse)
Duration:
Up to 30sec
Treatment:
Ethosuximide (Thalamic Ca-Channel Blocker)

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 o S a s Epilep ic s (Unremitting Seizure; or Multiple Successive Seizures):
= An Episode of Seizures of Any Type that Either:
1. Seizures Don’t Stop Spontaneously.
2. Seizures Occur in Rapid Succession Without Recovery.
A Status Epilepticus Seizure = Absolute Neurological Emergency:
High Risk of Cerebral Hypoxia
High Risk of Permanent Brain Damage
Often Results in Permanent Loss of Neurons due to Excito-Toxicity.
o (Hippocampus & Pyramidal Tracts are Particularly Sensitive Memory
& Motor)
Surviving Neurons may exhibit Synaptic Reorganisation.
The Problem = Cell Death:
Seizures can Trigger Cell Death; How?:
o In racell lar Ca+ from Ca-Mediated-NT-Release. Release of
Cytochrome-C from Mitochondria Triggers Apoptotic Pathway.
o Energy Depletion Free Radicals Widespread
Protein/Membrane/DNA Damage.
Also, Attempts made by the brain to Restore Function favour The Excitatory
Pathways Seizures.
Occurs mostly in the Young and the Elderly (Typically not middle-aged)
NB: Mortality is highest in Elderly Patients.
Average Mortality Rate 20
Treatment:
1st Line: Benzodiazepines (GABA-Channel Agonist)
o *Diazepam – (Generally #1; But Short Acting)
o Lorazepam – (Some argue that it’s #1 due to Higher Seizure-Termination
Rate)
o Midazolam
+/- Phenytoin – As an Adj nc o Ben os (Usage Dependent VG-Na Channel
Blocker):
o (Unless Absence Seizures or TLE)

- Treatment - Anti-Convulsants:
• The Jack of All Trades (Valproate):
• 3 Mechanisms of Action - (Na+ Channel Blocker, Ca+ Channel Blocker & GABA Activator):
• Repetitive Firing of Neurons.
• Prevents Spread of Signals from Epileptic Focus.
• General Neuronal Inhibition of the Brain.
• ALL Seizure Types
• VG-Na+ Channel Blockers (Carbamazepine[Tegretol], Lamotrigine, Phenytoin):
• Use Dependent VG-Na+ Channel Blockers
• Useful in All Seizures EXCEPT Absence Seizures
• VG-T-Ca+ Channel Blockers (Ethosuximide):
• Blocks VG-T-Ca+ Channels in the Thalamus Prevents Propagation of Seizure Activity.
• Used ONLY in Absence Seizures
• GABA Channel Modulators (Benzodiazepines - Diazepam):
• Activate GABA Channel Cl- Influx Hyperpolarises & :. Stabilises Neuron.
• Useful in All Seizures EXCEPT Absence Seizures
• NB: Benzodiazepines (Diazepam) = 1ST LINE FOR STATUS EPILEPTICUS
• GABA Analogues (Gabapentin):
• Activate GABA Channel Cl- Influx Hyperpolarises & :. Stabilises Neuron.
• Useful in Partial Seizures

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 Surgical Interventions:

Why Surgery:
- Up to 30% of Epilepsies are Unresponsive to Pharmacological Treatment
- If the Epilepsy is Unresponsive to drugs, Surgery is Essential to prevent Permanent Progressive Brain
Damage
o NB: Risk of Brain Damage Increases the longer the condition continues.
o NB: Seizures bring about More Seizures. (Ie. Untreated Seizures make Future Seizures more Likely)

Surgical Options:
- 1. Resections:
o Removal of Epileptic Focus.
o Hemispherectomy (Removal of an entire Hemisphere)
o Anteromedial Temporal Lobectomy
- 2. Disconnections:
o Cut the Corpus Callosum (Bridge between Hemispheres)
o Multiple Sub-Pial Transections (Small cuts made into cortex hoping to isolate neuronal networks)
Prognosis:
- 0 of Surgery Patients are Seizure-Free 10yrs later.
- (NB: Precise mapping of the Epileptic Focus is an Essential Prerequisite to Surgery to ensure that removal
won’t render the patient Paralysed/Unable to Speak/Other Serious Deficit.)

Dietary Intervention: The Ketogenic Diet:

What is the Ketogenic Diet?

- 1gram/KgBody-Weight of Protein.
- 5-10grams of Carbs/Day. (Ie. Virtually NO Carbs)
- Remainder of Calories is made up in Fats.
- NB: Side Effect – Bloating & Constipation (Lack of Fibre).

Proposed Mechanism/s of Action:

- GABA Availability:
o Through Metabolic Conversion of Ketone Bodies GABA.
GABA Availability General Inhibition of Neuronal Activity.
- Altered Metabolic Activity:
o Protein & Carbs Forced Re-Adaptation of Energy-Utilisation Glutamate Availability.
Glutamate Availability Decreased Stimulation of Neuronal Activity.
- Ac i i of Na K-ATPase:
o Drives Neurons Away from Threshold Hyperpolarises.

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 SENSORY Pathology:
EQUILIBRIUM DISORDERS

Common Equilibrium Disorders:

- Vertigo:
o Hallucinatory sensation of movement (Referred to dizziness)
o Labyrinthitis or vestibular neuronitis (subsequent to viral/bacterial infection/metabolic disturbance
– eg. hypoglycaemia)
o Elderly patients – due to reduced blood supply to the labyrinth.
- Menie e S nd me
o Labyrinthine disorder – affects both semicircular canals & cochlea:
Repeated attacks of vertigo, nausea & vomiting
Tinnitus is common & hearing is impaired
- Positional Vertigo:
o May often follow trauma
o May follow drug overdose
o Anxiety & depression may contribute (psychogenic)
- Motion Sickness:
o Mismatch between visual & vestibular information.

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 NEUROLOGICAL Pathology:
GUILLIAN-BARRE SYNDROME

- Guillain-Barre Syndrome:
o Aetiology:
Post-Viral Autoimmune
An Acute Inflammatory Demyelinating Peripheral Polyneuropathy that occurs following
an Acute Viral Illness
o Pathogenesis:
Acute Viral Illness Triggers a Misdirected Immune Response
T-cell Mediated, Autoimmune Attack & Demyelination of Peripheral Nerves
Motor: Ascending Paralysis (Weakness beginning in Feet & Hands Migrating
toward the Trunk)
Sensory: A cending Parae he ia Proprioception & Areflexia (Altered Sensation
in Feet/Hands Trunk)
(NB: Distinct from Multiple Sclerosis since it does not affect the CNS)
o Clinical Features:
Hx of Recent Viral Illness
Acute Progresses over Hours Days
Rapid, Symmetrical Ascending Paralysis & Paraesthesia (Initially Distal Limbs only, then
Proximal Muscles)
Areflexia
NO Fever
Is Life threatening - Death usually due to respiratory paralysis
o Diagnosis:
LP CSF Pro ein
EMG (Electromyography) & Nerve Conduction Studies.
o Treatment:
Hospitalisation
**Ventilation
Prompt IV-Immunoglobulins Or Plasmapheresis Recovery

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 SENSORY Pathology:
HEARING DISORDERS

Common hearing deficiencies:

- Ageing:
o Progressive loss of hearing receptors
- Acute Damage:
o Hair cells can be destroyed by a single explosive sound or continuous high-intensity sound tears
at the cilia
- Drugs:
o Some are ototoxic (damage the hair cells)
- Tinnitus:
o Ringing in the ear in the absence of auditory stimulus
o Symptom of nerve degeneration/inflammation of middle/inner ear.
o Can be caused by drugs. (Damage can be permanent)
Some antibiotics (Streptomycin, neomycin)
Loop diuretics (transient)
Salycilates
- Otitis Media:
o Inflammation of middle ear lining
o Is a common result of throat infections in infants & children (due to short Eustachian tube).
o Can be bacterial viral or bacterial
o Eardrum becomes inflamed and bulges – can perforate
o When large amounts of fluid - pus accumulate behind the eardrum, grommets may be inserted.
- Deafness:
o Conduction Deafness:
Problem with Soundwave Conduction (Ie. Mechanical Structures)
Eg. Earwax
Eg. Perforated Ear Drum
Eg. Fused Ossicles
o Sensorineural Deafness:
Problem with Soundwave Transduction (Ie. Neural Structures)
Eg. Damaged Hair Cells
Eg. Damaged Cochlear Nerve
Eg. Damaged Auditory Cortex

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 NEUROLOGICAL Pathology:
HERPETIC NEURALGIA (SHINGLES)

- Herpetic Ne ralgia Shingles

o Aetiology:
Herpes Zoster Virus Infection in Neural Ganglia
o Pathogenesis:
Trigger (Stress/Sunlight/Immunocompromise) Reactivation of Latent HZV Infection in
Neural Ganglia HZV Migrates down the Axons Painful Vesicular Lesions in the Sensory
Dermatome (Often Trigeminal Nerve)
o Morphology:
Vesicular Lesions over Sensory Dermatome
o Clinical Features:
Initially just paraesthesia & burning pain over Sensory Dermatome
Then Painful Vesicular Lesions over Sensory Dermatome
o Treatment:
Antivirals:
Famciclovir Shortens course of disease.
Pain Management:
Antidepressants / Anticonvulsants (For Neuropathic Pain)
Topical Anaesthetics (Lidocaine Patches / Capsaicin Lotion)
Opioid Analgesics

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 NEUROLOGICAL Pathology:
HUNTINGTONS DISEASE

- Huntingtons Disease:
o Aetiology:
Genetic - Autosomal Dominant
Defective Huntungton Gene (Chromosome 4) – Excess CAG Tandem Repeats
Onset Age & Severity depends on # of CAG Repeats in mutation.

o Pathogenesis:
Excess CAG Tandem Repeats in Huntington Gene Production of Mutant Huntingtin
Proteins in the Brain Increases Decay Rate of Certain Types of Neurons
Selective Marked Degeneration of the Basal Ganglia (incl. The Striatum
[Caudate + Putamen], Globus Pallidus & Substantia Nigra).
o NB: Loss of Basal Ganglia Dysfunctional Action Selection Chorea
Also loss of Cortical Tissue as well (Dementia as well as chorea)

o Morphology:
Macro:
Atrophy of Basal Ganglia (Striatum [Caudate & Putamen], Globus Pallidus &
Substantia Nigra)
Some Atrophy of Cortical Tissue as well.
Compensatory Hydrocephalus of Lateral Ventricles (Lateral Ventricular Dilatation)
o Clinical Features:
Onset in 40’s (NB: The more CAG repeats, the younger the onset & faster the progression)
H n ing n T iad
Dementia (Intellectual Decline)
Depression
Coreiform Movement (Involuntary Jerking) Unsteady Gait
Late Stages:
Slurred speech
Difficulty swallowing.
o Treatment:
Incurable
Tetrabenazine, Neuroleptics, Benzodiazepines Can Chorea
o Prognosis:
<20yr life expectancy after Symptoms Begin.

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 NEUROLOGICAL Pathology:
INTRACRANIAL HAEMORRHAGES

INTRACRANIAL HAEMORRHAGES:
- Aetiologies:
o Trauma:
Eg. Skull Fracture Extradural Haemorrhage (Arterial)
Eg. Low-Force Trauma Subdural Haemorrhage (Venous)
o Congenital Vascular Conditions:
Eg. Congenital Berry Aneurysms Rupture Subarachnoid Haemorrhage (Arterial)
Eg. Congenital AV Malformations Rupture Intracerebral Haemorrhage (Arterial)
o Hypertension:
Hypertensive Intracerebral Haemorrhage (Arterial)

EPIDURAL/EXTRADURAL HAEMORRHAGE:
- Aetiology:
o Trauma/Cranial Fracture Arterial Rupture Separation of Dura from the Skull Haematoma
- Pathogenesis:
o High pressure bleed Forced Splitting of the Dura Mata In ac anial P e e
- Morphology:
o Dura Mata gets separated from the skull
o Extent of Bleeding is Limited by Attached Dura, :. Clearly Defined Margin.
o Lens-shaped area
o Brain Underneath is Compressed
- Clinical Features:
o Severe headache, vomiting and altered consciousness.
o Course:
Rapid progression (due to arterial source of blood)
1. Acute Loss of Consciousness
2. Then Lucid Interval (Temporary Improvement)
3. Then Sudden Deterioration if Herniation (Vomiting, Ipsilateral Pupil Dilation, LOC)
o Signs:
Fixed & Dilated Pupil on side of injury.
Eye on side of injury may be down & out (CNIII Palsy)
Contralateral Weakness of Extremities
Contralateral Homonymous Hemianopsia (Loss of Contralateral Visual Field)
If ICP Cerebellar Tonsillar/Uncal Herniation Respiratory Arrest
- Investigations:
o Head CT (Biconvex Lens Appearance)
- Management:
o Good prognosis with Surgery (Burrhole Craniotomy Drainage)
Will C ne Die without surgery

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 AfraTafreeh.com exclusive

SUBDURAL HAEMATOMA (typically a venous bleed; happens slowly)

- Aetiology:
o Elderly + Low force trauma (Eg. Whiplash Injuries) Slow Venous Bleed
- Pathogenesis:
o Bleeding between the Dura Mata and the Arachnoid Mater
- Morphology:
o Wide distribution ie. Over the entire hemisphere
o Cerebral Oedema Flattening of the gyri, narrowing of sulci, shift of midline
o Abnormal Brain underneath (Ie. Pt. Is often demented, or alcoholic, or have severe cerebral
atrophy)
- Clinical Features:
o Acute Subdural Haematomas:
Typically Due to Mild Trauma
Acute Neurologic Dysfunction (Within Minutes)
High Mortality Rate
o Chronic Subdural Haematomas:
Typically a Spontaneous, Slow Venous bleed (Days Weeks)
Gradual headache, Somnolence, Confusion, Focal Deficits, Seizures.
Common in Elderly.
Signs/Symptoms within Days-Weeks.
o Signs/Symptoms:
Gradually Increasing Headache and Confusion
Dizziness/Tinnitus/Numbness
Blurred Vision
Disorientation/Amnesia
Weakness/Lethargy/Ataxia
Nausea/Vomiting/Anorexia
Irritability/Seizures
- Investigations:
o Head CT:
Acute Subdural = Crescent-Shaped Density.
Can compress lateral ventricle and cause midline shift
Chronic Subdural = Bleeding has Spread Throughout the Subdural Space Follows the
curve of the brain.
- Management:
o If Severe Bleed: D ill D ainage f Bl d ICP
o If Small Bleed: Conservative Management and Monitoring
- Prognosis:
o Brain is typically Abnormal Underneath, Therefore the prognosis is worse

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Subarachnoid Haemorrhage
- Aetiology:
o Berry Aneurysm Rupture in Circle of Willis
o Hypertension is a Contributing Factor
- Pathogenesis:
o #Congenital Berry Aneurysm (Rupture of Saccular Aneurysm on circle of willis)
MCA is Commonest, then ACA, then PCA rare

- Morphology:
o Blood in the sulci
o Blood pools around the Basal Cistern of the brain
- Clinical Features:
o (Pre-Rupture):
Fatigue, Loss of perception/balance, Dysphasia
o Post-Rupture:
Thunderclap Headache Sudden, Severe, Pulsating Headache
+ Vomiting
+ Meningism
+ Hemiparesis
+ Diplopia
Followed by Confusion Loss of Consciousness (+/- Seizures)
- Specific Investigations:
o Head CT/MRI: Blood Within the Sulci & Fissures
o Lumbar Puncture: Blood in CSF
o CT Angiography: To Identify Aneurysms
- Management:
o Stabilise Patient (Ie. Intubate/Ventilation, ICU Admission)
o Urgent Neurosurgical Consult & Intervention
o Prevent/Rx ICP
- Prognosis:
o <50% are Fatal.

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 NEUROLOGICAL Pathology:
ISCHAEMIC ENCEPHALOPATHY

- Global Ischaemia – (Ie. Hypoxemic Encephalopathy):

o Aetiology:
Impaired blood supply – Eg. Heart Failure, Hypotension, Shock, Carotid Thrombosis.
Impaired O2 carrying – Eg. Anemia, Hypoxia.
Impaired O2 utilization – Eg. Cyanide/Carbon-Monoxide Poisoning.
Excessive Neuronal Activity – Eg. Epilepsy/Seizure
o Pathogenesis:
Heart Failure, Anaemia, Hypotension, Hypoxia, Shock, Etc Global Brain Ischaemia
Sensitive Areas:
Adults:
o Watershed Zone (Between ACA & MCA Perfusion Zones)
o 3rd, 5th, 6th Layers of Cortex
o Hippocampus
o Purkinje Cells – Cerebellum Border Zone (watershed areas)
Infants:
o Brainstem Nuclei
o Morphology:
Watershed Zone Necrosis (Between ACA & MCA Perfusion Zones)
Laminar Necrosis – (Chronic – Short penetrating arteries) – the nuclear layers of the cortex
Hippocampus
Purkinje Cells of the Cerebellum
o Clinical Features:
Mild Transient Confusion Severe Irreversible Brain Death (Flat EEG = Vegetative = Coma)

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 NEUROLOGICAL Pathology:
MOTOR NEURONE DISEASES & POLIO

- Motor Neurone Disease (MND)/Amyelotrophic Lateral Sclerosis (ALS):

o *Remember:
Skeletal Muscles are Innervated by Lower Motor Neurons (Ventral Spinal Root Muscle)
LMN a e inne a ed b Uppe Mo o Ne one F om he Co ico pinal T ac
o Aetiology:
90% Sporadic; 10% Genetic
o Pathogenesis:
P og e i e Degene a ion of LMN UMN in he Spinal Co d
(+ Cranial Nerve Nuclei in the Spinal Cord)
UMN & LMN Degeneration Progressive Weakness, Muscle Wasting, Fasciculations,
Spasticity/Stiffness & Hyperreflexia.
Affects Voluntary Muscles (Ie. Walking, Speaking, Breathing, Swallowing)
o Morphology:
Macro:
Degeneration of the Ventral Horns of the Spinal Cord (Ie. LMN)
Degeneration of the Ventral Spinal Roots (Ie. LMN)
Degeneration of Ventral & Lateral Corticospinal Tracts in Spinal Cord (UMN)
Micro:
Neurons may show Spongiosis
Higher #s of Astrocytes
Neuronal Inclusions Skein-like Incl ion B nina Bodie Vac olisation.
o Clinical Features:
Highly Aggressive (Normal Severe within 1yr)
Voluntary Motor Only; Sensory System is Spared
LMN Signs:
o Progressive Muscle Weakness
o Am o oph No M cle G o h M cle A oph Wa ing
o Fasciculations & Cramps
o Hyporeflexia if Mo l LMN a e Affec ed Muscle Innervation)
UMN Signs:
o Spacticity/Stiffness/Rigidity
o Hyperreflexia - if Mo l UMN a e Affec ed D e o Co ical Inhibi ion
(+ Up-Going Plantars (Babinski Sign))
Clinical Diagnosis
o Treatment:
Supportive (Ventilation, Parenteral Nurtition)
o Prognosis:
Incurable
Death within 3yrs

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- Poliomyelitis:
o Aetiology:
Poliovirus Infection
o Epidemiology:
Non Existent in Aus (A single case would be an epidemic)
o Prevention:
Vaccination Available
Live Attenuated (Oral Polio Vaccine):
o Advantages:
Easy Administration - Given Orally
o Disadvantage:
Rarely causes paralysis (1 in 2.5million)
Inactivated Polio Vaccine (IPV):
o Advantages:
Carries NO risk of Vaccine-Associated Polio Paralysis
o Disadvantage:
Difficult Administration - Has to be injected
o Pathogenesis:
Transmission:
Faecal-Oral
or Respiratory
Initially Enteric Infection Spreads to Bloodstream Spinal Cord Preferentially Infect
& Destroy Motor Neurons
o Clinical Features:
90% Asymptomatic
<10% Minor Viral Illness:
Headache
Neck/Back pain
Abdominal Pain
Fever, Lethargy, Vomiting
1% CNS Infection Paralysis
Acute Asymmetrical Flaccid Paralysis + Areflexia
If Spinal Polio Paralysis of Legs(unilateral)
If B lba Polio Cranial Nerve Paralysis (eg. Dysphagia, Dysphasia, Dyspnoea)
Or Combination of Both.

o Treatment:
Self-Limiting, but Lasting Disability Only Supportive Rx (Eg. Ventilation, Physiotherapy)
But Vaccine Preventable

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 NEUROLOGICAL Pathology:
MULTIPLE SCLEROSIS & LEUKODYSTROPHIA

Multiple Sclerosis – (Demyelinating Disorder):

- (Formed Meylin gets Destroyed)
- Aetiology:
o Chronic Autoimmune Inflammatory Disease of the CNS
o Some Genetic Concordance
- Pathogenesis:
o Precise Mechanism Unknown.
o Autoimmune Demyelination within the Brain Spinal Cord (Stripping of Wire’s Insulation
Defective Impulse Transmission & Short-Circuits.
o Affects the CNS ONLY!!
- Morphology:
o Macro:
Patches/islands of Grey-matter-like material in the white matter (Demyelination)
Multiple Soft Pink plaques of Demyleination (Periventricular) (Seen as white periventricular
patches on MRI)
o Micro:
Areas of Loss of Myelin Firstly Around the blood vessels, extending outwards.
Perivascular Inflammation: T-Lymphocytes, Macrophages & Plasma Cells
Reactive Gliosis
- Clinical Features:
o Onset @ 20-40yrs
o Affects White Matter Only
Limb weakness
Ataxia
Paraesthesia
Optic Neuropathy
Vertigo + Nystagmus, but Without Tinnitus or Deafness.
o Relapsing & Remitting
o Progressive Spastic Quadraparesis Death in years (Typically due to paralysis of chest muscles
pneumonia)
- Diagnosis:
o MRI – Visible Plaques around the Ventricles in the White Matter.
o CSF Examination – Oligoclonal IgG
- Treatment:
o Currently Incurable
o Home Care & Supportive Therapy

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www.MedStudentNotes.com
Leukodystrophies – (Myelin Production Disorders):
- (Insufficient Production of Myelin)
- Many, Many Types
- Aetiology:
o Genetic Defect
- Pathogenesis:
o Insufficient Production of Myelin (Insufficient Insulation around Wires) Defective Impulse
Transmission & Short-Circuits.
- Morphology:
o Macro:
o Micro:
- Clinical Features:
o Gradual Decline in a Previously-Well Infant/Child:
Body Tone
Movements
Gait
Dysphasia
Dysphagia
Sensory Impairment (Vision/Hearing)
Behaviour
Slowed Mental/Physical Development
- Treatment:
o Incurable

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 NEUROLOGICAL Pathology:
MYAESTHENIA GRAVIS

Myasthenia Gravis
- Se ere M scle Weakness
o Myo(Muscle)
o Asthenia (Weakness)
o Gravis (Grave/Severe)
- Pathophysiology:
o MG is an Antibody-Mediated Autoimmune Disease which attacks the ACh-Receptors @ the NMJ,
leading to Failure of Neuromuscular Transmission.
o How? By 3 Mechanisms:
A) Complement Binding & Activation @ the NMJ:
Ab-Binding to the AChR activates the Complement Cascade.
Receptor Density Changed Physical Architecture of the Muscle
o Failure of Neuromuscular Transmission.
B) Antigenic Mod lation
Ab-Binding Cross-Links AChRs on NMJ.
Causes Endocytosis & Destruction of the Cross-Linked AChRs.
Leads to a Reduced Number of AChRs on the NMJ.
o Failure of Neuromuscular Transmission.
C) Functional AChR-Block by Antibodies: (Relatively Rare)
Ab-Binding to AChR @ the ACh-Binding Sites.
Causes functional block of the AChR by preventing ACh binding @ the NMJ.
o Failure of Neuromuscular Transmission.

- 2 Types of Myasthenia Gravis:

o Ocular MG:
Fatigable Muscle Weakness limited to Extrinsic Ocular Muscles of the Eye.
In 75% of Cases, Ocular MG is the Initial Manifestation of Generalised MG.
Ocular Muscles are susceptible due to constant rapid neuronal stimulation.
Symptoms:
Double Vision (Diplopia)
Drooping Eyelids
o Generalised (Whole Body) MG:
Fatigable Muscle Weakness involving Other Muscle Groups Including the Eye Muscles.
As mentioned above, Generalised-MG typically begins as Ocular-MG, and then progresses
to the rest of the body.

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 Symptoms (In addition to Ocular MG):
Unstable/Waddling Gait
Weakness in Arms/Hands/Fingers
Weakness in Legs
Weakness in Facial Muscle
Difficulty Swallowing
Shortness of Breath

- Diagnosis:
o Clinical (Pharmacological) Test:
Edrophonium (Short-Acting ACh-Esterase Inhibitor):
Repeated stimulation of remaining receptors.
If symptoms improve, then it s MG
o Serology Testing:
Test for Antibodies Against:
AChR (Acetylcholine Receptors)
MuSK (MuSK = Muscle-Specific Tyrosine Kinase)
Anti-Muscle (eg. Actin) Antibodies
o Electrophysiological Tests:
Repetitive Stimulation of Peripheral Nerves:
Single-Fibre Electromyography:
- Treatment:
o Acetyl-Cholinesterase Inhibitors:
Drugs that Inhibit the Cholinesterase Enzyme from degrading ACh in the Synapse.
Eg. Physostigmine/Organophosphates
Mechanism of Action:
Prolonged Action of ACh in the Synapse
ACh in the Synapse
Side Effects:
Short Term Excessive ACh-Signalling:
o Increases Mainly Parasympathetic Activity:
Increased Secretions (Salivary/Lacrimal/Bronchial/Intestinal)
Increased Peristaltic Activity
Bronchoconstriction
Bradycardia & Hypotension
Pupillary Constriction ( Fall in Intraocular Pressure)
Long Term Desensitisation of AChRs:
o Decreased Parasympathetic Activity.
o In Cholinergic Crisis Muscle & Respiratory Paralysis:
(Cholinergic Crisis = AChR Desensitisation due to ACh-
Stimulation)
ACh-E-Inhibitors Potentiate further Desensitisation.
In Myasthenic Crisis Original Dose is Ineffective:
o (Myasthenic Crisis = Disease Progression Number of ACh-Rs )
o Requires higher Dose for Therapeutic Effect.
o Immunomodulation:
Goal To Remove the Source of the Antibodies or the Antibodies Themselves.
Variety of Options:
Thymectomy
Plasma Exchange
Intravenous-Ig
Immunoadsorption.
o General Immunosuppression:
Goal To dial down the whole immune system slow progression of disease.
Immunosuppressive Drugs:
*Prednisone:

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 o Prednisone = A Corticosteroid = Powerful Anti-Inflammatory
*Azathioprine:
o A Purine-Analogue DNA Synthesis in Clonally Dividing Cells (B/T-
Cells).
- Complications:
o Cholinergic & Myasthenic Crises:
Cholinergic Crisis:
Rapid Desensitisation of the AChRs due to ACh-Stimulation.
Requires Instant Cessation of Acetyl-Cholinesterase Inhibitors.
Myasthenic Crisis:
The point at which the Disease Progression has rendered the current ACh-E-
Inhibitor Useless
Often causes Paralysis of Respiratory Muscles Pt. Requires Assisted Ventilation.
Ie. Requires a higher dose of ACh-E-Inhibitor to Maintain Therapeutic Effects.
o Rectifying these Complications:
Cholinergic Crisis:
Cessation of ACh-E-Inhibitors.
Myasthenic Crisis:
Dose of ACh-E-Inhibitors.

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 NEUROLOGICAL Pathology:
NEUROSYPHILIS

NEUROSYPHILIS:
- Aetiology:
o Infection of the Brain/Spinal Cord by Bacteria: Treponema pallidum.
- Pathogenesis:
o Chronic, Untreated Syphilis – Usually after 10-20yrs Tertiary Syphilis Brain/Spinal Cord
- Clinical Features:
o Weakness, Abnormal Gait
o Blindness, Argyll-Robertson Pupils (Bilateral Miosis, responsive to accommodation, but not to light)
o Confusion, Dementia, Irritability
o Depression
o Headache
o Paraeshtesia in Toes/Feet/Legs
o Seizures
- Treatment:
o 2wk Course of IV/IM Penicillin.

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 Week 11
Neuroscience Synthesizing Session Notes
Disorders of the Special Senses:

Visual Disorders
- Visual Acuity:
o The ability to discriminate fine detail in a visual image.
o Refers to the ability of one cone to be stimulated without its neighbour being stimulated
o Disorders are typically due to imperfections in lens/eyeball shape.
o Measured Using Snellen’s Charts @ 6m distance (See lecture notes for full description)
§ 20/20 (20ft) (6m) = Normal Acuity
§ 20/15 = Better than Normal Acuity
§ 20/60 = Less than Normal Acuity

- Glaucoma:
o A group of diseases characterised by raised intraocular pressure due to an imbalance between
Aqueous Humour Production & Drainage (via Canal of Schlemm)
o IOP produces ocular tissue damage
o One of the leading causes of blindness
o 3 Categories:
§ Angle-closure
• Aqueous humour produced by the ciliary body normally is emptied through the canal
of schlemm.
• Angle-Closure is an imbalance between production & drainage à ↑IOP
• “Angle” = the angle between the inside of the cornea & the iris.
• “Closure” = the angle is too small à blocks off the canal of schlemm.

§ Open angle
• The ‘angle’ is fine.
• But the part of the canal of schlemm is blocked à obstruction to drainage à ↑IOP
§ Congenital/juvenile
• Hereditary
• Infections can do it too.
o IOP à pressure on nerve fibres à axonal necrosis
§ à pressure on the blood vessels à ↓Blood flow

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 - Diabetic Retinopathy:
o Change in basement membranes of the retinal capillaries:
§ Microaneurysms
§ Microvascular obstruction
§ Non-perfusion of capillaries
§ Narrowing of arterial walls
§ Increase in Retinal Vein Calibre
- Cataracts:
o Opacity in the crystalline lens
o Causes are multifactorial:
§ Metabolic disease (eg. Diabetes)
§ UV Light
§ Smoking
§ Ocular diseases (eg. Glaucoma)
§ Skin diseases (eg. Dermatitis)
§ Drug induced (Eg. Corticosteroids)
§ Ageing (Idiopathic – unknown cause)
o Prevention is important –
§ Improving nutrition
§ Reducing diarrhoea
§ Wearing sunglasses with UV filters.
Common hearing deficiencies:
- Ageing:
o Progressive loss of hearing receptors
- Acute Damage:
o Hair cells can be destroyed by a single explosive sound or continuous high-intensity sound à tears at
the cilia
- Drugs:
o Some are ototoxic (damage the hair cells)
- Tinnitus:
o Ringing in the ear in the absence of auditory stimulus
o Symptom of nerve degeneration/inflammation of middle/inner ear.
o Can be caused by drugs. (Damage can be permanent)
§ Some antibiotics (Streptomycin, neomycin)
§ Loop diuretics (transient)
§ Salycilates
- Otitis Media:
o Inflammation of middle ear lining
o Is a common result of throat infections in infants & children (due to short Eustachian tube).
o Can be bacterial viral or bacterial
o Eardrum becomes inflamed and bulges – can perforate
o When large amounts of fluid - pus accumulate behind the eardrum, grommets may be inserted.
- Vertigo:
o Hallucinatory sensation of movement (Referred to dizziness)
o Labyrinthitis or vestibular neuronitis (subsequent to viral/bacterial infection/metabolic disturbance –
eg. hypoglycaemia)
o Elderly patients – due to reduced blood supply to the labyrinth.
- Meniere’s Syndrome:
o Labyrinthine disorder – affects both semicircular canals & cochlea:
§ Repeated attacks of vertigo, nausea & vomiting
§ Tinnitus is common & hearing is impaired
- Positional Vertigo:
o May often follow trauma
o May follow drug overdose
o Anxiety & depression may contribute (psychogenic)
- Motion Sickness:
o Mismatch between visual & vestibular information.

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 NEUROLOGICAL Pathology:
PARKINSON'S DISEASE

PARKINSON S DISEASE Shaking Pals

- Aetiologies:
o Parkinsonism Shaking Pals The Clinical S ndrome
(Drugs/Toxins/Post Encephalitis)
o Parkinson s Disease Primar Atroph of Substantia Nigra Dopaminergic System)
(Idiopathic)
- Pathogenesis:
o Loss of Substantia Nigra (Dopamine makers) Neurons Dopamine Deficiency in the Basal
Ganglia Basal Ganglia Dysfunction.
Dopamine is required by the basal ganglia to coordinate complex movements, therefore, a
lo of he ba al ganglia f nc ion m om of Pa kin on
o More Specifically:
S lemen a Mo o A ea i n ac i a ed o Fine-Tune Movement.
- Morphology:
o Macro:
Loss of Pigment Neurons (Melanin) in the Striatum

- Clinical Features:
o Onset: In second half of life (mean age of onset = 55yrs)
o Parkinson s Triad
1. Resting Tremor Ma be a Pill-Rolling emo
2. Rigidity (Hypertonia Re i ance o Pa i e Join Mo emen
Ma be Lead-Pi e Rigidi Con an o Cog-Wheel Rigidi Fl c a ing
3. Brady/Akinesia (Slowness/Inability to Initiate/Execute Movement)
o Other Symptoms:
+Diminished Facial Expressions
+Stooped Posture
+Shuffling/Hurried Gait
+Declined intellectual function
+Depression
+ Inability to pick up small objects, cups, do up buttons, write in small font etc.

- Treatment:
o Aim: To Do amine Le el in he B ain o o mimic he effec of Do amine
o Oral Levodopa: (L-Dopa can cross the bbb Converted to Dopamine in the Brain)
o Dopamine Agonist: Drugs that mimic Dopamine, binding to Dopamine receptors.
o Side effects:
B Do amine in he Ba al Ganglia Do amine i Globall Side Effects
On Off Phenomenon Symptomatic Relief is Random & Fluctuating
O e ime Le odo a Efficac Dec ea e B Side Effec Inc ea e

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 Week 12
Neuroscience Notes
Parkinson’s Disease (“Shaking Palsy”)

What is it?
- Onset:
o Insidious (Menacing/Unstoppable)
o In second half of life (mean age of onset = 55yrs)
o Progression is variable.
- Characterised by:
o Slowly progressive akinesia
o Rigidity (stiffness)
o Postural abnormality (Leaning forward, stiff, difficult to move, weight loss – difficult to swallow
without aspirating)
o Tremor
- 2nd most common neuro-degenerate disease after Alzheimer’s
- Prevalence:
o 1/1000 non-elderly
o 1/200 in elderly

Biochemistry – Basal Ganglia Dysfunction due to:

- Loss of Substantia Nigra (Dopamine makers) Neurons à Dopamine Deficiency in the Basal Ganglia.
o These neurons project to the striatum (Caudate & Putamen) – Part of the Basal Nuclei – Normally
involved in coordinating movements.
o 50-60% loss of Nigral neurons are required for symptoms.
o Dopamine is required by the basal ganglia to coordinate complex movements, therefore, a loss of
the basal ganglia’s function à symptoms of Parkinson’s.
- Unknown Aetiology
- Secondary Causes – eg. Illicit drug
- More Specifically:
o Without input from the Substantia Nigra, there’s no activation of Inhibitory Neurons of the Putamen,
meaning there’s No Inhibition of Inhibitory Neurons of the Globus Pallidus, Meaning Inhibitory
Neurons of the Globus Pallidus are unopposed in inhibiting Neurons of the VL-Thalamus that usually
activate the SMA (Supplementary Motor Area).
o à Supplementary Motor Area isn’t activated to Fine-Tune Movement.
- NB: Loss of Dopamine release in Striatum creates a NT Imbalance that favours ACh :. Anticholinergic Drugs
are used to treat Parkinson’s Disease.

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Symptoms:
- Most common presenting feature = Tremor:
o Usually unilaterally
o Present at rest
o Increased by emotion & stress
o ‘Pill rolling’ tremor (with fingers)
- Rigidity:
o Stiff muscles
o Cogwheel phenomenon (ratchet-like feeling during passive pronation)
- Slowness of movement
- Postural Chances
- Decline in intellectual function
- Depression
- à Inability to pick up small objects, cups, do up buttons, write in small font etc.

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Treatment:
- Aim: to try to increase the level of Dopamine in the brain, or to mimic the effect of Dopamine, or to relieve
competition of dopamine receptors by anticholinergics.
- Oral Levodopa (Dopamine – NB: L-dopa can cross the bbb, but dopamine can’t)
o Converted to dopamine in the brain by dopa-decarboxylase.
o However, if taken orally, less than 5 % reaches the brain as most is converted to dopamine
systemically. Therefore, it is usually administered with decarboxylase inhibitors to prevent
conversion in systemic.
- Dopamine Agonist:
o Drugs that mimic Dopamine, binding to Dopamine receptors.

NB: Remember, The Dopamine Deficit is only in the Striatum. Other Dopamine pathways are Unaffected. Hence
this poses a problem of side-effects with Dopamine supplementation & Dopamine Agonist drugs.

- Anticholinergic drugs – to prevent competition in the brain. (Loss of Dopamine release in Striatum creates a
NT Imbalance that favours ACh :. Anticholinergic Drugs are used to treat Parkinson’s Disease)
- Surgery
o Sterotactic – using instruments to make a lesion to the brain resulting in decreased symptoms.
o Today – rather than making a physical lesion, an electrical probe is inserted into the brain à ‘lesions’
the brain à stimulates response.
o However, the aim is to 1. Find the area of the brain you want to target, & 2. Find a way to get there
safely while minimising the damage to the brain.
o Benefits – Good control of tremor and on/off phenomenon – stimulator inhibits the sub-thalamic
nuclei (can also be used in some severe OCD’s and other psychiatric disorders)
o Disadvantage – dangerous, and only beneficial for a small subgroup of parkinsons patients.
- Physical Therapy
- Side effects:
o On off phenomenon – Symptoms range from either well controlled or poorly controlled at random
times
o Over time, Levodopa decreases in Efficacy & Side effects Increase.
o Increased severity of symptoms after a while of DOPA administration
o Therefore, treatment is delayed until symptoms are sufficient to impact on the person’s life.

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 Other Facets of Parkinson’s: By Speech pathologist

Psychosocial Impact:
- Myths:
o Only old people get it. – wrong - +10% of diagnoses are in people under 40yrs.
o They only get shaking – wrong – people have postural, balance, speech, swallowing, breathing
problems.
o Sufferers are unemotional and non-feeling – wrong – this is often due to inability to show facial
expression
- Personal Impact:
o Tremor
o Stooped posture
o Masklike face
o Rigidity
o Arms flexed at elbows & wrist
o Bradykinesia
o Postural/balance instability
o Short shuffling steps
o Other CNS symptoms:
§ Speech difficulties (Disarthria of speech
muscles)
§ Swallowing difficulties (dysphagia)
§ Masklike facial expression
§ Constipation/urinary problems
§ Sweating
§ Pain & sensory disturbances.
o Behavioural/Psychological:
§ Sleep disturbances
§ Fatigue (Fatigue very quickly)
§ Mood/depression
§ Anxiety & obsessiveness
§ Thought & memory disturbances (dementia in the end-stage)
§ Psychosis.
- Impact on Carers:
o Depression
o Financial stress
o Strained relationships
o Frustration
o Anger
o Change in roles
o Changed plans for the future
- Impact on families:
o Helplessness
o Financial stress
o Change in roles
o Frustration
o Resentment
- Impact on community:
o Loss of social capital
o Increased healthcare costs
o Increased social benefits
o Loss of productivity
o Ageing population.

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Role of Health Professionals:
- Role of the GP:
o Coordinate lifetime, holistic care
o Plan of management
o Give patient an idea of what the future may hold
o Aim of management:
§ Encourage healthy lifestyle
§ Help the family & patient
§ Manage symptoms as they arise
- Allied Health:
o Specialist (Neurologist)
o Geriatrician
o Physiotherapy
o Occupational therapy
o Speech path
o Social work
o Psychologist
- Other management issues:
o Conselling
o Continuing to work
o Continuing to drive
o Help for carers.

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 AfraTafreeh.com exclusive

NEUROLOGICAL Pathology:
PERIPHERAL NEUROPATHIES

- Diabetic Neuropathy:
o Aetiology:
Chronic Hyperglycaemia
Demyelination
& Arteriolosclerosis
o Pathology:
1. Hyperglycaemia Focal Osmotic Demyelination of Axons Exposure of axon
Affects SENSORY nerves first because they are the ones covered with myelin.
Remember Motor ne rons aren t co ered in m elin
2. Hyperglycaemia Arteriolosclerosis in Vasa-Nervorum (Nerve Blood Supply)
Ischaemic Neuropathy
o Morphology:
Arteriolosclerosis (Amyloid Thickening of the Basement Membrane of Capillaries)
Myelin Loss in Nerve Seen on Myelin Stain (Myelin Stains Black)
Diabetic Neuropathy Normal

o Clinical Features:
Distal, Symmetric Sensory Neuropathy (Paraesthesia, Loss of Sensation)
Autonomic Neuropathy
Progression:
o 1. Sensory Neuropathy
Glo e Stocking Paraesthesia Pain Night-Time Pain
Loss of Proprioception
Risk of Ulcers due to Chronic Painless Injuries.
NB: Bilateral, Symmetrical
o 2. Motor Neuropathy
Muscle Atrophy
3rd Nerve Palsy (Eye is Down & Out)
o 3. Autonomic Neuropathy
Postural Hypotension
GI Motilit Constipation Diarrhoea
Urine Retention/Urgency/Incontinence
Erectile Dysfunction

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- B12 Deficiency:
o Aetiology:
B12 Deficiency Due to:
Dietar Intake Eggs meat, milk, shellfish Ie. Vegetarian/Vegan)
Malabsorption Eg Pernicio s Anaemia GI S rger Coeliac Crohn s
Loss
o Pathogenesis:
B12 is necessary for Maintenance of the CNS
:. B12 Deficiency Demyelination, Axonal Oedema, Neuronal Sclerosis
Particularly Affects Spinal Cord:
(1) Dorsal Column ML Pathway (Sensory Paraesthesia)
o Vibration Proprioception fine to ch
(3) Corticospinal Pathway (Motor Weakness)

o Clinical Features:
Weakness and Paraesthesiae in the Lower Limbs
Loss of Balance
Megaloblastic Anaemia
o Treatment:
Supplemental B12

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 NEUROLOGICAL Pathology:
PRION DISEASES

- Eg. Creutzfeldt Jackob Disease, Gertsmann-Straussler Syndrome, Fatal Familial Insomnia, Kuru Kuru:
o Aetiology:
Prion Infection of the Brain
Prions Proteinaceous, Infectio s on
= Abnormally folded Host-Proteins that accumulate in the brain
NO DNA or RNA!! (Important for Exams)
Prion Proteins (PrP):
Normal Form = PrPc (Cellular)
o Normal -Helix form. (Functional & Denaturable)
o Found throughout the body (Also in mammals).
Abnormal Form = PrPsc (Scrapie)
o Abnormal -Sheet form. (Non-Functional & Non-Denaturable)
o Accumulates in plaques in the brain Tissue Damage & Cell Death.
o EXTREMELY STABLE – Resists denaturation :. Difficult disposal.
o Pathogenesis:
Prions cause Neurodegenerative Disease by aggregating Extra-Cellularly in the CNS form
amyloid plaques Plaques are Internalised Vacuole formation in Neurons Spongy
Architecture.
Propagation Conversion of Normal Proteins -helix -sheet):
Prions propagate by transmitting a Mis-Folded Protein State, not replicating.
Ie. They convert Pre-Existing, Normal forms of the protein to the Abnormal Form.
o Morphology:
Macro:
Empty cystic lesions in the brain Spongiform Encephalopathy
Micro:
Neuronal Vacuolation & Plaque Formation
o Clinical Features:
Initially Subtle Memory & Behavioural Changes Then Rapidly Progressive Dementia
Convulsions (Myoclonus)
Dementia
Ataxia, Dysarthria, Dysphagia, Nystagmus
Behavioural/Personality Changes
o Prognosis:
All known Prion Diseases affect the Brain and are currently Untreatable & Universally
Fatal
7mths life expectancy

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 NEUROLOGICAL Pathology:
RAISED INTRACRANIAL PRESSURE

Intracranial Pressure:
Normal ICP:
o 10mmHg
ICP leads to :
o Cerebral blood flow (Due to reduced perfusion pressure)
(Perfusion Pressure = Sys.BP Intracranial Pressure)
(NB: Perfusion only occurs when Perfusion Pressure is Positive)
o ICP may = Arterial Pressure?
If Arterial Pressure ICP then Perfusion Pressure
Nil Perfusion
Signs of Raised Intracranial Pressure:
o C hing Re pon e Refle C hing Triad
Hypertension
Bradycardia
Irregular Breathing
Treating Raised ICP:
o Osmotic Diuretics (Eg. Mannitol)
o Hyperventilation Hypocapnia Vasoconstriction of Cerebral Vessels
o Continuous CSF Drainage/Surgical CSF Shunt

NB DON T do a L mbar P nc re if Intracranial Pressure is High:

o If ICP is high, and you drain CSF Can ca se Coning
Aka Cerebral Herniation Aka Cistern Obliteration
Brain can herniated through the foramen magnum Puts extreme pressure on parts of
the brain and thereby cuts off their blood supply.
Is often Fatal
o Signs:
ALOC (GCS 3-5)
Vomiting (Compression of Emetic Centre in Medulla)
Can cause 3rd Nerve (Oculomotor) Palsy:
Ptosis = Unable to Open Eyelid (Levator Palpebrae Superioris)
Blo n P pils Dila ed Unresponsi e o Light.
Eye faces Downwards & Outwards
Decerebra e Pos ring (Abnormal Extension to Pain)

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CEREBRAL OEDEMA:
- Cerebral Oedema = Fluid Accumulation in the Intracellular and/or Extracellular Spaces of the Brain
- Aetiologies & Pathogeneses 4 Types:
o Vasogenic - Cap Permeabilit (Ie. Trauma, Ischaemia/Infarction, Infection/Inflammation)
o Cytotoxic Na & H2O Retention in Injured Neurons (Eg. From Hypoxia or Neurotoxin)
o Osmotic CSF Osmolality > Plasma Osmolality (Eg. Overhydration, Hyponatraemia)
o Interstitial Obstructive Hydrocephalus
- Clinical Features:
o (Features of Aetiology Fever if Meningitis, Concussion if Trauma, Stroke if Infarction, etc)
o Fea res of ICP
C shing s Triad - (Hypertension, Bradycardia, Cheyne-Stokes Respiration)
Headache
ALOC
Vomiting
Pupil Dilation
- Management:
o Osmotic Diuretics (Eg. Mannitol)
o Hyperventilation Hypocapnia Vasoconstriction of Cerebral Vessels
o Continuous CSF Drainage/Surgical CSF Shunt

Chronic In racranial Press re Due to Space-Occupying Lesions (See Wk 3 for Cerebral Oedema & Herniation):
- Aetiologies:
o *Space-Occupying Tumours
- Clinical Features of Raised Intracranial Pressure:
o Signs (Cushings Response/Reflex/Triad):
1. Hypertension
2. Bradycardia
3. Cheyne-Stokes Respiration
o Symptoms:
Headache; Drowsiness; Altered level of Consciousness (GCS 3-5)
Vomiting
Seizures
- Treating Raised ICP:
o Elevate Head 30-40o
o Hyperventilate Hypercapnia Vasoconstriction of Cerebral Vessels
o Neurosurgery (if Trauma Haemorrhage)
o Continuous CSF Drainage/Surgical CSF Shunt
o Osmotic Diuretics (Eg. Mannitol) Plasma Osmolarit Extracts Water from Brain Tissue.

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BRAIN HERNIATIONS:
- Aetiology An hing ha Ca ses ICP
o Eg. Cerebral Haemorrhage
o Eg. Cerebral Oedema
o Eg. Obstructive Hydrocephalus
o Eg. Space-Occupying Lesions

- Cerebellar Tonsil Hernia ion Coning

o Pathogenesis:
General ICP Herniation of Cerebellar Tonsils through Foramen Magnum
Compresses the Brainstem Brainstem Ischaemia Cardio/Respiratory-Centre
Dysfunction (Death)
o Specific Signs/Symptoms:
Decerebrate Posturing Abnormal E tension to Pain

ALOC (GCS 3-5)

One Both Pupils Blo n Dilated Unresponsi e to Light
Vomiting (Compression of Emetic Centre in Medulla)
- Uncal Hernia ion
o Pathogenesis:
Unilateral Lesion Lateral Herniation of the Uncus Inferomedial Temporal Lobe against
the midbrain Then, Inferior Uncal Herniation below the Tentorium Cerebelli.
o Specific Signs/Symptoms:
May compress the Occulomotor Nerve Third Ner e Pals
Ipsilateral Pupil Dilation & Unresponsive to Light
Ptosis = Unable to Open Eyelid (Levator Palpebrae Superioris)
Eye Down & Out
o NB: May Progress to Cerebellar Tonsil Herniation Coning Death

- S bfalcine Hernia ion

o Pathogenesis:
Frontal Lesion Posterio-Lateral Herniation of the Cingulate Gyrus (Medial Frontal Lobe)
under the Rigid Falx Cerebri.
o Specific Signs/Symptoms:
May compress the ACA Stroke Contralateral Para-Hemiplegia
Abulia (Frontal Dysexecutive Symptoms)

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 NEUROLOGICAL Pathology:
SPINAL CORD SYNDROMES

Revision of Spinal Cord Tracts:

Changes in Motor Reflexes with Spinal Cord Injury:

o Immediate Consequences:
Reflexes are conserved since they aren’t mediated by the brain.
(NB: Reflexes are only lost if the lesion is @ the level of that reflex)
o Consequences Over Time:
Muscle movement diminishes over a period of time
Due to Progressive Muscle Atrophy (not Nerve Atrophy)

Different Spinal Cord Lesions (Pathways Affected & Clinical Consequences):

o B o n-Sequard S nd ome
(seen if someone is stabbed in the back with a knife or shot with a handgun causing a hemi-
transection of the spinal cord)
Pathways Affected & Clinical Consequences:
Dorsal Column Medial Lemniscal Pathway
o Loss of Discriminative Touch & Proprioception
o (Ipsilateral to & below the level of the lesion)
Spinothalamic Tract
o Loss of somatosensation (Touch, Pain, Temperature)
o (Contralateral to & below the level of the lesion)
Lateral Corticospinal:
o Loss of voluntary movements
o (Ipsilateral to the side of the lesion. Because it decussates in the pyramidal
tracts)

o Anterior Spinal Artery Syndrome:

(Due to Lesion of the Anterior Spinal Artery. Eg. Diving injury)
Pathways Affected & Clinical Consequences:
Doesn’t affect the Dorsal Column Medial Lemniscal pathway.
o No loss of Discriminitive Touch & Proprioception
Doesn’t Affect the Corticospinal Tract
o Conserves Motor Function)
Affects Spinothalamic Tract
o Loss of Somaosensation Contralateral to & below the level of the lesion.

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o Central Cord Syndrome:
(Usually secondary to spinal trauma and, affects the centre of the spinal cord.)
Pathways Affected & Clinical Consequences:
Mainly Corticospinal Tracts
o Motor Impairment (Mostly in Upper Extremities)
o (Why? Motor Fibres supplying Upper limbs tend to be more Central than
those supplying the lower limbs)
Dorsal Column & Spinothalamic Tracts:
o Variable sensory losses below the Lesion.

o Dorsal Column Syndrome:

(Very Unusual)
Pathways Affected & Clinical Consequences:
Dorsal Column Medial Lemniscal Tracts:
o Ipsilateral Loss of Discriminitive Touch & Proprioception Below the Lesion
Doesn’t Affect Spinothalamic Tract:
o Somatosensation (Touch, Pain, Temperature) Unaffected.
Doesn’t Affect Corticospinal Tract:
o Motor Functions Conserved

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 NEUROLOGICAL Pathology:
STROKES

Strokes:
- TIA vs. CVA vs. Stroke:
o TIA = TRANSIENT ISCHAEMIC ATTACK Mini-Strokes = A brief stroke (<24hrs)(episode of
neurologic dysfunction) due to a temporary focal cerebral ischemia NOT associated with cerebral
infarction.
Typically Thromboembolic
Clinical Course:
Temporary Ischaemia, Resolves within 24hrs
o CVA = CEREBRO-VASCULAR ACCIDENT = Any cerebro-vascular pathology that leads to lack of blood
supply to the brain Stroke >24hrs
Clinical Course:
Evolving CVA = Increasing Ischaemia, Longer than 24hrs, Typically Thrombosis
Completed CVA= Complete Ischaemia, No Change, Typically Embolism
o Stroke = Rapid Loss of Brain Function s due to Disturbance in the Blood Supply to the Brain.
(Stroke is the clinical syndrome of a CVA)

- Common Causes of Stroke:

o 1. Ischaemic Strokes (Focal, Thrombo/Embolic):
Atherosclerosis
Rupture Thrombosis Cerebral Ischaemia Stroke.
Or Athero-Emboli in a Cerebral Artery Cerebral ischaemia Stroke
Heart Disease
Eg. Atrial Fibrillation Thrombo-Emboli Cerebral Ischaemia Stroke
o 2. Haemorrhagic Strokes Global ICP Hypoperfusion):
Hypertension
Blood vessel bursts under pressure Bleeding ICP Compresses other
Cerebral Arteries Blood Flo Cerebral Ischaemia Stroke.
Congenital Vascular Conditions
Eg. Congenital Berry Aneurysms Rupture Subarachnoid Haemorrhage
(Arterial) ICP Compresses other Cerebral Arteries Blood Flo
Cerebral Ischaemia Stroke.
Eg. Congenital AV Malformations Rupture Intracerebral Haemorrhage
(Arterial) ICP Compresses other Cerebral Arteries Blood Flo
Cerebral Ischaemia Stroke.
Trauma
Eg. Skull Fracture Extradural Haemorrhage (Arterial)
Eg. Low-Force Trauma Subdural Haemorrhage (Venous)

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 CAUSES OF ALOC VASCULAR:

TRANSIENT ISCHAEMIC ATTACK Mini-Strokes

- Aetiology Typically Transient Embolism:
o Thrombo-Embolism from Carotids
o Cardioembolism from a mural thrombus (Post-MI, AF, Valve disease, Prosthetic Valve)
- Pathogenesis:
o Thrombo-Emboli Lodged in Cerebral Artery Ischaemia Temporary Neurological Deficit (TIA)
When Blood Flow Returns, Neurons are still Functional Recovery
NB: Prolonged Ischaemia Infarction Stroke.
- Morphology:
o No Physical Changes Only Metabolic.
- Clinical Features:
o Signs/Symptoms:
Mimic those of stroke (But <24hrs)
Cerebral hemisphere Contralateral Hemiplegia
Brainstem Quadriplegia, Vision Disturbances etc
Lacunar (Basal Ganglia) Pure Motor, Pure Sensory etc
Emboli in Retinal Artery Amaurosis Fugax (Unilateral Descending Curtain of Blindness)
o DDX:
Hypoglycemia
Migraine Aura
Focal Epilepsy
Hyperventilation
Retinal Bleeds
- Investigations:
o Physical Examination:
Causes? Carotid Bruit, HT, Murmur, ECG (AF?), Fundoscopy
o Lab:
FBC, ESR, U&Es, Glucose, Lipids,
o Imaging:
CT Brain (Rule out Haemorrhagic Since Rx Contradict Each Other)
Carotid Doppler +/- Angiography
- Management:
o Control CV risk factors
Lower lipids (Simvastatin / Atorvastatin)
Stop smoking (Champix)
Lower BP (Perindopril/Candesartan +/- Atenolol)
Antiplatelet (Aspirin)
o Anticoagulation (Warfarin with Heparin Cover)
o +/- Carotid Endarterectomy

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80% ISCHAEMIC STROKE (Thrombo/Embolic Infarction):
- Aetiologies:
o 50% Thrombotic Infarct (Sudden Onset At Rest)
Eg. Rupture of Atherosclerotic Plaque
Eg. Hypercoagulable Syndromes (Eg. Oral Contraceptives, Clotting Disorders)
o 30% Embolic Infarct (Sudden Onset Following Exercise)
Eg. Embolus from Atherosclerosis (eg. From internal carotid)
Eg. AF Blood Stasis in Atria Thrombus Formation
Eg. Paradoxical Embolism (Embolus from DVT Through ASD CVA)
- Pathogenesis:
o Thrombosis/Embolism Focal Ischaemia Infarction Focal Neurology
- Locations:
o MCA (Most Common)
o ACA (Common)
o PCA (Rare - 4% clinically)
- Morphology:
o Early: Oedema (Narrow Sulci, Flattened Gyri)
o NB: Thrombolytic Therapy can Pin-point Haemorrhages around Capillaries
o 1wk: Liquefactive Necrosis & Cavitation
- Clinical Features (Depend on which arteries/functional areas are affected/occluded):
o Middle CA Stroke (#1 Most Common):
Contralateral Whole Body Hemiplegia (Primary Motor Cortex) +/- Dysarthria
Generalised Reduced Sensation (Primary Somatosensory Cortex)
Homonymous Hemianopia (Or sometimes Homonymous Quadrantonopia)
Expressive Aphasia If on LEFT (Dominant) Side Left Broca s Area

o Anterior CA Stroke (#2 Most Common)

Contralateral Lower-Limb Hemiplegia (Primary Motor Cortex)
Lower-Limb Numbness (Primary Somatosensory Cortex)
D se ecutive S ndrome Abulia Slo ness Prolonged Dela s to Perform Acts
Cognitive Impairment (Frontal)
Flat Affect (Limbic System)

o Posterior CA Stroke (#3 - Rare - 4% clinically)

Primarily Visual Defects
Memory Deficits (Short Term)

- Investigations:
o Clinical Examination
o FCB, Coags, Lipids
o CT Brain (Rule out Haemorrhagic)
- Treatment:
o Supportive (O2, Fluids)
o Rapid Reperfusion (Thrombolysis [Tissue Plasminogen Activator] +/- Thrombectomy)
o Anticoagulation (Clopidogrel/Aspirin + Warfarin with Heparin Cover)
o Stroke Rehabilitation (Speech Therapy, OT, Physio)
- Prognosis/Complications:
o 40% Mortality; 75% Mobidity (Eg. Hemiplegia, Aphasia, Dementia, Epilepsy, Mental Dysfunction)

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20% HAEMORRHAGIC STROKES (Bleeds):
INTRACEREBRAL HAEMORRHAGE ICH Haemorrhagic Stroke CVA :
o Aetiologies:
Head Trauma.
Congenital Arteriovenous Malformations
= Tufts of Blood Vessels where they shouldn’t be
Highly Susceptible to Rupture Intracerebral Haemorrhage & Cystic Change

Hypertension
Hypertension Vessels Burst Bleeding ICP Compresses other Cerebral
Arteries Blood Flo Cerebral Ischaemia Stroke.
Morphology:
o Slit Haemorrhages Microhaemorrhages heal as slits with pigment
o Lacunar Infarcts in the Brainstem Small cavity-like areas of pale infarcts

o Clinical Features:
Sudden onset Headache/Vomiting/Meningism
Anisocoria (Uneven Pupils), Nystagmus
Signs of ICP (Hypertension, Bradycardia & Cheyne-Stokes Respiration)
+ Potentially Fatal Herniation Syndromes (Cerebellar Tonsillar/Uncal/Subfalcine).
ALOC
+Focal Neurological Deficits:
o Investigations:
Head CT/MRI (Bleeding within the Brain or Ventricles)
Transcranial Doppler
o Management:
Supportive (Intubation, IV Fluids)
Medical:
Antihypertensives (B-Blocker, ACEi/ARB, Ca-Ch-Blocker)
Coagulation Factor VIIa
Mannitol (Osmotic Diuretic) ICP
Paracetamol Hyperthermia
FFP, Vit.K, Platelets (if Coagulopathy)
Corticosteroids Swelling
Surgical (If Haematoma >3cm)
o Prognosis:
>40% Mortality
75% of Survivors are Disabled

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 NEUROLOGICAL Pathology:
TRAUMATIC BRAIN INJURIES

Focal Primary Injury:

- CONCUSSION:
o Aetiology:
Moderate-Force Blunt Trauma to Head
o Pathogenesis:
Brain Trauma Metabolic/Ionic/Neurotransmitter Disruption Impaired
Neurotransmission
o Morphology:
Macro:
No structural damage
No visible Bleed
o Clinical Features:
Course = Acute, Temporary Unconsciousness (Secs-Mins) Normal Arousal
Symptoms:
Temporary Loss of function
Likely to fully recover (unless secondary injury)
Anterograde & Retrograde Amnesia Memor before after Injur
Headache
“Post Concussion Syndrome” 3wks Post injury
Memory Problems
Dizziness/Loss of Balance
Visual Disturbances/Photophobia
Tiredness
Sickness
Depression/Irritability/Restlessness
Rarely, Post-Traumatic Seizures
o Investigations:
History (Mechanism & Duration of LOC)
Concussion Grading Systems:
Grade I: Confusion, No LOC
Grade II: Confusion, Amnesia, No LOC
Grade III: Any LOC
Physical Examination
Neurological Examination
Including GCS
If GCS is <14 CT
o Management:
Usually Benign :. Just Supportive Treatment (Analgesics, Rest, Sleep, Avoid Drugs/Alcohol)
Avoid Further Head Trauma to Prevent “Second-Impact Syndrome” (Dangerous cerebral
oedema following second impact. Occurs days-weeks after an initial concussion)

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- CONTUSION:
o Aetiology:
Higher-Force Blunt Trauma to Head
(Often a “Contre-Coup injury” Brain Injury on the Opposite Side of Impact Due to
Rebound of the Brain)
(NB: “Coup Injuries” Brain Injury on the Side of Impact)
o Pathogenesis:
Higher-Force Trauma Coup &/or Contre-Coup Injury Bruising & Swelling of the Brain.
o Morphology:
Macro:
Contusion = Local Injury + haemorrhage
Some damage
Localised, Visible Injury with Bleeding (Bruising)
o Clinical Features:
Headache
Confusion/Sleepiness/Loss of Consciousness
Dizziness/Nausea/Vomiting
Cognitive Impairment
Sensory Impairment
Seizures
Ataxia
o Specific Investigations:
CT/MRI:
Focal Cerebral Oedema and often Surrounding Brain tissue
Transtentorial Herniation
o Management:
ICU management
Goal Treat ICP
Prevent Hypotension, Hyponatraemia, Hypercapnia.
May require surgical Intervention
Usually heal without other treatments.
o Prognosis:
Expect a reasonable recovery (but decreased memory, concentration; but still retain
normal function)

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- LACERATION:
o Aetiology:
Penetrating Head Trauma
An incised wound of brain tissue (Eg. Bullet/knife/etc)
o Pathogenesis:
Mechanical Destruction of Brain Matter due to Invading Object
Usually SEVERE damage
o Morphology:
Macro:
Visible tear in the tissue
Haemorrhage
o Clinical Features:
High Velocity:
Instant Death due to Blast Effect Immediate Supratentorial Pressure
Brainstem Herniation through Foramen Magnum.
Low Velocity:
May have Lucid Interval and No LOC
May have LOC as the laceration bleeds into the skull ICP
o Specific Investigations:
CT:
Frequently Associated with Skull Fractures &/or Diffuse Axonal Injury
Cerebral Laceration
Large amounts of Blood
o Management:
Pre ent ICP
o Prognosis:
Typically a Poor Prognosis.

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Diffuse Primary Injury:
- DIFFUSE AXONAL INJURY:
o Aetiology:
High-Force Blunt Trauma to Head
o Pathogenesis:
Shearing of neurons.
(Grey matter of whole areas of the brain have been sheared right off)
o Morphology:
Macro:
Small Haemorrhagic Lesions In the Corpus Callosum and Dorsolateral Brainstem
o Clinical Features:
Unconsciousness
Persistent Vegetative State (Coma) NB: 90% Never regain constiousness.
10% Regain Constiousness BUT significant mental impairment.
o Specific Investigations:
Difficult Doesn t sho up ell on CT/MRI.
CT may appear normal initially
May see small bleeds in Basal Ganglia/Corpus Callosum/Cerebral Cortex on MRI.
o Management:
No Specific Treatment Exists
(Stabilise Patient, & Control ICP)
o Prognosis:
Poor (Brain Damage GCS 3 Organ donor)

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 SENSORY Pathology:
VISION DISORDERS

Focal Disorders:
- Myopia (Short Sighted) Eye is too long
- Hyperopia (Far Sighted) Eye is too short

- Astigmatism:
o The lenses are not perfectly round (more football shaped)
o C ec ed b a T c (Football shaped) lens which is oriented in the opposite direction

- Presbyopia:
o As you get older, the ability to Accommodate gets less Presbyopia
Ie. A progressively diminished ability to focus on near objects with age.
Why? Because the lens loses its elasticity with age.
o Inability to focus on Near Objects (Similar to Hyperopia, but different aeitiology)
o Corrected by Corrected by Plus lenses.

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Glaucoma:
- = A State of Increased Intraocular Pressure
- Aetiology:
o Imbalance between Aqueous Humour Production & Drainage (via Canal of Schlemm)
- Pathogenesis:
o Imbalance between Production & Drainage IOP Damages Optic Nerve & Causes Retinal
Ischaemia Loss of Vision (Typically Peripheral Vision First)
- 3 Categories:
o De e d he A g e be ee he C ea The Iris Which determines patency of the Canal
of Schlemn)
o Open Angle Glaucoma:
The a g e f e, But the Canal of Schlemm is Blocked for another reason obstruction
to drainage IOP
NB: Progresses slower and vision loss may be insidious until the disease has progressed
significantly.
o Closed Angle Glaucoma:
The Angle is too acute Blocks Canal of Schlemn Drainage IOP
NB: Acute onset - Often Painful; visual loss can progress quickly but the discomfort often
leads patients to seek medical attention before permanent damage occurs.
o Congenital/juvenile
Hereditary
Infections can do it too.
- Acute Glaucoma Symptoms:
o Sudden onset headache, nausea, vomiting
o Loss of vision
o Red Eye
o Commonly Unilateral
o Pupils are Dilated
- Treatment:
o Pupillary Constrictors
o NB: Pupillary Dilation will make glaucoma worse; or precipitate glaucoma in predisposed
individuals. (Eg. At night)

Production of aqueous humour & drainage through canal of schlemn

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“Red Eye”
- Common Causes:
o Foreign bodies
o Conjunctivitis(baterial,viral,allergic)
o Sub-conjunctival haemorrhage
o Corneal abrasion
o Corneal ulcer(bacterial/viral)
o Uveitis
o Acute Glaucoma
- Questions to ask:
o Ascertain History of Injury:
Have you been welding
Have you been using contact lenses (notorious for causing problems)
Have you been handling acids/alkalines?
o Is it Uniocular or Binocular?:
If Binocular Probably conjunctivitis
If Monocular These are the ones to be concerned about:
Uveitis
Glaucoma
o Watery or Sticky?
If watery More concerning Eg. Uveitis, Glaucoma, corneal ulcer
If Sticky - Less concerning Prob Conjunctivitis
o Painful/Sensitive to light OR Just uncomfortable?
o (If Vision is Blurred & Painful, Flourescein is used to determine corneal staining)
- Red Flags:
o Unilateral
o Blurred vision
o Severe pain
o Photophobia
o Haloes.
- Common Causes of Red-Eye:
o Foreign Body:
Must know the mechanism of injury

o Subconjunctival haemorrhage:
Just a simple bruise
Common Causes
Coughing fit
Hypertensive
Anticoagulants
Requires no treatment but check BP hether the re on anticoagulants

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o Conjunctivitis:
Inflammation of conjunctiva
Sticky eyes common due to exudates (sometimes purulent)
NB: The cornea is nice and clear
Common Causative Organisms
Staph epiderm
Staph aureus
Strep
adenovirus

o Corneal Abrasion:
Diagnosed by Flourescine + Blue Light
Stains areas of epithelial loss
Must be able to distinguish between a simple corneal abrasion & a corneal ulcer
S perficial abra ion Heal i hin hr and don car

o Corneal Ulcers:
Require Urgent Specialist Care
Viral:
Commonest is Herpetic (Herpes Simplex Virus)
Characteristic feature = has branches :. A Dendritic Ulcer.

Bacterial:
More concerning
Most dangerous organism is Gonorrhea (Can penetrate the eye even without break
in the epithelium)
Pseudomonas Spreads Very Quickly Opaque (Most sight-threatening)

o Uveitis:
Very common cause of Red Eye
Inflammation of the entire uveal tract
Different from iritis
Very sensitive to light
Watery Eyes
NB: There is pus collecting in the anterior chamber.

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Diabetic Retinopathy:
- Change in basement membranes of the retinal capillaries:
o Microaneurysms
o Microvascular obstruction
o Non-perfusion of capillaries
o Narrowing of arterial walls

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Cataracts:
- Opacity in the crystalline lens
- Causes are multifactorial:
o Metabolic disease (eg. Diabetes)
o UV Light
o Smoking
o Ocular diseases (eg. Glaucoma)
o Skin diseases (eg. Dermatitis)
o Drug induced (Eg. Corticosteroids)
o Ageing (Idiopathic unknown cause)

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- Chalazion:
o A cyst in the eyelid that is caused by inflammation of a blocked meibomian gland, usually on the
upper eyelid.

- Strabismus:
o Where eyes are not properly aligned with each other.
o Very important to treat in children because it can cause Amblyopia (Where the brain ignores input
from the deviated eye. Can also be a cosmetic problem)

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SS Quiz Cases: - What is Most Likely in Each Patient?

1.A 23 yr old male presented to A&E with a red left eye .He was grinding metal at work.
- Foreign Body

2.A 13 yr old girl presented with complaints of a red right eye and blurred vision. She has also noticed some cold
sores around her lips.
- Herpetic ulcer

3.A 65yr old male presents with a painless red right eye following a coughing fit. He happens to be on
anticoagulants for a heart condition.
- Subconjunctival Haemorrhage

4.A 35yr old lady who wears contact lenses comes with a 2 day history of a painful red left eye. Her vision is
blurred and her eye is watery.
- Acanthomeba or Pseudomonas infection

5.A 27 yr old male comes with a 2 day history of red eyes. Both eyes are affected. He tells you that his vision
appears OK but they are sticky. He has recently had a sore throat.
- Conjunctivitis (Probably Bacterial)

6. 78 yr male presents with sudden loss of vision in the right eye.Over the past few months he has episodes of
loss of vision lasting for a couple of minutes. He has raised cholesterol.
- transient ischaemic attacks due to embolic atherosclerotic lesions lodging in the eye.

7. 80 yr old woman presents with blurring of central vision.She complains that whem she looks at your face she
cant see anything clearly but can see around it.She tries to read but all the letters are wavy and distorted.
- Age Related Macular Degenration

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