Nerve Tracts in the Spinal Cord

Nerve tract in Spinal Cord

Ascending Tracts Functions
Posterior column tract Carries position, fine touch, pressure & vibration sensation
Anterior spinocerebellar tract
Carries unconscious proprioceptive sensation
Posterior spinocerebellar tract
Anterior spinothalamic tract Carries crude touch & pressure sensation
Lateral spinothalamic tract Carries pain & temperature sensation
Descending Tracts Functions
Anterior corticospinal tract Motor control of voluntary muscles (uncrossed fibres)
Rubrospinal tract Motor tone control
Lateral corticospinal tract Motor control of voluntary muscles (crossed fibres)
General overview

 Ascending tracts - Sensory

 Descending tracts – Motor

General arrangement of both tracts

 1st order neuron

 2nd order neuron
 3rd order neuron

The only difference is the different locations where each order of neuron ends.

Decussation is the cross-over of the tract from one side to the other. Therefore, there are instances
where the left side of the body is controlled by the right brain hemisphere. Decussation occurs at
different locations for each tracts.
General arrangement of descending tracts

 1st order neuron

First-order neurons conduct impulses from receptors of the skin and from proprioceptors (receptors
located in a join, muscle or tendon) to the spinal cord or brain stem, where they synapse with second-
order neurons. First-order neuron’s cell bodes reside in ganglion (dorsal root or cranial). It starts at the
cerebral cortex in the somatomotor area.

 2nd order neuron

2nd neuron to carry an order. The order could be a sensory stimulus or a motor stimulus. The axon of
the 1st order neuron will synapse with the 2nd order neuron at the level of the brain stem, which
commonly decussate (crosses over) to the opposite side.

 3rd order neuron

The 3rd order neuron is located in the ventral horn of the spinal cord, which will exit with the spinal
nerve to supply the muscle.

Types of descending tracts:

 Lateral corticospinal tract

 Anterior corticospinal tract

Therefore, the descending tract is also known as corticospinal tract.

Flow of arrangement of the corticospinal tract:

Corticospinal tract arise from long axons of the pyramidal cells (extrapyramidal layer) of the precentral
gyrus (primary motor centre of the cerebral cortex) which lies in front of the central sulcus

Homunculus arrangement

 arranged upside down

 the finer the movement, the more the cortical representation
 fingers, face, tongue – more
 trunk, lower limbs – less
 medial surface: lower limbs
 superolateral surface: everything else
1) 1st order neuron
 Fibres of the 1st order neuron arise from the precentral gyrus
 These fibres converge and enter a small area
 internal capsule
 like a bunch of flowers with a ribbon tied around it
 ALL the fibers (from ascending & descending tracts) converge here
 Function: separates the caudate nucleus and the thalamus from
the lenticular nucleus
 Ques: location of internal capsule
 bounded medially by the thalamus and caudate nucleus
 bounded laterally by the lenticular nucleus
 Parts of internal capsule (not homunculus arrangement, normal head to
toe)
 anterior limb
 head & neck fibres most anterior
 posterior limb
 lower limb fibres most posterior
 The descending fibres passes through the
 LATERAL half of the posterior limb of internal capsule
 After the internal capsule, the fibres enter the brain stem
 midbrain
 pons
 medulla

2) 2nd order neuron

 Fibres of the 1st order neuron ends when it enters the brain stem and synapse with the
2nd order neuron
 The fibres pass through the brainstem
 1st – through the (mid 5th) crus cerebri of midbrain
 2nd – through the anterior part of the pons
 3rd – in the medulla oblongata
 80-85% of the fibres cross to the opposite side
 Motor decussation
 uncrossed fibres
 Enters the spinal cord
3) 3rd order neuron
 2nd order neuron fibres in the medulla oblongata enters the spinal cord and synapse
with the 3rd order neuron
 Motor decussation
 in the spinal tract, the crossed tract descend as the lateral corticospinal
tract
 Therefore, the motor cortex of the cerebral hemisphere controls the
opposite side of the body (L – R, R – L)
 contra-lateral side
 In upper motor neuron lesions:
 above the motor decussation (above medulla)
 opposite side of body affected
  below the motor decussation
 same side of body affected
 ipsilateral side
 Uncrossed fibres
 in the spinal tract, the uncrossed tract descent as the anterior
corticospinal tract
 its fibres cross at spinal level?

Ascending tracts (sensory)

Types of ascending tracts:
 Spinothalamic tracts
 Lateral
 pain & temperature
 Anterior
 light touch & pressure
 Dorsal column tract
 deep touch & pressure
 proprioception
 vibration sensation
 Spinocerrebellar tract
 posture & coordination
Flow of arrangement of Spinothalamic tracts:
1st order neuron:
 Arise from sensory receptors of the body
 The fibres enter the white mater and ends at the substantia gelatinosa
 tip of posterior gray horn
2nd order neuron:
 The fibres of 1st order neuron synapse with the 2nd order neuron at the substantia
gelatinosa
 These fibres then cross to the opposite side
 Pain & temperature fibres
 enters the lateral spinothalamic tract
 Light touch & pressure fibres
 enters the anterior spinothalamic tract
 These tracts ascends to brainstem
 to medulla oblongata, pons and midbrain
  tracts flattened in the brainstem
 spinal lemniscus
 Reaches the ventral posterolateral nucleus of the thalamus
 ends here
3rd order neuron:
 The 3rd order neurons arise from the thalamus and pass through the internal capsule
 thalamocortical fibres pass through the medial part of the posterior limb of the
internal capsule
 Enters the postcentral gyrus
 sensory cortex of the cerebrum
 behind the central sulcus
 Same homunculus arrangement
 more sensitive areas in the body have a greater representation

Flow of arrangement of the dorsal column tracts:

 Arise from the sensory receptors of the body
 Fibres enter the dorsal column of the SAME side (post column of spinal cord)
 ascends to the medulla oblongata
 (does not synapse and end here like spinothalamic tract)
 Enters medulla oblongata
 ends in the gracile and cuneate nucleus
2nd order neuron:
 Starts at the gracile & cuneate nucleus of the medulla oblongata
 These fibres crosses to the opposite side of the medulla oblongata
 Ascends through the brain stem
 as flattened bundle
 medial lemniscus
 Ends in the ventral posterolateral nucleus of the thalamus
3rd order of nucleus:
 Arise from the thalamus
 Pass through the internal capsule
 medial aspect of the posterior limb of internal capsule
 Reaches the postcentral gyrus
 ends here

Flow of arrangement of Spinocerebellar tract:

1st order neurons:
 Arise from the sensory receptors of the body
 Enters the spinal cord
 Ends in the Clarke’s Column of the posterior grey horn
 synapse
2nd order neurons:
 Arise from the Clarke’s Column
 synapse with 1st order neurons
 Ascends in the spinocerebellar tracts
 Enters the cerebellum
 through the interior and superior cerebellar peduncles
 the only tract that enters the cerebellum
Actual decussation of these tracts:
 These tracts decussate 2 times
 therefore cerebellum controls same side of body
 ipsilateral
 eg. right spinocerebellar tract controls the right side
 vice versa

Clinical anatomy:
 Lesion of one half of the spinal cord may lead to
 Opposite side of body
 loss of pain, temperature, light touch, pressure sensations
 Same side of body
 loss of the other sensations
 Sensory cortex of the cerebral hemisphere controls the opposite side of the body
 contralateral
 Lesion above the sensory decussation
 all the sensations of the OPPOSITE side of the body are lost
 Lesion below the sensory decussation
 sensations of the SAME side of the body are lost
 Cortical lesions
 affected areas are usually limited
 paralysis/parasthesia is localized
 Internal capsule lesions
  all ascending & descending tracts are affected
 hemiplegia/hemiparasthesia

Upper motor neuron & Lower motor neuron lesions

Definitions
Upper motor neuron
 Corticospinal neuron
 Corticonuclear neuron
Cerebral cortex (pyramidal tract) –> Precentral gyrus (motor strip) → internal capsule (posterior
limb) → brainstem → spinal cord

 85% cross to opposite side

Upper motor neuron lesions
 Interruption of the corticospinal and corticonuclear tract along its course

Lower motor neuron

 Neurons from the brain stem & spinal cord
 efferent motor fibres
 terminal axons & motor end plates
 muscle fibres
Anterior horn cells in spinal cord→nerve roots→nerve plexus →peripheral nerves

Lower motor neuron lesions

 Degeneration of the motor neuron & peripheral nerves

Clinical features – Upper motor neuron lesion

 Initial phase
 limbs flaccid
 loss of tendon reflexes
 Several days to a week
 return of motor function, but tone increases
 Long term
 Spasticity
 Hyperreflexia
 Ankle & patella clonus
 Barbinski sign +ve
 extensor plantar response
 Absent abdominal reflexes
Examples of UMN lesion
 Cerebrovascular accident
 stroke! most common
 Intracranial tumour
 Cervical spine injury
Clinical features – Lower motor neuron lesion
 Muscle wasting
 Muscle weakness
 reduced power
 Hypotonia
 Loss of reflexes
 Fasciculations
 Fibrillations
 Associated changes in
 skin, nail, hair
Examples of LMN lesion
 Motor neuron disease
 Peripheral nerve neuropathy
 Diabetic neuropathy?
 Poliomyelitis
 anterior horn cell affected
 Spinal cord injury
 with nerve root compression
Examples of BOTH UMN & LMN lesion
 Demyelinating disease
 Multiple sclerosis
Spinal cord injury
 C1 – C5
 Upper limbs: UMN
 Lower limbs: UMN
 C6 – T2
 Upper limbs: LMN
 Lower limbs: UMN
 T3 – L3
 Upper limbs: normal
 Lower limbs: UMN
 L4 – S2
 Upper limbs: normal
 Lower limbs: LMN

Facial nerve lesion

 Upper motor neuron lesion
 Contralateral lower quadrant weakness
 Angle of the mouth
 Opposite side
 Lower motor neuron lesion
 Ipsilateral orbicularis oculi muscle and facial muscles involved
 Half of face
 unable to close eyes
 weakness of angle of the mouth
 cannot elevate eyebrows
 Same side
Pyramidal tract

The pyramidal tract, also known as the corticospinal tract, is an important part of the central nervous
system. It is responsible for all voluntary movements made by the body. Damage to this tract can
lead to a number of problems, including paralysis, muscle weakness, loss of muscle control, and
tremors.
The origins of the pyramidal tract lie in the “motor strip,” an area in the cerebral cortex where signals
that trigger voluntary movement originate. A group of pyramidal neurons create a dense network of
fibers that travels through the brain, along the brain stem, and into the spinal cord. Once in the spinal
cord, the lower motor neurons connect with the nerves that innervate muscles all over the body.
When a voluntary movement is made, the signal is passed along from neuron to neuron along the
corticospinal tract until it reaches the desired nerves. This transmission takes place in a fraction of a
second, allowing people to respond in a way that may feel instantaneous. The level of control
available through the pyramidal tract is extremely precise and highly detailed, allowing people to do
everything from controlling the movement of the hands during brain surgery to running a marathon.
Certain neurological diseases can cause lesions in the pyramidal tract, leading to a loss of muscle
control because nerves become damaged and can no longer transmit signals. The cells can also be
damaged through stroke and trauma, such as a traumatic brain injury. Patients with pyramidal tract
dysfunction are usually treated by a neurologist, a doctor who specializes in the treatment of
diseases that involve the nervous system.
Patients who have sustained damage to their corticospinal tract have a prognosis that varies,
depending on the nature of the damage. Some patients may be able to regain motor control over the
course of the healing process. Others may permanently lose motor control, leading to the  atrophy of
muscles that are never used. Some patients can also develop issues like contractures, in which
muscles or tendons become permanently shortened. Physical therapy can sometimes help patients
retain muscle strength and control.
Problems with the pyramidal tract can be identified during a neurological examination in which a
medical professional checks for classic signs, such as muscle weakness and the Babinski reflex, a
reflex normally only seen in young children, and which is indicative of a problem when it is seen in
adults.

Neural Pathways

Pyramidal system – Direct Activation Pathway. All of the motor impulses that

orginate at the cortical level (in cortex of brain) travel through this tract. This pathway
supplies the voluntary muscles of the head, neck, and limbs. Neurons of this tract
originate in the post-central gyrus or primary motor cortex.

The pyramidal system has two tracts: corticospinal and corticobulbar. The nerve

fibers of the corticospinal tract travel down through the internal capsule down to the
medulla. At the inferior level of the medulla, 70-90% of the nerve fibers on each side
will deccusate, or cross over to the other side. Those that cross over continue down
the spinal cord and are collectively known as the lateral corticospinal tract, and
these fibers exert contralateral control. The remaining 10-30% travel down the
ipsilateral side and are collectively known as the ventral corticospinal tract, and
these fibers exert ipsilateral control. These will continue to travel down the spinal cord
until they reach the level of the muscles they will serve, where they will then synapse
with the nuclei of lower motor neurons.

The nerve fibers of the corticobulbar tract initially follow the same pathway as the
corticospinal tracts. However, these will begin to synapse with the motor nuclei of the
cranial nerves beginning at the level of the upper pons. These fibers will deccusate at
various levels of the brainstem. Of interest is that the nuclei of the facial nerve receive
bilateral innervation for some muscles and unilateral representation for others.
Generally speaking, the upper face is more bilaterally innervated, and the bottom half
is more unilaterally innervated (but by contralateral fibers).

Extrapyramidal system – Indirect Activation Pathway

The pyramidal system was the primary pathway for voluntary movement. The
extrapyramidal system is another motor system that is important for control of
movements. Neuronal activity for this motor system begins in the cerebral cortex and
ultimately exerts an influence on the lower motor neurons. The pathways are indirect,
as opposed to the direct pathways of the pyramidal system. The long axons of the
corticospinal tract and corticobulbar tract make only one synapse with the lower
motor neuron, so the pyramidal system is called monosynaptic. The extrapyramidal
system, however, is polysynaptic.

The major extrapyramidal nuclei are the basal ganglia. Remember that the basal
ganglia is composed of the Globus Pallidus, Putamen, and Caudate Nucleus.
Together, the Globus Pallidus and Putamen are called the Lenticular Nucleus.
Together, all three are called the Corpus Striatum. Other structures related to the
extrapyramidal system include the substantia nigra, red nucleus, subthalamic
nucleus, and reticular formation of the mesencephalon. The cerebellum is also
thought of as contributing to the extrapyramidal system.

The extrapyramidal system works by modifying neural impulses that originate in the

cerebral cortex. Impulses generated at the primary motor strip are sent via the
extrapyramidal fibers to the basal ganglia. In a complex network of pathways, the
structures of the basal ganglia modify impulses and send information to each other.
Some fibers will then be directed down to synapse with the lower motor neurons.
Other fibers are routed through the thalamus and back up to the cortex.

The role of the extrapyramidal system includes the following: (1) selective activation
of movements and supression of others (2) Initiation of movements (3) setting rate
and force of movements (4) coordinating movements.

Damage to the extrapyramidal system, but especially damage to the basal ganglia, will
result in movement disorders known as dyskinesias. Different types of dyskinesias
include:

Myoclonus - characterized by involuntary single or repetitive jerks of a body part. If

the jerks are repetitive, they can be rhythmic or non-rythmic. They can be isolated to
one muscle group or a number of muscles at the same time. These movements can
occur spontaneously, but also to stimuli (visual, tactile or auditory). Hiccups are a
form of myoclonus (brief spasm of diaphragm.).

Tics - these are rapid, repeatingly coordinated or patterned movemetns that are under
partial control by the affected person. Often, the person will relate that they have an
irresistible urge to perform the movements. They can often supress the movements
temporarily. Simple tics may appear similar to dystonia or myoclonus. Complex tics
are coordinated and can involve jumping, noises, lip smacking, and other rapid,
repeated movements.

Chorea - characterized by rapid, involuntary, random, purposless movements of a

body part. Can be present at rest, during sustained postures, and during movement.

Can be subtle or obvious. These movements can often be modified by the person after
initial onset so that they are made to appear intentional in order to cover them up.

Ballism - characterized by gross, abrupt contractions of axial and proximal muscles of

the extremities that can produce flailing.

Athetosis - a relatively slow, writhing, purposless movement of a body part. Athetosis

and choreaic movements often combine with eachother, and called choreoathetosis.
Athetosis is a major category of the effects of Cerebal Palsey.

Dystonia - a slow form of hyperkinesia characterized by involuntary abnormal

postures resulting from excessive co-contraction of antagonistic muscles. Writers
cramp is a form of this.

Spasm - a general term that designates a variety of muscular contractions. Tonic

spasms are prolonged. Clonic spasms are repetitive, have a rapid onset, and are brief.

Tremor - Rhythmic (periodic) movement of a body part. Resting tremors occur

when a body part is at rest. Postural tremor occurs when the body part is maintained
against gravity. Action tremor occurs during movement. Terminal tremor occurs as
the body part nears a target. Can be caused by cerebellar circuit problems.
Lower motor neuron signs are pyramidal not extrapyramidal.
To put it super simply any lesion is the direct route from motor cortex-->corticospinal tract (upper
motor neuron)-->lower motor neuron = WEAKNESS = PYRAMIDAL. Weakness is key as both
upper and lower motor neurons lesions cause it. Of course, intrinsic muscle pathology and a whole
load of other non neuro things can cause weakness.

As mentioned by the poster above MOVEMENT DISORDERS =EXTRAPYRAMIDAL. EPS are

errors in MOTOR PLANNING pathways (not on the direct path from motor cortex to motor neuron)
and do NOT characteristically cause weakness or spasticity (though cerebellar lesions can cause
hypotonia). The primary motor cortex, the UMN, and the LMN (pyramidal tract) directly give the
"marching orders" signals where as the extrapyramidal system refines them and removes the
meaningless noise. So knock out the pyramidal "motherboard" and you cant move (weakness) but
knock out the EPS "adjusters" and you can still move, but you'll move funny (ataxia) or get stuck
(rigidity, bradykinesia, torticollis) or randomly flail (hemiballism) or have an overshoot tremor
(cerebellar) or have writhing athetosis or dancing chorea (Huntingtons) etc etc

1.  Motor centers and pathways

 o Pyramidal tracts (corticospinal and corticobulbar) pass through the medullary
pyramids.
o All others are extrapyramidal tracts and originate primarily in the following
structures of the brain stem:
o Rubrospinal tract
 originates in the red nucleus and projects to interneurons in the lateral spinal
cord.
 Stimulation of the red nucleus produces stimulation of
flexors and inhibition of extensors.
o Pontine reticulospinal tract
 originates in the nuclei in the pons and projects to the ventromedial spinal
cord.
 Stimulation has a general stimulatory effect on both extensors and
flexors, with the predominant effect on extensors.
o Medullary reticulospinal tract
 originates in the medullary reticular formation and projects to spinal cord
interneurons in the intermediate gray area.
 Stimulation has a general inhibitory effect on both extensors and flexors,
with the predominant effect on extensors.
o Lateral vestibulospinal tract
 originates in Deiters’ nucleus and projects to ipsilateral motoneurons and
interneurons.
 Stimulation causes a powerful stimulation of extensors and inhibition of
flexors.
o Tectospinal tract
 originates in the superior colliculus and projects to the cervical spinal cord.
 is involved in the control of neck muscles.
2. Effects of transections above the spinal cord
o Lesions above the lateral vestibular nucleus
 cause decerebrate rigidity because of the removal of inhibition from higher
centers, resulting in excitation of α- and γ-motoneurons and rigid posture.
o Lesions above the pontine reticular formation but below the midbrain
 cause decerebrate rigidity because of the removal of central inhibition from
the pontine reticular formation, resulting in excitation of α- and γ-
motoneurons and rigid posture.
o Lesions above the red nucleus
 result in decorticate posturing and intact tonic neck reflexes.
Chapter 10. Upper Motor Neuronal Tracts
In order to reach the muscles, motor commands generated in the central nervous system must travel on
upper motor neurons and synapse with lower motor neurons.

Upper motor neurons (UMN) are a type of first order neuron. They are unable to leave the central
nervous system. The pyramidal tract is a very important upper motor neuron tract. The extrapyramidal
tract also consists of upper motor neurons, and is multi synaptic.

As upper motor neurons must remain inside the neuraxis, they synapse with neurons of another type
called lower motor neurons which can carry messages to the muscles of the rest of the body. When
children have neuromuscular problems due to UMN lesions that occur before, during, and shortly after
birth they are said to have cerebral palsy.

Lower motor neurons, or second order neurons are cranial and spinal nerves. The cell bodies of these
neurons are located in the brain stem, but their axons can leave the central nervous system and synapse
with the muscles of the body.

All lower motor neurons are either spinal or cranial nerves. All spinal nerves have a lower motor neuron
component as they are mixed nerves. However, not all cranial nerves have lower motor neuron
components. Some of the cranial nerves contain only sensory fibers and therefore cannot be classified as
lower motor neurons. For example, CN I, the olfactory nerve, CN II the optic nerve, and CN VIII, the
auditory nerve, do not have motor components.

The Pyramidal Tract

This group of fibers carries messages for voluntary motor movement to the lower motor neurons in the
brain stem and spinal cord.

Approximately 80% of the cell bodies of the pyramidal tract are located on the precentral gyrus of the
frontal lobe, which is also known as the motor strip. Particularly large cells located here whose axons are
part of the pyramidal tract are called pyramidal cells. Approximately 20% of the pyramidal tract fibers also
originate in the postcentral gyrus of the parietal lobe, in Brodmann's areas 1, 2, and 3. Regardless of the
location of their cell bodies, pyramidal tract fibers begin their descent from the cortex as a corona radiata
(radiating crown) before forming the internal capsule.

This tract is direct and monosynaptic, meaning that the axons of its neurons do not synapse with other
cells until they reach their final destination in the brain stem or spinal cord. These direct connections
between the cortex and the lower motor neurons allow messages to be transmitted very rapidly from the
central nervous system to the periphery.

The fibers that synapse with cranial nerves form the cortico-bulbar tract. Bulbar refers to the brain stem
(midbrain, pons and medulla). The ancients anatomists thought that the medulla looked like a plant bulb.

The fibers of the pyramidal tract that synapse with spinal nerves sending information about voluntary
movement to the skeletal muscles form the cortico-spinal tract. These axons are among the longest in
the central nervous system, as some of them travel all the way from the cortex to the inferior part of the
spinal cord. As they descend through the brain, they form part of the posterior limb of the internal
capsule.

At the pyramids in the inferior part of the medulla, eighty-five to ninety percent of cortico-spinal fibers
decussate, or cross to the other side of the brain. The remaining ten to fifteen percent continue to
descend ipsilaterally. The fibers that decussate are called the lateral cortico-spinal tract or the lateral
pyramidal tract. Because they descend along the sides of the spinal cord,
the uncrossed or direct fibers that synapse with spinal nerves on the ipsilateral side of the body are
called the direct pyramidal tract. They may also be referred to as the ventral pyramidal tract or
the anterior cortico-spinal tract since they travel down the ventral aspect of the spinal cord.
The spinal nerves receive only contralateral innervation from the cortico-spinal tract. This means that
unilateral pyramidal tract lesions above the point of decussation in the pyramids will cause paralysis of the
muscles served by the spinal nerves on the opposite side of the body. For example, a lesion on the left
pyramidal tract above the point of decussation could cause paralysis on the right side of the body.

The fibers of the pyramidal tract that synapse with cranial nerves located in the brain stem form the corti-
cobulbar tract. Obviously, this is the part of the pyramidal tract that carries the motor messages that are
most important for speech and swallowing. Corticobulbar axons descend from the cortex within
the genu or bend of the internal capsule.

Almost all of the cranial nerves receive bilateral innervation from the fibers of the pyramidal tract. This
means that both the left and right members of a pair of cranial nerves are innervated by the motor strip
areas of both the left and right hemispheres.

This redundancy is a safety mechanism. If there is a unilateral lesion on the pyramidal tract, both sides of
body areas connected to cranial nerves will continue to receive motor messages from the cortex. The
message for movement may not be quite as strong as it was previously but paralysis will not occur.

The two exceptions to this pattern are the portion of CN XII that provides innervation for tongue protrusion
and the part of CN VII that innervates the muscles of the lower face. These only
receive contralateralinnervation from the pyramidal tract. This means that they get information only from
fibers on the opposite side of the brain. Therefore, a unilateral upper motor neuron lesion could cause a
unilateral facial droop or problems with tongue protrusion on the opposite side of the body. For example,
a lesion on the left pyramidal tract fibers may cause the right side of the lower face to droop and lead to
difficulty in protruding the right side of the tongue. The other cranial nerves involved in speech and
swallowing would continue to function almost normally as both members of each pair of nuclei still
receives messages from the motor strip.

Because most cranial nerves receive bilateral innervation, lesions of the upper motor neurons of the
pyramidal tract must be bilateral in order to cause a serious speech problem. (The effects of the inability
to protrude the tongue and of paralysis of the lower face on speech are negligible.)

On the other hand, unilateral lesions of the lower motor neurons may cause paralysis. This occurs
because the lower motor neurons are the final common pathway for neural messages traveling to the
muscles of the body. At the level of the lower motor neurons, there is no alternative route which will allow
messages from the brain to reach the periphery. Muscles on the same side of the body as the lesion will
be affected.

Lesions on the cranial nerve nuclei located in the brain stem are called bulbar lesions. The paralysis that
they produce is called bulbar palsy.

Lesions to the axons of the cranial nerves are called peripheral lesions.

As cranial nerves are lower motor neurons, both bulbar and peripheral lesions are lesions of the final
common pathway.

When bilateral lesions of the upper motor neurons of the pyramidal tract occur, they produce a paralysis
resembling that which occurs in bulbar palsy. For this reason, the condition is known as pseudo-
bulbar palsy.

If a lesion occurs in the brain stem and damages both the nucleus of a cranial nerve and one side of the
upper motor neurons of the pyramidal tract, a condition known as alternating hemiplegia may result.
This involves paralysis of different structures on each side of the body. The lesion on the nucleus of the
cranial nerve will cause a paralysis of the structures served by that nerve on the same side of the body as
the injury. Because the pyramidal tract provides only contralateral innervation to the spinal nerves,
damage to the upper motor neurons will meanwhile cause a paralysis of different structures on the other
side of the body. For example, a lesion that affected the right nucleus of the trigeminal cranial nerve and
the right side of the pyramidal tract would cause paralysis of the right side of the jaw and the left arm or
leg.

Both the cortico-spinal and cortico-bulbar tracts send some axons to the pontine nuclei as they descend
to synapse with lower motor neurons. These fibers that end in the pons form the cortico-pontine tract.
This pathway carries information to the cerebellum (cortico-pontine-cerebellar) about the type and
strength of the motor impulses generated in the cortex. While the cortico-pontine fibers actually end in the
pontine nuclei, second order neurons carry their message to the cerebellum via the middle cerebellar
peduncle. This tract may be considered to be a part of the extrapyramidal system rather than a
component of the pyramidal tract since it does not synapse directly with lower motor neurons.

This system is involved in automatic motor movements, and in gross rather than fine movement. It works
with the autonomic nervous system to help with posture and muscle tone and has more influence over
midline structures than those in the periphery. Facial expression is one important communicative behavior
that is mediated by the extrapyramidal tract. This is the reason that some Parkinson's patients have little
facial expression. In contrast to the pyramidal tract, the extrapyramidal tract is an indirect, multisynaptic
tract.

Components of the extrapyramidal tract include the basal ganglia, the red nucleus, the substantia
nigra, the reticular formation and the cerebellum. All of these structures send information to the lower
motor neurons.

Some sources, including the text by Love and Webb, 1992, consider the basal ganglia to be the sole
constituent of the extrapyramidal system, saying that the other structures listed above synapse with the
extrapyramidal tract but are not part of it.

The basal ganglia acts to inhibit the release phenomenon, or the rapid firing of motor neurons. It is aided
in this function by the substantia nigra of the midbrain. The muscles most often affected by this inhibitory
functions are those controlling the head, the hands, and the fingers.

The neurotransmitters involved in the inhibitory function of the basal ganglia include dopamine, which is
produced by the substantia nigra, acetylcholine, and GABA (gamma amino butyric acid), which is a
glutamate. Dopamine is an especially powerful inhibitor.

Extrapyramidal Projections to Lower Motor Neurons

The extrapyramidal tract has an important role in motor movement. It has projections that carry autonomic
motor impulses to voluntary muscles in the body, including the muscles for speech and swallowing.
During speech, muscles are receiving input from both the pyramidal and extrapyramidal systems. it is
involved in gross motor movement rather than fine. It is responsible for facial expression such as
sadness, irony and happiness.

The rubrospinal tract passes through the red nucleus. The cerebellum sends messages to the spinal
nerves along this tract. Information flows from the superior cerebellar peduncle to the red nucleus and
finally to the spinal nerves. This information is very important for somatic motor, or skeletal muscle control
and the regulation of muscle tone for posture.

The reticulospinal tract runs from the reticular nuclei of the pons and medulla to the spinal nerves. It is
involved in somatic motor control like the rubrospinal tract and also plays an important role in the control
of autonomic functions.

The tectospinal tract has points of origin throughout the brain stem, but especially in the midbrain area,
and ends in the spinal nerves. It is involved in the control of neck muscles.

The vestibulospinal tract runs from the vestibular nuclei located in the lower pons and medulla to the
spinal nerves. It is involved in balance.

(Note that all of these tracts receive input from the cerebellum.)

Extrapyramidal Diseases and Syndromes Affecting Communication/Swallowing

Lesions in the extrapyramidal tract cause various types of diskinesias or disorders of involuntary
movement.

The problems most commonly affecting the extrapyramidal tract

include degenerative diseases, encephalitis, and tumors.

Parkinson's Disease, which is a degenerative disease, is probably the most frequently occurring illness
that results from extrapyramidal tract lesions. It occurs when the dopaminergic neurons of the substantia
nigra are destroyed. Its symptoms include:

Tremor

Festinating movements, especially a festinating gait. (Festinating movements are movements which
become increasingly rapid and uncontrolled).

Hypokinetic dysarthria

Weak Voice

Mask-like facial expression

Diseases associated specifically with lesions of the basal ganglia include Huntington's

Chorea and Sydenham's Chorea. The term "chorea" comes from the Greek "khoros" which means
dance. Both of these diseases are associated with jerky, uncontrolled movements of the limbs.
Sydenham's chorea was probably the cause of the malady that was known as St. Vitus' Dance during the
middle ages. Huntington's Chorea is an inherited degenerative disease. Sydenham's tends to clear up
spontaneously.

Essential Tremor Syndrome, which is associated with Spastic Dysphonia may also be the result of
basal ganglia lesions.

Lesions of the basal ganglia will also cause hyperkinetic dysarthria.

Note that not only is the definition of the extrapyramidal system controversial, but also many sources say
that it is very difficult to make functional distinctions between the extrapyramidal and pyramidal systems.
When upper motor neuron lesions occur, it is sometimes difficult to determine which tract has been
damaged.