Approach To A Case Of

Quadriparesis
-

Dr DEEPAK SHARMA
 HISTORY
 Age: young vs old

Onset and Duration:

Is it acute- Is it subacute- Is it chronic-

within minutes or within days or within months or
hours? weeks? years?
Progression of weakness: constant/progressing/intermittent
 History of :

• Trauma to cervical spine

• Pain in neck

• Recent history of vaccination(Rabies, H1N1, COVID)

• History regarding infections/fever(Viral illness/Tuberculosis)

• Any comorbid illness: Diabetes, Hypothyroidism, HIV

 History of:

 Any loss of sensations?

Any sphincter disturbances( bladder and bowel involvement) ?

 Past History:
Enquire about Malignancy;
Swellings or bone tenderness?
Surgery for tumors?
Chemotherapy or radiation?

 Personal History: diet(veg/non veg, vitamins deficiencies, excess

alcohol intake), Drugs intake
Occupational exposure(regarding toxins(OP), heavy metals)

Family history: hereditary? Familial periodic paralysis

ALWAYS RULE OUT MALINGERING IF HISTORY IS NOT SUGGESTIVE OF ANY

NEUROLOGICAL DISEASE.
 QUADRIPARESIS

UMN SIGNS LMN SIGNS

-Anterior horn cell

-Roots
SPINAL CORD
BRAIN
(Cervical) -Nerves
-Neuro-muscular jn
Non
Compressive
Compressive
-Muscle
 Approach to UMN Lesions
• Cerebral Palsy- leading to spastic quadriplegia along with other
associated features

• Young adult/quadriparesis along with visual disturbances(one or more

episodes)/relapses and remissions

MULTIPLE SCLEROSIS
 Approach to UMN Lesions
• Consciousness retained/paralysis of limbs and oral structures/
voluntary blinking and vertical eye movements remain intact

Bilateral ventral pontine damage

LOCKED IN SYNDROME
Approach to UMN
Lesions(Cervical Cord)
FEATURES COMPRESSIVE NON-COMPRESSIVE
Bony deformity Present Absent
Bony tenderness Present Absent
Upper level of sensory loss present Absent
Root pain Present Absent
Onset and progress Gradual May be acute
Symmetry Asymmetrical Majority are symmetrical
Bladder and bowel involvement Late Early(acute transverse myelitis)
Features Extramedullary Intramedullary

Radicular pain Common Unusual

Funicular pain Rare Common

Motor deficit Ascending motor weakness .i.e. Descending pattern of loss .i.e.
Sacral>lumbar> thoracic> cervical Cervical >thoracic>lumbar> sacral

Reflexes Brisk, early feature less brisk.

Sensory deficit Ascending sensory loss.i.e. • Descending pattern of loss .i.e.

Sacral>lumbar> thoracic> cervical Cervical >thoracic>lumbar> sacral
• Dissociative sensory loss

Sacral sensastions Lost early Sacral sparing

Bowels and bladder involvement Late Early

Lesion at Foramen Magnum:

• Motor: “Around the clock” type of motor weakness

may be seen (Ellsberg phenomenon)
• Sensory: Suboccipital pain in the distribution of great
occipital nerve
• Downbeat nystagmus
• Cerebellar Ataxia
• Papilledema(Due to CSF obstruction)
 Lesions of High Cervical
Cord(C1-C4)
• Pain at suboccipital region(C2)
• Lhermitte’s symptoms: Due to lesions of posterior cord

Electric shock like sensations radiating down spine which may be

transmitted to extremities & may occur with neck flexion

• Inability to elevate shoulders(Compromise of Cr. N XI supplying

Sternocleidomastoid and Trapezius in compressive lesions of C1-C4)
 Lesions of High Cervical
Cord(C1-C4)
• Diaphragmatic paralysis(particularly lesions involving C3-C5)

• Biceps jerk(C5,C6) Exhaggerated

• False localizing signs including thoracic sensory levels, proprioceptive

sensory loss, paraesthesias of hands, clumsiness and atrophy of hands
can occur with disorders afflicting upper cervical cord.(? Ant. Spinal
artery ischemia, venous congestion) {Sonstein et al, 1996}-
{Localization in Clinical Neurology, 6th edition}
 Lesions of High Cervical
Cord(C1-C4)
CAUSES:
• Cranio-vertebral junction anomalies
• Cervical spondylosis
• Tumors(Meningioma, neurofibroma, gliomas)
• Basilar invagination(e.g in Pagets Disease)
• Atlanto-axial subluxation( e.g. Rheumatoid Arthritis)
• Multiple Sclerosis
• Syringomyelia
• Chiari-I Malformation
• Morquio disease
 Lesions affecting C5/C6
• Lesions affecting C5&C6 leads to LMN paresis of arms and spastic
paresis of lower extremities. Diaphragmatic functions may be
compromised(C5 affection)
Lesions at C5:
• Sensory loss over entire body below neck.
• Biceps jerk(C5,C6) Absent/Diminished
• Brachioradialis jerk(C5-C6)
• Triceps reflex(C6-C7) Exaggerated
• Finger flexion reflex(C8-T1)

Lesion at C5 leads to inversion of supinator reflex.

Lesions at C6:
• Sensory loss over entire body below neck except that lateral arm is
spared
• Biceps jerk(C5,C6)
• Brachioradialis jerk(C5-C6) Depressed/Absent
• Triceps reflex(C6-C7)
• Finger flexion reflex(C8-T1) Exaggerated
Lesions at C7:
• Sensory loss at and below the third and 3rd and 4th digits(including the
medial arm and forearm)
• Paresis involves the flexors and extensors of wrists and fingers
• Biceps jerk(C5,C6)
Preserved
• Brachioradialis jerk(C5-C6)
• Finger flexion reflex(C8-T1) Exaggerated

• Paradoxical triceps reflex may be seen(flexion of elbow in percussion

to triceps tendon)- afferent arch of triceps reflex is injured in injuries
of C7
 Lesions affecting C8/T1
• Sensory loss involves the fifth digit and the medial forearm and arm
as well as the rest of the body below the lesion.
• Weakness predominantly involves the small hand muscles with
associated spastic paraparesis
• Biceps jerk(C5,C6)
• Brachioradialis jerk(C5-C6) Preserved
• Triceps reflex(C6-C7)
• Finger flexion reflex(C8-T1) Diminished

• May be associated with unilateral or bilateral Horner Syndrome

 Syringomyelia
• Fluid filled, gliosis lined cavity within spinal cord(mostly b/w C2-T9)
• Symptoms more pronounced in upper limbs-
• Distal muscle wasting seen
• “Suspended” and “dissociated” sensory loss- loss of pain &
temperature sense with preserved light touch, joint position and
vibration sense
 Motor Neuron Disease
• Degenerative disease of the motor neurons in which both UMNs and
LMN are involved almost exclusively.
• Course is not relapsing and remitting, but rather INSIDIOUSLY
PROGRESSIVE
• UMN+LMN- Amyotrophic Lateral Sclerosis(ALS)- MOST COMMON
• Can be associated with bulbar/pseudobulbar palsy.
• Asymmetric limb weakness is the most common presentation.
• Upper extremity onset is most often heralded by hand weakness and
lower extremity onset of ALS most often begins with foot drop
• Cognitive functions are usually preserved
The diagnosis of ALS is further
suggested by an ABSENCE of
history of:
• Neuropathic or radiculopathic pain

• Sensory loss

• Bladder and bowel involvement

• Ptosis (Motor neurons for ocular motility remain unaffected)

 Sub acute combined degeneration
of Spinal cord
• Vit. B12 deficiency leading to degeneration of dorsal and lateral
white matter of spinal cord

DORSAL COLUMN LATERAL SPINOCEREBELLAR

• Impaired tactile CORTICOSPINAL TRACT TRACT
discrimination, • Muscle weakness • Sensory Ataxia
proprioception, • Hyperreflexia (Romberg sign)
vibration sense • Spasticity
• Paraplegia/quadriplegia
• Bladder and bowel
involvement in advanced
cases
Anterior spinal artery syndrome
• Abrupt onset of symptoms
• Loss of motor functions, pain/temperature sensations
• Relative sparing of proprioception and vibratory sense below the level
of lesion
 QUADRIPARESIS

Sensory level on examination

yes
No

Deep Tendon Reflexes

Compressive Non compressive
myelopathy myelopathy,
Transverse myelitis
Symmetric
ascending paralysis
Ocular/bulbar

Prolonged ICU
Symmetric Intermittent involvement + GBS
proximal muscle weakness,
stay, sepsis precipitating factors
weakness Descending Fluctuating
weakness , weakness, fatigue
Critical illness Periodic bradycardia
polyneuropathy paralysis
DeRmatomyositis, Neurotoxic Myasthenia
Botulism
polymyositis snake bite Gravis