Two (contralateral to each other) or three limbs (upper and lower limbs), e.g. right upper limb and

left lower limb or left arm and both legs, both arms and one leg.

Patterned weakness:

The pattern of pyramidal weakness is weakness of upper limbs extensors and lower limbs

flexors.

For example: Right MCA territory embolic infarct—history of sudden onset, complete loss of power

in left upper limb, lower limb associated with left UMN facial palsy. Weakness—maximum at onset,

nonprogressive.

Causes of monoplegia affecting the

lower limb

Causes of monoplegia affecting the upper limb

Stroke, affecting anterior cerebral

artery territory.

Cerebral venous sinus thrombosis

affecting superior sagittal sinus.

Trauma, head injury, with contusion

in the frontal lobe.

Infection, such as granuloma

affecting frontal lobe.

Trauma to the lumbosacral plexus,

diabetic lumbosacral plexopathy.

Functional or psychogenic.

Stroke, affecting superior division of contralateral middle cerebral artery

territory, affecting parietal lobe, or unpaired anterior cerebral artery.

Head injury, with contusion in the parietal lobe.

Trauma to the brachial plexus.

Injury to multiple cervical nerve roots.

Functional or psychogenic.

Causes of hemiplegia

Ischemic or hemorrhagic stroke, affecting contralateral cerebral hemisphere, internal capsule, brainstem or ipsilateral

upper cervical cord.

Cerebral venous sinus thrombosis with venous infarction of contralateral cerebral hemisphere.

Acute central nervous system infection, such as meningitis or encephalitis, brain abscess, granulomatous infections.

Head injury causing contusion/bleeding in the contralateral cerebral hemisphere, internal capsule, basal ganglia, or

brainstem.

Tumor affecting cerebral hemisphere, internal capsule, basal ganglia, brainstem or cervical cord.

Bleeding into a brain tumor on the contralateral side.

Demyelinating illness, such as acute disseminated encephalomyelitis (ADEM) or multiple sclerosis (MS).

Todd’s paresis.

Mill’s hemiplegic variant of motor neuron disease (MND).

Causes of Quadriplegia (Table 6C.1)

Table 6C.1: Causes of quadriplegia.

UMN causes LMN causes

Cerebral palsy

Bilateral brainstem lesion (glioma)

Craniovertebral junction anomaly

High cervical cord compression

Multiple sclerosis

Motor neuron disease

Acute anterior poliomyelitis

GB syndrome

Peripheral neuropathy

Myopathy or polymyositis

Myasthenia gravis

Periodic paralysis

Snake bite, organophosphorous poisoning, etc.

Causes of Paraplegia

Causes of Flaccid Paraplegia (LMN type)

UMN lesion in shock stage, i.e. sudden onset or history of long duration as in extradural transverse myelitis and spinal

injury

Lesion involving anterior horn cells:

Acute anterior poliomyelitis

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Progressive muscular atrophy (a variety of motor neuron disease)

Diseases affecting nerve root: tabes dorsalis, radiculitis, GB syndrome

Diseases affecting peripheral nerves:

Acute infective polyneuropathy (GB syndrome)

High cauda equina syndrome

Disease of peripheral nerves involving both the lower limbs

Lumbar plexus injury (psoas abscess or hematoma)

Diseases affecting myoneural junction:

Myasthenia gravis, Lambert-Eaton syndrome

Periodic paralysis due to hypo- or hyperkalemia

Diseases affecting muscles: Myopathy.

Onset and Progression

Acute, subacute, or chronic.

Reversible, stable nonreversible, fluctuating, stuttering or step-ladder, or progressive.

Ascending weakness—first lower limbs→upper limbs→GB syndrome, extramedullary

compressive myelopathy

Descending weakness—first upper limbs→lower limbs→Miller Fisher variant of GB syndrome,

intramedullary compressive myelopathy.

Ellsberg phenomenon—compressive lesions near the high cervical cord produce weakness of

the ipsilateral shoulder and arm followed by weakness of the ipsilateral leg, then the contralateral

leg, and finally the contralateral arm, an “anticlock-wise” pattern that may begin in any of the four

limbs.

Table 6C.2: Causes of spastic paraplegia [upper motor neuron (UMN) type lesion].

A. Gradual onset B. Sudden onset

Cerebral causes

Parasagittal meningioma

Hydrocephalus

Thrombosis of unpaired anterior cerebral artery or superior

sagittal sinus

Spinal causes

Compressive or transverse lesion in the spinal cord: Cord

compression

Noncompressive or longitudinal lesion or systemic disease

of the spinal cord

Motor neuron disease (MND), e.g. amyotrophic lateral

sclerosis

Multiple sclerosis, Friedreich’s ataxia

Subacute combined degeneration (i.e. from vitamin B12

deficiency)

Lathyrism, Syringomyelia, Erb’s spastic paraplegia, Tropical

spastic paraplegia

Radiation myelopathy

Compressive causes

Injury to the spinal cord (fracture-dislocation or collapse

of the vertebra)

Intervertebral disc prolapse

Spinal epidural abscess or hematoma

Noncompressive causes

Acute transverse myelitis

Thrombosis of anterior spinal artery

Hematomyelia (from arteriovenous malformation,

angiomas, or endarteritis)

Muscles/Limb(s) Involved

Proximal upper limb—

shoulder/arm:

Difficulties combing hair, reaching for high objects, winging of scapula

Distal upper limb—forearm/hand: Finger/wrist drop, poor hand grip, cannot open jar, difficulty in

buttoning/unbuttoning

Proximal lower limb—pelvic/thigh: Cannot rise from chair or squatting position, waddling gait

Distal lower limbs—leg/foot: Difficulty in gripping chappals, cannot walk on heels/toes, foot drop

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Neck muscles Dropped head/broken neck

Trunk Inability to roll on the bed

Variation throughout day—fatigability: In postsynaptic neuromuscular junction disorders like

myasthenia gravis the weakness worsens on exertion. Wasting/loss of muscle bulk—wasting is a feature of LMN disease. Florid wasting is seen in

motor neuron disease. Usually associated with fasciculations. In late stages of UMN disease

disuse atrophy may be seen. Wasting of muscles also results in undue prominence of underlying bones.

Stiffness of limbs—increased tone of the limbs resulting in stiffness and heaviness of limbs is a

characteristic feature of UMN disease. Patients may complain that the limbs are heavy as log of

wood in spasticity, while they may say that the limbs are floppy in LMN diseases.

Gait abnormalities: It may aid in the diagnosis.

Limp or dragging foot—might suggest LMN disease/foot drop

Scissoring/circumduction may suggest UMN disease.

Involuntary movements:

Type

Symmetrical/asymmetrical

Part of the body involved

Present at rest

Functional disability.

SENSORY DYSFUNCTION

Numbness/loss of feeling

Altered feeling:

Paresthesia

Dysesthesias (tingling, pin-needles)

Spontaneous pain

Pattern of sensory loss:

Pattern of sensory loss Site of the lesion

Hemisensory loss—same side face and body Internal capsule/thalamus

Crossed sensory—one side face, opposite side body Lateral medulla

Ascending sensory loss—lower limbs → upper limb Extramedullary compressive myelopathy

Descending sensory loss—upper limbs → lower limb Intramedullary compressive myelopathy

Dissociative sensory loss (only pain and temperature lost, posterior column

sensations preserved)

Intramedullary compressive myelopathy

Lateral medullary syndrome

Anterior cord syndrome

Definite sensory level (below which all sensations lost) Suggestive of spinal cord disease

Graded sensory loss—glove and stocking Suggestive of peripheral

neuropathy

Positive and Negative Symptoms

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Abnormal sensory symptoms can be divided into two categories: positive and negative.

Positive Symptoms

Altered sensation that are described as pricking, bandlike, lightning-like shooting feelings

(lancinations), aching, knifelike, burning, scarring, electrical. Such symptoms are often painful.

Positive phenomena usually result from trains of impulses generated at sites of lowered threshold

or heightened excitability along a peripheral or central sensory pathway.

Because positive phenomena represent excessive activity in sensory pathways, they may or may

not be associated with a sensory deficit (loss) on examination.

Negative Symptoms

Represent loss of sensory function and are characterized by diminished or absent feeling that

often is experienced as numbness and by abnormal findings on sensory examination.

It is estimated that at least one-half of the afferent axons innervating a particular site are lost or

functionless before a sensory deficit can be demonstrated by clinical examinations.

Subclinical degrees of sensory dysfunction may be revealed by sensory nerve conduction

studies. Whereas sensory symptoms may be either positive or negative, sensory signs on examination

are always a measure of negative phenomena.

Sense Test device Endings activated Fiber size mediating

Pain Pin prick Cutaneous nociceptors Small

Temperature

(heat)

Warm metal object Cutaneous thermoreceptors for hot Small

Temperature

(cold)

Cold metal object Cutaneous thermoreceptors for cold Small

Touch Cotton wisp, fine brush Cutaneous mechanoreceptors, also naked

endings

Large and small

Vibration Tuning fork, 128 Hz Mechanoreceptors, especially Pacinian

corpuscles

Large

Joint position Passive movements of specific

joints

Joint capsule tendon endings, muscle

spindles

Large

CEREBELLAR EXAMINATION

Coordination and Balance

Difficulty in walking

Unsteadiness

Falls

Staggering

Loss of balance in dark.

AUTONOMIC DYSFUNCTION

Bladder Dysfunction (Table 6C.3)

History of:

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