Hemiplegia

Neurological symptoms

HEMIPLEGIA RIGHT HEMIPLEGIA

• Cortical • Test for Aphasia (think of cortical lesions; also know province and background) • Name objects (eg. Pen,tie,etc.); repeat (no. if’s, and’s or but’s); read and check comprehension; listen to spontaneous speech for errors • Check cortical sensory loss • Position sense, point localization, graphesthesia (write number on palm); stereognosis (coin, pen comb)

• Are face and arm more involved than leg? (Middle cerebral AA territory) or Is leg more involved? (Anterior cerebral artery) • Is there eye deviation? • Eyes deviate to hemisphere involved and away from the hemiparesis in cortical lesions • Check field defect • NB: field defect suggests subcortical deficit except when occipital lobe is involved in which case the field defect is due to a lesion in the cortex. • “Cortical” type eye deviation maybe found in subcortical lesions • Hemiparesis and seizure suggest cortical lesion • Determine if lesion is of same distribution as the weakness • Normal primary sense but impaired higher sense like stereognosis

• Subcortical • Impaired primary sense such as vibration and pinprick but not higher senses • Internal capsule • Basal ganglia (globus pallidus and putamen) • Thalamus • Face, arm and leg equally involved – characteristic lesion of the internal capsule • Dystonic posture- basal ganglia • Dense sensory loss to pinprick and touch in the face, arm, leg (thalamic lesion) associated with hemiplegia (involvement of adjacent internal capsule) • Eye deviation and field defect

• Left Brainstem • Look for crossed hemiplegia – classic feature of brainstem lesion • -right hemiplegia from left sided brainstem lesion often produces left sided brainstem signs (e.g. left sided dysmetria or cranial nerve palsies at the level of the lesion) • Check for cerebellar signs • -finger to nose test (FTNT) ataxia, alternate pronation and supination test (APST), heel to toe (tandem gait) • -limb ataxia is on the same side as the lesion • Nystagmus (oscillating movement of the eye; slow component is pathologic because that’s the involuntary movement) • -marked when the patient gazes towards the side of the lesion • Ipsilateral hearing loss

1 and ½ syndrome. There is L internuclear ophthalmoplegia (A) with L gaze paresis(B)

Vertical skew deviation in patient with MS( intrinsic brain stem or cerebellar lesion).

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Sensory findings: -pain, temperature and corneal loss on the left side of the face (involvement of descending tract of V); -with pain and temperature loss on right side of the body (spinothalamic tract) Dysarthria and difficulty in swallowing -pseudobulbar palsy (usually secondary to multiple bilateral vascular lesion above the brainstem), also causes dysarthria and dysphagia -with pseudobulbar palsy, there is hyperactive instead of decreased gag, brisk jaw jerk, emotional lability and history of previous stroke Check for abnormal eye movement -example, right hemiplegia secondary to left brain lesion have trouble gazing to the left or in getting the left eye to cross the midline when looking to the right (Internuclear ophthalmoplegia) Tongue deviation is to the left with lesion on left 12th nerve or its nucleus (the stronger right hypoglossus muscle pushes the tongue to the left ; above the nucleus, tongue deviates to the right)

• Eg……

Lateral Medullary (Wallenburg) Syndrome) • Most common encountered vascular lesion (or syndrome) affecting the medulla (due to occlusion of ventral or posterior inferior cerebellar artery). • Ipsilateral to the lesion – facial numbing, limb ataxia, Horner’s Syndrome (meiosis, ptosis, anhydrosis), eye pain. • Contralateral to lesion - pinprick and temperature loss in arms and legs, then vertigo nausea, hiccups, hoarseness, difficulty swallowing, diplopia. • 7th nerve is not in the medulla. • 12th or hypoglossal – lesion cause ipsilateral fasciculation, tongue deviation to the side of the lesion. • 9th and 10th – dysphagia (laryngeal and pharyngeal muscles)

• Basic structure of the PONS • medial involvement cause motor dysfunction, internuclear opthalmoplagia or gaze palsy to side lesion. • lateral involvement – cause pain and temperature dysfunction. • vertical nystagmus – sign of brainstem dysfunction at level of pontomedullary junction or upper midbrain (unless the patient is on barbiturates). • 6th n – cochlear and vestibular components. • trigeminal n. exits from the middle of the pons – • if involved in this level → produce pain and ipsilateral loss of corneal reflex. • high pontine lesion → pain and sensory loss are contralateral to lesion in both face and extremity. • below the high pons → pain and temperature senses are lost ipsilateral in the face and contralateral in limbs.

Pontine(ipsilateral) lesion in MS.There is partial failure of abduction of the right eye(VI nn. Palsy) associated with b. incomplete facial weakness of the lower motor neurone type.

MIDBRAIN Medial longitudinal fasciculus lesion result to internuclear opthalmoplagia. MLF lesion – difficulty in right eye abduction, nystagmus to abduct-ing left eye when the patient looks to the left. Most prominent disturbance in the midbrain 3rd n. nucleus or exiting fibers. Dilated pupils and opthalmo-plagia.

MS. Bilateral internuclear ophthalmoplegia.

Midbrain lesion just below the superior colliculus produce difficulty with upward gaze convergence and pupillary light reflexes (PARINAUD’S SYNDROME) • Tumors pressing superior colliculus (pinealoma) • Red Nucleus Lesions • Contralateral ataxia and tremor (rubral tumors) • Substancia nigra is located at this level and plays an important role in PARKINSON’S DISEASE • 4th n. nucleus is seen in midbrain at lower level and is seldom involved alone, if involved alone (e.g. – trauma), 4th n. injury causes a head tilt • Optic Tract fibers concerned with pupillary response synapse at region of 3rd n. nucleus • Midbrain lesion may impair pupillary reaction to direct light but leave contraction to accomodation intact

Crossings in the CNS PATHWAY

FUNCTION

CROSSES

INTERPRETATIONS

Pyramidal tract

motor

Lower medulla

Lesion below cross gives ipsilateral sign

Spinothalamic tract

Pain and temp (body)

On entry to spinal cord

Lesion is always contralateral to pain and temperature loss (except in the face)

Spinal tract of 5th n.

Pain and temp (face)

Midpons (runs throughout the medulla)

If lesion is in the medulla or lower pons, there is ipsilateral loss If above midpons – there is contraleteral loss

Spinal dorsal column

Position and vibration

Lower medulla

Lesion below crossing gives ipsilateral signs

Cerebellar tracts

Coordination of movement

Crosses 2 times (on entry to cerebellum and in the midbrain)

Due to “double crossing” lesions of cerebellum or its tracts produce sings ipsilateral to lesion

Gaze fibers

Coordinates lateral gaze

Midpons

See eye deviation in neural disease

CN palsy

CN

Just above CN

Lesion is ipsilateral when CN nuclei is involved

• Spinal Cord Lesion • Face is not involved, so are language and cranial nerves • Paralysis on the same side of lesion • -pinprick and temperature loss on opposite side maybe seen (BROWNSEQUARD SYNDROME) • Sensory level to pinprick or vibration maybe present • Bowel and bladder disturbance are common

Ascending tracts 1. The dorsal column carry position and vibratory sense, fibers rise ipsilateral and cross in the medulla. 2. Lateral spinothalamic tract – carry pain and temperature sensation, fibers cross on entering the cord, cord lesions affecting them cause contralateral loss,? laminate with sacral fibers most laterally placed, therefore expanding lesions in the center of the cord gives sacral sparing (pinprick and sensory loss to temp are least prominent in the sacral area). Descending tracts 3. Lateral corticospinal tract – carry motor fibers, which synapse at anterior horn cells, fibers, have already crossed in the medulla. Lesion in this area causes weakness, spasticity, and hyperreflexia, upgoing toes? 4. Anterior horn cells – lowers motor neurons, lesion produces weakness, muscle wasting, fasci-culation, loss of reflex and tone.

5. Anterior spinal artery – supplies the entire cord except the dorsal column Anterior spinal syndrome produces paralysis and loss of pain and temperature sense, position and migratory sense intact. • Clinical correlation • Combined systemic disease affects 1 and 3. • Amytrophic lateral sclerosis affects 3 and 4. • Multiple sclerosis affects 1, 2 and 3 (alone or in combination). • Poliomyelitis affects 4. • Brown Sequard syndrome (hemi section of the cord), ipsilateral paralysis with contraleteral loss of pinprick.

• Spinal cord • Sensory level → band of sensory change around thorax or abdominal or a sharp level below which sensation is lost • Distal usually symmetric weakness • Bowel bladder changes • PHYSICAL EXAM • Distal weakness usually worse in the leg then arm, worse in extensors than flexors • Tone is increased • DTR is brisk • There is BABINSKY sign • Superficial reflex commonly lost (like anal wink, anal tone, cremasteric reflex, and abdominal reflex • Sensory level can be sound

• Root diseases (radiculopathies) • Hallmark is pain • Other features are the same as above such as denervation (weakness, atrophy, fasciculation) with sensory loss • Weakness can be proximal • Radiculopathies of arm commonly involves C5 and C6 which is proximal, but can be distal • Common radiculopathies in the leg involve the L5 and S1

• Radiculopathy • Pain is usually severe often described as sharp, hot or electric and commonly radiates down an arm or leg • PHYSICAL EXAM • Weakness in one myotomal group of muscles (e.g. C5 and C6 in arm, L5 and S1 in leg, sometimes atrophy and fasciculation) • Tone is normal or decreased • DTR? 0 decreased or absent • Sensory loss to dermatomal distribution maneuvers may stretch the root eliciting pain e.g. straight leg raising

• Peripheral neuropathies • Causes distal, often asymmetric, weakness, with sensory changes, atrophy and fasciculations may also appear • HISTORY • Does the patient wear out his shoes? Catches his toes and trip (foot drop)? (to test for distal weakness of the leg) • Does the patient have trouble with grip or frequently drop things? (this is a sign of distal strength of the hands) • Is the process asymmetric? (some are symmetric e.g. stocking and glove neuropathy, but most are asymmetric e.g. carpal tunnel syndrome, radial nerve palsy, etc) • Does the patient notice shrinkage or wasting of muscles (atrophy) or quivering, twitching (fasciculations) • Is there numbness, tingling or parasthesia?

CARPAL TUNNEL SYNDROME

• PHYSICAL EXAM • Distal often asymmetric weakness with atrophy, fasciculations, and sensory loss e.g. decrease pinprick, vibration and occassionally position sense • Tone is normal or decreased • Reflexes are decreased • Sometimes trophic changes are seen such as loss of hair and nail and smooth and shiny skin

• Neuromuscular Junction Disease • Same as above? But with fatigability, weakness worsens with use, improves with rest • Diseased muscles are usually extremely proximal • Often involves the muscles of the face (like drooping of the eye lids, double vision, difficulty in swallowing or chewing, slurred speech, and facial weakness. • PHYSICAL EXAM • Repetitive test of muscle strength will produce progressive weakness while rest improves the strength

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Muscle disease (MYOPATHY) proximal muscle weakness, symmetric, without sensory loss HISTORY Can the patient arise from the chair, get out of a car seat, go upstairs without using hands? (this is to check proximal muscle weakness) OR can the patient lift or carry objects? (to check proximal arm weakness) Is weakness relatively symmetric? (minor difference is allowed since slight asymmetrical weakness may be observed) Is there sensory loss? (pain, cramping and other sensations may occur with some myopathies but with no sensory loss PHYSICAL EXAM Proximal symmetric muscle weakness with NO sensory loss Tone is normal or slightly decreased Reflex is normal or slightly decreased Significant atrophy absent except in advanced stage

END OF LECTURE