Hemiplegia - أ.د.عمرو حسن الحسني أستاذ المخ والأعصاب 

Definition: Paralysis of one side of the body
Causes:
I. Vascular Causes: These are the most common.
A. Thrombotic: resulting in cerebral infarction.
1. Vessel wall diseases:
 Cerebral atherosclerosis (most important).
 Vasculitis e.g.: Polyarteritis nodosa & SLE.
2. Blood diseases causing hyperviscosity: result in thrombosis.
 Polycythemia 1ry & 2ry. -Thrombocytosis
 Hypergammaglobulinaemia
3. Circulation diseases: slow circulation results in thrombosis.
 Heart failure.
 Systemic hypotension (after myocardial infarction, shock, excessive hypotensive drugs, severe blood loss).
B. Embolic: resulting in cerebral infarction. The source of the embolus may be:
1. Heart (commonest): in cases of mitral stenosis with A.F.
2. Distal vessels
C. Haemorrhagic: Intracranial haemorrhage may be:
1. Intracerebral: the bleeding is in the brain substance
2. Subarachnoid: the bleeding is in the subarachnoid space.
The causes of intracranial haemorrhage are:
 Hypenension
 Rupture of an intracranial aneurysm, angioma or A-V malformation: commonest cause of subarachnoid haemorrhage.
 Haemorrhagic blood diseases: purpura, haemophilia.
 Anticoagulants.
 Trauma to the head: commonest of subdural haematoma.
II. Infective: ;
 Encephalitis
 Meningitis - Brain abscess.
III. Neoplastic: e.g. Meningioma.
IV. Demyelination: multiple sclerosis may present with hemiplegia.
V. Traumatic: e.g. Cerebral laceration and subdural haematoma.
VI. Hysterical: patient suffering from paralysis in the absence of organic lesion.
Clinical picture:
A. The classical clinical picture
Onset & course:
 Acute onset & regressive course (vascular, infective & traumatic lesions).
 Gradual onset & progressive course (neoplastic lesions).
 Relapsing remitting course (M.S.).
Symptoms & signs: Vary according to the onset:
Acute lesions: the clinical picture passes through 2 stages:
 Stage of flaccidity due to neuronal shock.
 Stage of spasticity
3-Exaggerated deep reflexes:
 Deep reflexes in both U. & L.L. are exaggerated on the paralysed side (biceps, triceps, brachioradialis, knee & ankle reflexes).
 Pathological deep reflexes (normally absent) may appear e.g. finger reflex.
 Clonus may be elicited in the ankle, less frequently in the knee or wrist.
4-Lost superficial reflexes e.g. abdominal and cremasteric reflexes are lost on the paralysed side.
5-Positive Babinski sign
6-Gait: If the patient can walk, his gait is circumduction due to spasticity of the extensors & adductors of L.L.
B. According to the site of the lesion
The lesion causing hemiplegia may occur at 3 main levels:
1. Spinal cord.
2. Brain stem.
3. Cerebral.
1. Spinal Cord
The lesion is on one side of the cord & is situated between Cl & C5 segments, it is caused by: stab wound, disc prolapse, M.S. or tumour resulting in the picture of Brown-Sequard syndrome (see fig.36) characterised by:
a) At the level of the lesion:
 Ipsilateral localised L.M.N.L. of the muscles supplied by the affected segments.
 Ipsilateral loss of all sensations in the area supplied by the dorsal roots of the affected segments.
b) Below the level of the lesion:
 Ipsilateral hemiplegia.
 Ipsilateral deep sensory loss.
 Contralateral superficial sensory loss for pain & temperature.
 Touch diminishes on both sides.
3. Cerebral
Cortical: characterised by one or more of the following:
 Coma if the lesion is extensive.
 Convulsions if the lesion is irritative.
 Contralateral cortical sensory loss if the parietal lobe is involved.
 Aphasia and agraphia (Cannot speak or write) if the lesion is in the dominant hemisphere.
 Homonymous hemianopia if the lesion involves the parieto-occipital region.
 The paralysis usually involves one limb (monoplegia) specially in vascular lesions.
Subcortical: It is indistinguishable from cortical hemiplegia except that the paralysis is more extensive.
Capsular: Characterised by the following:
 Hemiplegia associated with U.M.N. facial and hypoglossal paralysis on the opposite side of the lesion.
 Hemihyposthesia on the opposite side of the lesion.
 Hemianopia may occur, if the fibres of the optic radiation in the capsule are involved.
 No convulsions.
 No aphasia.
 No coma.
Investigations:
A. Labs: blood glucose, liver and kidney functions, lipid profile, CBC.
B. Imaging:
1. CT brain: to detect presence of infarction, haemorrhage , brain tumor.
2. MRI brain: to detect presence of infarction, haemorrhage, brain tumor, encephalitis, M.S. plaques.
Management of hemiplegia
I. General: in the acute (shock) stage of hemiplegia & in the comatosed patient:
II. Specific: It is the treatment of the cause.