Hemiplegia - أ.د.عمرو حسن الحسني أستاذ المخ والأعصاب
ฝัง
- เผยแพร่เมื่อ 5 พ.ค. 2023
- 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.
So grateful for your valuable lectures, dear professor ❤
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