1.Cerebral atherosclerosis is the most important cause. This may or may not be associated with hypertension.
2. Syphilitic endartertis obliterans.
3.Pressure effect of a tumour.
5.Acute febrile illness in children.
6.Carotid artery occlusion (Carotid hemiplegia).
10. Use of oral contraceptives.
12. Idiopathic thrombocytosis.
13. Sickle cell disease.
14. Takayasu’s syndrome.
15. Giant cell arteritis.
Cerebral thrombosis is the commonest form (85%) of CVA and the commonest cause of hemiplegia. The site of lesion in pyramidal tract may be at various sites which can be seen in adjoining diagram but all these sites will not produce hemiplegia. From corona radiata to upper part of spinal cord lesion can produce hemiplegia. However, the common site is the internal capsule and commonest vessel involved is the middle cerebral artery. The resultant cerebral infarction depends on the size of the vessel obstructed and the development of collateral circulation. Due to ischaemia some excitatory and other neuropeptides are released which in turn augment calcium influx into the neurons which is responsible for cell death and augmentation of neurologic deficit.
Onset is insidious.
Usually the attack occurs at rest particularly during sleep due to sluggish circulation. Premonitory symptoms such as transient aphasia, amblyopia, etc. may develop, which are usually absent in cerebral haemorrhage. There may be convulsive seizure at the onset. Patient is often dazed for several hours after which usually he becomes conscious. Complete unconsciousness is rare. Hemiplegia occurs due to infarction of the territory of the middle cerebral artery. There Left-sided lesion will result in right-sided upper motor neurone paralysis. In cortical lesion monoplegia, corona radiata, internal capsule, mid-brain and pontine lesion will have variable effect. When the lesion is bilateral and upto Cs anywhere there will be quardriplegia but below Cs bilateral lesion will produce paraplegia. Lower motor neurone lesion will produce same-sided lower motor пеurone paralysis.
may be hemianopia and hemianaesthesia opposite to the side of lesion. Some improvement in hemiplegia occurs for about first 1-2 months after which little weakness of the paralysed side persists. This is called residual hemiplegia. In some cases no residual paralysis persists.
Features of Classical hemiplegia after the shock stage is over
Usually normal except right-handed persons where left- sided lesion may produce aphasia due to involvement of the Broca’s area. Speech may show slurring dysarthria.
Supranuclear type 7th nerve paralysis is seen Upper half of the face escapes because that part is controlled by pyramidal tracts of both sides. Sometimes supranuclear type of 12th nerve palsy is also seen, characterised by deviation of the tongue to the side of hemiplegia.
(i) Nutrition of muscles is usually normal but in long- standing cases there may be disuse atrophy
(ii) Power is lost on the paralysed side or it may be weak which is called paresis.
(iii) Tone is increased, called clasp knife or jack knife type of rigidity.
(iv) Co-ordination is normal on the non-paralysed side. On the paralysed side this test cannot be done.
(v) Involuntary muscular movement are usually absent but rarely post-hemiplegic fine tremor may develop.
No change is usually seen
(i) Superficial: Abdominal reflexes are lost on the side of paralysis. The lower one is lost earlier than the upper ones. Afterwards they reappear in a reversed manner. Planter reflex on the paralysed side is extensor (Babinski’s sign). Cremasteric reflex may be diminished or absent.
(ii) Deep reflexes: On the paralysed side, ankle-jerk, knee- jerk, biceps-jerk, triceps-jerk and supinator-jerks are all exaggerated. Ankle and patellar clonus may also be present. Rarely finger clonus may be seen. Hoffmann’s reflex may be present. On the non-paralysed side jerks are normal.
(iii) Sphincteric reflexes are normal.
Hemiplegic or circumduction gait is seen in a classical case. Patient stands with adducted arm, flexed elbow, wrist and small joints. During walk the pelvis is tilted on the healthy side and the foot is dragged along the ground forming a semicircle.
Cerebral infarction may develop due to obstruction of:
(i) Carotid circulation,
(ii) Vertebrobasilar circulation.
Obstruction of Carotid circulation
Anterior cerebral artery: Obstruction distal to anterior communicating artery causes motor weakness of contralateral leg and slight weakness of proximal arm and cortical sensory loss in the lower limb. Grasp reflex, paratonic rigidity, frank confusion and abulia or lack of initiative are also present. Expressive aphasia and apraxia on the non-paralysed side are also seen. When behaviour disturbances are present urinary incontinence may be present. When the obstruction is bilateral marked behavioural changes and memory loss will be present. When the obstruction is proximal the anterior communicating artery no deficit develops as there is collateral supply from the opposite side. Occlusion of the ophthalmic artery is usually symptomless because of the rich orbital collaterals. Of course in embolic obstruction Amaurosis fugax may develop.
Middle cerebral artery occlusion may give rise to contralateral hemiplegia, hemisensory loss and homonymous hemianopia with conjugate deviation of eyes to the side of lesion. Scintillating scotoma is also present. Involvement of dominant hemisphere gives rise to global aphasia also. It is difficult to distinguish this from occlusion of internal carotid artery. In extreme cases, there is severe post-infarctive oedema leading to drowsiness, stupor and coma. Involvement of the anterior main devision gives rise to contralateral paralysis with loss of sensation on the face and arm and to a lesser extent in the leg. On the other hand posterior branch obstruction gives Rise to receptive aphasia (Wernicke’s aphasia) and homonymous field defect; but involvement of non-dominant hemisphere may be associated with confusional state, dress and constructional apraxia with special deficits.
Obstruction of Vertebrobasilar circulation
Obstruction of posterior cerebral artery gives rise to thalamic syndrome associated with contralateral hemisensory disturbance followed by spontaneous pain (Thalamic pain) and hyperpathia. There may also be homonymous hemianopia with Macular sparing and very mild transient hemiparesis. Involuntary movements and alexia may also be seen. When the main artery beyond the penetrating branches is occluded macular sparing with hemianopia may result.
Vertebral artery occlusion below the origin of anterior spinal and posterior inferior cerebellar artery may remain without any signs as the circulation is maintained by the opposite vertebral artery. Of course clinical signs similar to vertebral artery insufficiency may develop if the opposite vertebral artery is congenitally small or markedly obstructed previously by severe atheroma. Occlusion of small paramedian arteries arising from vertebral artery gives rise to contralateral hemiplegia, sensory loss with cranial nerve palsy. Obstruction of posterior inferior cerebellar artery gives rise to sensory loss with cranial nerve palsy. Obstruction of posterior inferior cerebellar artery or vertebral artery before it branches to this artery gives rise to sensory loss (spinothalamic type) on the face, ataxia of limbs with numbness, Horner’s Syndrome with 9th and 10th nerve palsy but contralateral sensory loss of limbs (spinothalamic type). Obstruction of both vertebral or basilar artery gives rise to deep coma, pin-point pupil, flaccid quadriplegia, sensory loss, cranial nerve palsy and syncopal attacks. But if the basilar artery is partially occluded, diplopia, visual loss, vertigo, ataxia, nystagmus, dysarthria, weakness of all four limbs, staggering gait, sensory loss of all or some of the limbs and cranial nerve palsy may develop.
In pontine lesion hemiplegia is crossed (facial palsy on the ipsilateral side with contralateral hemiplegia called Millard Gubler’s syndrome), pin-point pupil, reversed conjugate deviation of eyes are seen
Subclavian and innominate artery obstruction will cause features of vertebral artery insufficiency due to subclavian steal syndrome.
When there is occlusion of major cerebellar artery there may be nausea, vomiting, vertigo, ipsilateral ataxia of limbs, nystagmus and spinothalamic type of sensory loss on the opposite limbs. With the involvement of superior cerebellar artery ipsilateral facial sensory loss (spinothalamic type) is also present. If anterior inferior cerebellar artery is occluded ipsilateral facial sensory loss (spinothalamic type) along with facial weakness and deafness are present.
When there is obstruction of posterior inferior cerebellar artery (Wallenberg’s or Lateral medullary syndrome) there will be vertigo, vomiting, hiccough, paresthesia or pain over the trigeminal area, muscular hypotonia, incordination, nystagmus, paralysis of soft palate, pharynx, vocal cord (9th and 10th nerve), Horner’s syndrome, loss of pain and thermal sensation over face on the ipsilateral side and in trunks and limbs on the contralateral side. Hemiparesis on the contralateral side may also develop.
If cerebellar infarction is massive, coma, tonsillar herniation and death may rapidly ensue.
INFARCTION AT SPECIAL SITES
Brain stem Infarction
This produces bizarre manifestations depending on the site of lesion. Bilateral involvement may cause coma due to involvement of reticular formation; there may be Pseudobulbar palsy, Weber’s Syndrome, Millard Gubler’s Syndrome, Lateral medullary or Wallenberg’s Syndrome (see later). Sometimes there may be “Locked in syndrome” when the lesion is in the upper brain stem characterised by inability to speak, swallow or move the limbs though consciousness is well-preserved.
These are very small infarctions (< 5 mm) usually encountered in post-mortem. Though they are symptomless there may be pure motor or sensory loss, sudden ataxia, dysarthria or even clumsiness of hand. These are seen in the distribution of short penetrating arterioles in the basal ganglia, pons cerebellum, anterior limb of the internal capsule and rarely deep cerebral white mater. These are seen to be associated with poorly controlled diabetes or hypertension. The neural deficit may be stabilised after 24-36 hours. Infarction may or may not be
visible in CT scan. Usually there is partial or complete resolution after 4-6 weeks.
During prolonged hypotension cerebral perfusion is much impaired. This causes damage of the border zones in the supplying territory of the anterior, middle and posterior cerebral artery. There may be cortical visual loss and impairment of memory and intelligence.
Multiinforct dementia (MID)
Multiple small infarcts or larger infarcts may produce generalised loss of intelligence. This may also give rise to dementia, pseudobulbar palsy and Parkinsonian gait.
Cortical blindness or Anton’s syndrome
Hemianopia or cortical type of visual loss may be seen in thrombosis of posterior cerebral arteries (see later).
1. Serum cholesterol, LDL cholesterol and triglyceride may be high in some cases indicating hyperlipidaemia.
2. Cerebral angiography may show the site of obstruction. In normotensive young stroke cases angiography should always be considered. Carotid angiography may show stenosis. Vertebral and arch angiography are rarely done now-a-days.
3. CSF is usually normal but there may be increased pressure if there is post-infarctive cerebral oedema; increased cell count and xanthochromia may be seen if the infarct is superficial and haemorrhagic. Protein level rarely inceased.
4. EEG may sometimes show slow frequency and low voltage of the electrical activity.
5. CT scan may demonstrate the infarction. This can differentiate haemorrhage from infarction. Moreover mass lesion, e.g., haematoma, abscess or neoplasm may also be distinguished. CT scan is superior to MRI in the acute stage because haemorrhage cannot easily be detected within 48 hours after onset.
6. VDRL test may be positive in syphilitic cases.
7. ESR, PPBS, Antiphospholipid antibodies may show some changes in appropriate cases.
8. ECG for evidences of arrhythmia or infarction may be seen.
9. Echocardiogram for heart disease, Holter’s monitoring for arrhythmia are also useful.
Main causes are Thrombosis, haemorrhage and embolism. The differentiating points are given in the table.
To prevent post-infarctive cerebral oedema Mannitol infusion or oral Glycerine may be used. 20% mannitol IV over 20-30 mins. 3-4 times a day and glycerine 30cc orally mixed with fruit juice 3-4 times a day may be given. Steroids and Diuretics (Frusimide 20 mgm IV 2-3 times a day) may also be of value to reduce cerebral oedema. Neurotropic vitamins may also be given. For secondary infection antibiotics may be required. If the patient becomes comatose all management for coma should be done. When the neural shock stage is over and residual hemiplegia persists physiotherapy can be done. For aphasic individual, gradual physiotherapy and speech therapy useful. Low molecular weight Dextran, platelet inhibitors and thrombolytic agents are sometimes helpful. Anticoagulants are of value in cases of stroke in evolution. Reconstructive surgery may be done in selected cases. Internal carotid endarterectomy or extra cranial bypass surgery may be done in selected cases. Associated underlying causes and risk factors should also be treated. Aspirin in small doses and Dipyridamole 100 mg thrice daily may prevent further episodes of stroke. Baclofen (GABA antagonist) may be used for spasticity. If BP is high that should be gradually brought down. Acute hypotension is harmful. High sugar and lipid should be controlled. Aspirin 300 mg daily may be beneficial.