Cerebral thrombosis

Cerebral thrombosis means occlusion of one of the branches of the carotid artery and is often preceded by one or two transient, ischemic attacks. Common sites may be carotid artery in the head, basilar or vertebral artery in the neck. Cerebral thrombosis commonly results due to atherosclerosis when there is narrowing of the lumen of the vessel, thickening of the intima of the vessel wall and a thrombus results because of increased coagulability of blood and slowness of circulation.

Though cerebral atherosclerosis remains the commonest cause yet other diseases like syphilitic, thromboangitis obliterans and acute infections also are causative factors in some cases. Obstruction of the artery leads to an area of infarction in the brain and softening may take place at the site.

Symptoms of Cerebral thrombosis

Onset is often preceded by prodromal symptoms in the form of transient attacks of paresis, and confusion. Sometimes this may take few days to evolve. Headache and giddiness are usually present. Deterioration in neurological symptoms starts within 48 hours when the thrombus extends and cerebral oedema develops. Commonly lesion is in internal capsule and patient has got an acute upper motor neuron lesion of body of one side. Face is also involved. At first the limbs are flaccid because of a state of shock. Aphasia is present if lesion is on the dominant side. Gradually there is recovery, tone in the limbs is increased, deep reflexes become exaggerated and plantar reflex is extensor (Babinski reflex).

Cerebral thrombosis

In addition to a full fledged picture of hemiplegia, some patients have lacunar infarcts which are smaller in size (less than 2 cm) and occur in the sub cortical area in the distribution of perforating arteries. Common sites are internal capsule, basal ganglia and pons. Generally the patient is dazed and unconsciousness does not occur. Multiple lacunar or large infarcts may produce a picture of generalized intellectual impairment. Depending on various localizing signs, site of lesion can be clinically judged.

In lesion at the cortex, there is generally monoplegia. There is aphasia and sensory loss of cortical type. Convulsions may occur.

Sub Cortical – No convulsions, Weakness as well as sensory loss in contra lateral limb may develop. Homonymous hemianopia if optic radiations involved.

Internal capsule. Complete hemiplegia, face may be involved.

Mid brain. Ipsilateral 3rd nerve palsy with crossed hemiplegia.

Brain stem lesion. Diplopia, nystagmus, vertigo, ipsilateral ataxia with contra lateral sensory loss and hemiparesis.

Pons. Nuclear type of facial paralysis with crossed hemiplegia.

Progress of the case

It shall depend on the size and site of vessel involved. Cerebral thrombosis of the basilar artery carries poor prognosis. Depending on underlying conditions like hypertension, diabetes and atherosclerosis the progress of further attacks shall be assessed. Many patients fall prey to inter current infections. But once recovery starts taking place the limbs tend to regain their power though it may take months to recover.

Investigations:

1. CSF is generally normal.

2. CT scan skull is essential to make a diagnosis. It will show low frequency infarct areas or a low dense lesion.

3. Doppler echo flow studies will demonstrate narrowing of carotid vessels in its extra cranial course.

Management

It consists of supportive and specific measures.

In general measure care of the patients nutrition, and feeding. Hydration and electrolyte balance be maintained. Prevention of bed sores passive movements of hemiplegic side daily and active exercises as power returns, Massage of the limb is equally beneficial.

Specific treatment consists of decongestant therapy

Injection Mannitol 1 vial IN twice a day. Injection dexamethasone 4 mg I/V 6 hourly along with prophylactic cover of antibiotics (Injection Ampicillin 500 mg IN 6 hourly) and anti platelet drug dispirin 75 mg daily orally. If a patient comes within three hours after formation of clot. Tissue type plasminogen. Activator is administered 100 mg IN slowly. This is called clot buster regimen and helps in supply of blood to dead part of brain. Attempt should be made from the very beginning to do physiotherapy and massage of the paralyzed limb.

Role of anticoagulants in cerebral thrombosis is controversial and should not be employed because of the danger of start of hemorrhage in the brain. As the patient improves, mannitol is replaced by glycerol 15 ml twice a day along with dispirin (75 mg) orally once a day. Other anti platelet drug Dipyradimole 75 rug once a day has also been employed. While giving anti platelet drugs look for any bleeding tendencies.

In patients with aphasia language training must be started at the earliest. Recovery in a case of thrombosis depends on the extent of lesion, presence of accompanying diseases like diabetes, hypertension, age of the patient (very old and debilitated patients have poor prognosis) and response of the patient to drug therapy as well as physiotherapy. Patients who become ambulatory early their prognosis is definitely better since they are saved from development of bed sores, contractures and inter current infections.