Cerebrovascular Diseases - Cerebral Thrombosis
Approximately 30% of all strokes is due to atherosclerotic thrombosis.
Usually, the major occlusion is preceded by one or more transient ischemic attacks.
Sometimes, there is only a single attack.
The stuttering intermittent progression of neurologic deficits over several hours or days (stroke-in-evolution) is often diagnostic of thrombosis.
Headache is an infrequent symptom.
It is located on one side of the head in carotid occlusion, in the occiput in basilar occlusions, and behind the ear in vertebral occlusions.
In the initial 48 hours, there is gradual deterioration of neurological status due to the development of cerebral edema.
The patient may become comatose during this period and the condition may end fatally.
The course of the stroke is often unpredictable.
Deterioration of the condition is usually due to extension of the thrombus along the vessel, increasing stenosis of the artery or acute brain edema.
Intercurrent infections of the respiratory or urinary tract are constant dangers, which lead to rapid deterioration if they set in.
On the other hand, hemiparesis start improving within hours and become completely alright in a week.
The term "lacunar infarcts" is applied to infarcts smaller than 2cm in diameter, placed subcortically in the distribution of the perforating arteries, commonly seen in the internal capsule, basal ganglia, and pons.
Delay in recovery suggests a poor prognosis.
The paralyzed limbs are flaccid in the acute stage and this flaccidity persists for the first few days or weeks.
Gradually spasticity develops and the tendon jerks become brisk.
The upper limb assumes a flexed adducted posture while the lower limb remains extended.
This is the classic picture of an internal capsular stroke.
Incomplete capsular strokes may be associated with involvement of the lenticular nucleus and thalamus.
This results in hemichoreo-athetosis or hemitremor of the paralyzed side.
This is called striatal hemiplegia.
Diagnosis: The CSF is normal, except in those areas of cerebral thrombosis secondary to infection.
The electroencephalogram (EEG) shows low voltage records of a lower frequency over the infracted area.
The CT scan usually shows the infracted area as a low dense lesion within a few days of the stroke.
Ultrasound investigations (Doppler echo flow studies) will detect the presence of narrowing of extracranial carotid system.
Radionuclide scans and positron emission techniques reveal the infarct before it is recognized by computerized tomography.
Arteriography is the definitive diagnostic procedure for identifying the abnormal vessel.
Since there is the risk of causing complete occlusion in a partially occluded artery, this procedure should be undertaken only if the diagnosis is uncertain or if surgical treatment is contemplated.
Usually, the major occlusion is preceded by one or more transient ischemic attacks.
Sometimes, there is only a single attack.
The stuttering intermittent progression of neurologic deficits over several hours or days (stroke-in-evolution) is often diagnostic of thrombosis.
Headache is an infrequent symptom.
It is located on one side of the head in carotid occlusion, in the occiput in basilar occlusions, and behind the ear in vertebral occlusions.
In the initial 48 hours, there is gradual deterioration of neurological status due to the development of cerebral edema.
The patient may become comatose during this period and the condition may end fatally.
The course of the stroke is often unpredictable.
Deterioration of the condition is usually due to extension of the thrombus along the vessel, increasing stenosis of the artery or acute brain edema.
Intercurrent infections of the respiratory or urinary tract are constant dangers, which lead to rapid deterioration if they set in.
On the other hand, hemiparesis start improving within hours and become completely alright in a week.
The term "lacunar infarcts" is applied to infarcts smaller than 2cm in diameter, placed subcortically in the distribution of the perforating arteries, commonly seen in the internal capsule, basal ganglia, and pons.
Delay in recovery suggests a poor prognosis.
The paralyzed limbs are flaccid in the acute stage and this flaccidity persists for the first few days or weeks.
Gradually spasticity develops and the tendon jerks become brisk.
The upper limb assumes a flexed adducted posture while the lower limb remains extended.
This is the classic picture of an internal capsular stroke.
Incomplete capsular strokes may be associated with involvement of the lenticular nucleus and thalamus.
This results in hemichoreo-athetosis or hemitremor of the paralyzed side.
This is called striatal hemiplegia.
Diagnosis: The CSF is normal, except in those areas of cerebral thrombosis secondary to infection.
The electroencephalogram (EEG) shows low voltage records of a lower frequency over the infracted area.
The CT scan usually shows the infracted area as a low dense lesion within a few days of the stroke.
Ultrasound investigations (Doppler echo flow studies) will detect the presence of narrowing of extracranial carotid system.
Radionuclide scans and positron emission techniques reveal the infarct before it is recognized by computerized tomography.
Arteriography is the definitive diagnostic procedure for identifying the abnormal vessel.
Since there is the risk of causing complete occlusion in a partially occluded artery, this procedure should be undertaken only if the diagnosis is uncertain or if surgical treatment is contemplated.
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