IPHREHAB : Embolic infarction

IPHREHAB


Embolic infarction
This is one of the most common cause of stroke. In most cases of cerebral embolism, the embolic material consists of a fragment that has broken away from a thrombus within the heart. Embolism due to fat, tumor cells, fibrocartilage, amniotic fluid, or air is a rare occurrence and seldom enters into the differential diagnosis of stroke.

Clinical Picture

Of all strokes, those due to cerebral embolism develop most rapidly. The embolus strikes at any time of the day or night. Getting up to go to the bathroom is a time of danger. The neurologic picture will depend on the artery involved and the site of obstruction.

It  is important to repeat that an embolus may produce a severe neurologic deficit that is only temporary; symptoms disappear as the embolus fragments. In other words , embolism is a common cause of a single evanescent stroke that may reasonably be called a prolonged TIA. Also as already pointed out, several emboli can give rise to two or three transient  attacks of differing pattern or , rarely , of almost identical pattern.

Causes of cerebral embolism:

Cardiac origin

Noncardiac origin

Undetermined origin

Laboratory Findings

Not infrequently the first sign of myocardial infarction is the occurrence of embolism; therefore it is advisable that an ECG and echocardiogram be obtained in all patients with stroke of uncertain origin. Prolonged study of heart rhythm with Holter monitoring should be undertaken.

In some 30 percent of cases, cerebral embolism produces a hemorrhagic infarction. CT scanning or MRI may be helpful in showing the more intense hemorrhagic infarcts, particularly if the scan is repeated on the second or third day.

Course and prognosis

Most patients survive the initial insult, and in many the neurologic deficit may recede relatively rapidly, as  indicated above. The eventual prognosis is determined by the occurrence of further emboli and the gravity of the underlying illness- cardiac failure myocardial infarction, bacterial endocarditis  and so on.

Treatment and prevention

Three phases of therapy : General medical management in the acute phase, Measures directed to restoring the circulation Physical therapy and rehabilitation These are much the same as described above the prevention of atherothrombotic infarction.

IPHREHAB : CEREBRAL ISCHEMIA AND INFARCTION

IPHREHAB :

 CEREBRAL ISCHEMIA AND INFARCTION


Cerebral ischaemia and infarction
Anatomy and pathology
The principal pathological process under consideration here is the occlusion of arteries supplying the brain. The two internal carotid arteries and the basilar artery form the Circle of Willis at the base of the brain, which acts as an efficient anatomotic device in the event of occlusion of arteries proximal to it.

CIRCLE OF WILLIS

Anatomy and pathology

VERTEBRAL ARTERY

Occlusion leads to sudden severe ischaemia in the area of brain tissue supplied by the occluded artery, and recovery depends upon rapid lysis or fragmentation of the occluding material: Reversal of neurological function within minutes or hours gives rise  to the clinical picture of a transient ischaemic attack.

When the neurological deficit lasts longer than 24 hours, it may be called a reversible ischaemic neurological deficit ( RIND ) if it recovers completely in a few days, or a completed stroke if there is a persistent deficit. Sometimes recovery is very slow and incomplete.

Neurological symptoms and signs  

The loss of function that the patient notices, and which may be apparent on examination, entirely depends on the area of brain tissue involved in the ischaemic process.      

 Neurological symptoms and signs

BASIC

The following suggest middle cerebral territory:

Dysphasia; Dyslexia, dysgraphia, dyscalculia; Loss of use of contralateral face and arm; Loss of feeling in contralateral face and arm.

• The following suggests anterior cerebral territory:

Loss of use and/ or feeling in the contralateral leg.

• The following suggests posterior cerebral territory:

Development of a contralateral homonymous hemianopia.

Neurological symptoms and signs

The following suggests a deep-seated lesion affecting the internal capsule which is supplied by small perforating branches of the middle and posterior cerebral arteries close to their origins: Complete loss of motor and sensory function throughout the whole of the contralateral side of the body with a homonymous hemianopia.

Neurological symptoms and signs

The following suggests ophthalmic artery territory (the ophthalmic artery arises from the internal carotid artery just below the Circle of Willis): Monocular loss of vision.

Neurological symptoms and signs

The following suggest vertebro-basilar territory: double vision( 3,4,6);

facial numbness(5);

facial weakness(7);

vertigo (8);

dysphagia (9, 10);

dysarthria ( 9, 10, 12);

ataxia; drop attacks;

motor or sensory loss in both arms or legs.