Onset is usually abrupt, and there may then be very little progression except that due to brain swelling. Clinical evaluation always includes examination of the heart and auscultation over the subclavian and carotid vessels to determine whether there are any bruits.
Cerebral Infarction an ischemic condition of the brain, producing local tissue death and usually a persistent focal neurological deficit in the area of distribution of one of the cerebral arteries. Called also cerebral ischemia. A stroke caused by interruption or blockage of blood flow to the brain; also called ischemic stroke. Brain-tissue damage caused by interrupted flow of oxygen to the brain. A stroke is an interruption of the blood supply to any part of the brain. A stroke is sometimes called a "brain attack."
Cause of Cerebral Infarction
Some common are causes of Cerebral Infarction follows:
Symptoms of Cerebral Infarction
There are some symptoms of Cerebral Infarction follows:
Treatment of Cerebral Infarction
If the neurologic deficit progresses over the following minutes or hours, heparinization may be of value in limiting or arresting further deterioration. Since the signs of progressing stroke may be simulated by an intracerebral hematoma, the latter must be excluded by immediate CT scanning or angiography before the patient is heparinized.
Intravenous thrombolytic therapy with recombinant tissue plasminogen activator (0.9 mg/kg to a maximum of 90 mg, with 10% given as a bolus over 1 minute and the remainder over 1 hour) is effective in reducing the neurologic deficit in selected patients without CT evidence of intracranial hemorrhage when administered within 3 hours after onset of ischemic stroke, but later administration has not been proved effective or safe. Recent hemorrhage, increased risk of hemorrhage (eg, treatment with anticoagulants), arterial puncture at a noncompressible site, and systolic pressure above 185 mm Hg or diastolic pressure above 110 mm Hg are among the contraindications to this treatment.
Early management of a completed stroke otherwise consists of attention to general supportive measures. During the acute stage, there may be marked brain swelling and edema, with symptoms and signs of increasing intracranial pressure, an increasing neurologic deficit, or herniation syndrome. Corticosteroids have been prescribed in an attempt to reduce vasogenic cerebral edema. Prednisone (up to 100 mg/d) or dexamethasone (16 mg/d) has been used, but the evidence that corticosteroids are of any benefit is conflicting. Dehydrating hyperosmolar agents have also been prescribed in efforts to reduce brain swelling, but there is little evidence of any lasting benefit.
Likewise, clinical benefit from treatment with vasodilators such as papaverine is minimal. Neither hypercapnia nor hypocapnia has been shown to have any benefit. Barbiturates are known to decrease neuronal metabolism and energy requirements and have been reported to improve functional recovery in experimental stroke models; their use in humans, however, is experimental.
Attempts to lower the blood pressure of hypertensive patients during the acute phase (ie, within 2 weeks) of a stroke should generally be avoided, as there is loss of cerebral autoregulation and lowering the blood pressure may further compromise ischemic areas. However, if the systolic pressure exceeds 200 mm Hg, it can be lowered with continuous monitoring to 170–200 mm Hg and then, after 2 weeks, the blood pressure reduced further to less than 140/90 mm Hg.
Some treatment of Cerebral Infarction :
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