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Intracerebral hemorrhage Intracerebral hemorrhages account for 10-15% of all strokes and have a poorer prognosis and a higher mortality rate when compared to cerebral infarctions. Intracerebral hemorrhage may be clinically indistinguishable from cerebral infarction, hence the importance of CT scan evaluation. Patients with intracerebral hemorrhages are more likely to have headache, lethargy, nausea and vomiting. They tend to occur in a younger population of patients, and they more commonly present with marked hypertension. Patients with intracerebral hemorrhage are more likely to rapidly deteriorate with an increased need for intubation. The majority of intracerebral hemorrhages are associated with chronic hypertension. Bleeding occurs directly into the brain parenchyma; this is thought to be due to blood leakage from small intracerebral arteries damaged by chronic hypertension. Other causes include bleeding diathesis from iatrogenic anticoagulation, amyloidosis and cocaine abuse. A small area of brain is probably irreversibly damaged by the hemorrhage. However, surrounding the hemorrhage there is likely to be an area of reversible damage. The surrounding tissue is damaged by increased pressure and local vasospasm due to the release of vasoactive substances. It is believed that damage can be reduced by clot removal to reduce pressure and pharmacologic measures to counteract the vasoactive toxic substances released. At present, surgical evacuation of the hematoma remains controversial. Early neurosurgical consultation is mandatory for all patients with intracerebral hemorrhage. Subarachnoid hemorrhage: Subarachnoid hemorrhage classically presents as the sudden onset of a severe headache (the worst headache of one*s life). The headache is often occipital or nuchal. It is often associated with vomiting and a decreased level of consciousness or may present with syncope or seizures. It may present with focal neurologic deficits secondary to the aneurysm or blood compressing adjacent brain or cranial nerves. Subarachnoid hemorrhages occur in a younger patient population accounting for half of all strokes in patients under age 45. They are associated with a very high mortality accounting for 10% of all deaths from stroke. The diagnosis of subarachnoid hemorrhage can be made on CT scan in up to 95% of cases.. However, in cases of suspected subarachnoid bleed, a "normal" CT is not definitive, and a lumbar puncture is required. Subarachnoid hemorrhage results when a blood vessel ruptures directly into the subarachnoid space. The majority are due to berry (saccular) aneurysms most often located in the anterior portion of the Circle of Willis. A smaller number are due to arteriovenous malformations. There is an immediate increase in intracranial pressure which can result in irreversible brain damage. In those who survive the initial hemorrhage, management focuses on the prevention of rebleeding, and treatment or prevention of vasospasm and hydrocephalus which may cause further morbidity and mortality. The risk of rebleeding is greatest in the first 48 hours and is associated with a high mortality rate. Surgical clipping of the involved aneurysm is of proven benefit, though the timing of surgery remains under debate. Deterioration due to delayed ischemia is a result of cerebral vasospasm. Vasospasm is caused by the irritant effect of blood surrounding the blood vessels in the basal cistern. The vasospasm is probably in part induced by breakdown products of hemoglobin. Vasospasm is prophylactically treated with the calcium channel blocker nimodipine which has been shown to improve outcome. It is recommended that therapy with nimodipine 60 mg be started in the emergency department and continued for 21 days. Hydrocephalus is a serious complication of subarachnoid hemorrhage. Acute obstructive hydrocephalus is associated with stupor or coma. Early consultation with neurosurgery is imperative in all cases of subarachnoid hemorrhage. Special Situations Cerebellar stroke: Cerebellar infarction and hemorrhage warrant separate consideration because of the rapid and life-threatening brainstem compression they may produce. Patients with cerebellar strokes may present with sudden onset of dizziness, nystagmus, vomiting, truncal ataxia, gait disturbance, gaze palsy, or stupor. The hematoma from a cerebellar hemorrhage or the swollen cerebellar hemisphere in an infarction can cause brainstem compression. Symptoms of brainstem compression include decreasing level of consciousness, facial weakness, and gaze palsy. Patients may rapidly progress to coma and herniation therefore prompt surgical decompression is indicated. All cerebellar strokes are neurosurgical emergencies requiring early neurosurgical consultation. Transient Ischemic Attacks: Transient ischemic attacks (TIAs) are neurologic deficits that resolve within twenty-four hours with most resolving within thirty minutes. Patients usually present for evaluation after the neurologic signs have ceased and therefore the diagnosis is often based on history. A TIA is a warning of an impending stroke. Approximately 10% of patients with TIA will have a subsequent stroke within 3 months of the TIA, 50% of whom will have the event within 48 hours. |
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Antiplatelet therapy with aspirin is of proven benefit in the prevention of stroke following TIA. Ticlopidine is another antiplatelet agent of proven benefit but is more expensive, takes several days for maximum effect and requires careful hematologic monitoring because it can cause pancytopenia. However, ticlopidine is useful for aspirin allergic patients. Anticoagulant therapy is not routinely recommended for patients following a TIA as there is no evidence to support its efficacy unless there is a cardiac source of embolism. Despite the lack of available data some recommend consideration of anticoagulation for patients with: a pattern of crescendo TIAs, development of a TIA while on aspirin, known high grade carotid stenosis and posterior circulation TIA. All patients presenting with a possible TIA require a CT scan to exclude other etiologies of their neurologic symptoms. The remainder of the work-up is individualized based upon the patient*s characteristics and the type of TIA. The evaluation of carotid arterial blood flow by doppler technology is often performed for screening but results do not always correlate with angiography. Carotid endarterectomy is of proven benefit in patients with TIA who have angiographically demonstrated carotid stenosis of 70% or greater, are at low risk for surgical complications, and for whom a skilled surgeon is available. Patients with TIAs are at high risk for stroke and management should be expedient. The need for close observation, rapid determination of etiology and institution of appropriate therapy justify admission for patients with a recent TIA (less than 72 hours) or crescendo TIAs. Neuroprotective therapy: There are several different classes of agents under active investigation which are thought to provide neuronal protection. In stroke, the disruption of blood flow results in numerous cellular and biochemical events. The ischemia causes energy failure and depolarization with release of neurotransmitters, influx of intracellular calcium, and release of free radicals. With better understanding of the mechanisms of neuronal damage and death new cytoprotective therapies are being studied. Many of these agents have demonstrated reduction of stroke volume in animal models of stroke and are undergoing clinical trials. Several of these agents have shown promise for the treatment of traumatic brain injury and neurodegenerative diseases such as amyotrophic lateral sclerosis and Huntington*s disease. Agents currently under study include excitatory antagonists, free radical scavengers, gangliosides, and leukocyte inhibitiors; unfortunately all of these agents remain experimental with no defined role in acute stroke management. |
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