Aneurysm - Cerebral
Alternate Names : Cerebral Aneurysm, Aneurysm in the Brain
In cerebral aneurysm, localized dilation of a cerebral artery results from a weakness in the arterial wall. Its most common form is the berry aneurysm, a saclike out pouching in a cerebral artery. Cerebral aneurysms usually arise at an arterial junction in the circle of Willis, the circular anastomosis forming the major cerebral arteries at the base of the brain. Cerebral aneurysms often rupture and cause subarachnoid hemorrhage.
The prognosis is guarded. About half of all patients who suffer a subarachnoid hemorrhage die immediately; of those who survive untreated, 40% die from the effects of hemorrhage and another 20% die later from recurring hemorrhage. With new and better treatment, the prognosis is improving.
Cerebral aneurysms may result from a congenital defect, a degenerative process, or a combination of both. For example, hypertension and atherosclerosis may disrupt blood flow and exert pressure against a congenitally weak arterial wall, stretching it like an overblown balloon and making it likely to rupture.Such a rupture is followed by subarachnoid hemorrhage, in which blood spills into the space norm by cerebrospinal fluid (CSF). Sometimes, blood also spills into brain tissue and subsequently forms a clot. This may result in potentially fatal increased intracranial pressure (ICP) and brain tissue damage. Incidence is slightly higher in women than in men, especially those in their late 40s or early to middle 50s, but a cerebral aneurysm may occur at any age, in both women and men.
Signs and symptoms
Occasionally, rupture of a cerebral aneurysm causes premonitory symptoms that last several days, such as headache, nuchal rigidity, stiffback and legs, and intermittent nausea. Usually, however, the rupture occurs abruptly and without warning, causing a sudden severe headache, nausea, vomiting and, depending on the severity and location of bleeding, altered level of consciousness (LOC), including a deep coma.Bleeding causes meningeal irritation, resulting in nuchal rigidity, back and leg pain, fever, restlessness, irritability, occasional seizures, and blurred vision. Bleeding into the brain tissues causes hemiparesis, hemisensory defects, dysphagia, and visual defects. If the aneurysm is near the internal carotid artery, it compresses the oculomotor nerve and causes diplopia, ptosis, dilated pupil, and inability to rotate the eye.
In cerebral aneurysm, diagnosis is based on the patient history; a neurologic examination; a computed tomography (CT) scan, which reveals subarachnoid or ventricular blood; and magnetic resonance imaging or magnetic resonant angiography, which can identify a cerebral aneurysm as a "flow void" or by computer reconstruction of cerebral vessels.
Cerebral angiography remains the procedure of choice for diagnosing a cerebral aneurysm. Lumbar puncture may be used to identify blood in CSF when CT is negative. However, its use is contraindicated in patients with signs of increased ICP.
Other baseline laboratory studies include a complete blood count, urinalysis, arterial blood gas (ABG) analysis, coagulation studies, serum osmolality, and electrolyte and glucose levels.
The risk of vasospasm and cerebral infarction is reduced by repairing the aneurysm. Usually, surgical repair (by clipping, ligation, or wrapping the aneurysm neck with muscle) takes place 7 to 10 days after the initial hemorrhage; however, surgery performed within 1 to 2 days after the hemorrhage has also shown promise in grade I and II aneurysms.
When surgical correction is risky, when the aneurysm is in a dangerous location, or when surgery is delayed because of vasospasm, treatment includes:
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