Impairment of one or more vessels in the cerebral circulation, caused by thrombosis, embolus, stenosis, or haemorrhage, which interrupts the blood supply and results in ischemia of brain tissues.
Causes and Incidence
A cerebrovascular accident (CVA) is caused by occlusion of a cerebral vessel. Most cerebrovascular occlusions occur secondary to atherosclerosis or hypertension, or a combination of the two. Other risk factors are diabetes mellitus, myocardial infarction, bacterial endocarditis, rheumatic heart disease, aneurysms, head trauma, sick sinus syndrome, and a history of previous stroke or transient ischemic attacks (TIAs). CVA is the second most common cause of neurological disability and the third most common cause of death in the Western Hemisphere. More than 500,000 people are diagnosed with CVA each year in the United States, and of those 200,000 die. The incidence increases with age, with adults 65 years of age or older at greatest risk.
The general pathophysiology of a CVA involves occlusion of a cerebral vessel, which leads to ischemia of the brain tissue supplied by that vessel. If the obstruction is not removed, the affected tissue infarcts and dies, causing permanent neurologic deficit or death. The severity of the CVA depends on the location and extent of the obstruction, the degree of collateral circulation, and the promptness of diagnosis and treatment.
Thrombotic strokes account for approximately 40% of ischemic cerebrovascular disease. The occlusion develops slowly over time as the atherosclerotic plaque builds up in the large-vessel walls. A TIA is a common precursor. Symptoms often evolve over hours or even days and frequently are noticed when the person awakens in the morning. Damage from a CVA is generally extensive because of the large vessels involved and the likelihood that collateral circulation is diminished or absent.
Emboli, which cause 30% of strokes, arise when platelets, cholesterol, fibrin, or other miscellaneous hematogenous (originating in, or carried by, the blood) material breaks off from the arterial walls or the heart and travels to and blocks a cerebral vessel. The onset of symptoms generally is sudden and usually occurs in small distal cortical vessels, affecting cortical functions.
Lacunar strokes, which account for 20% of all CVAs, occur where small perforating arterioles branch off large cerebral vessels in the basal ganglia, internal capsule, and brainstem. The small subcortical arterioles are exposed to the constant high-pressure flow of the large branch arteries. Over the years the smaller vessels become thickened, thrombosed, and then obstructed. The resulting damage is distinctive, and these strokes are often labeled ipure motori or ipure sensoryi strokes.
Intracerebral hemorrhage accounts for 10% of all strokes and is the most catastrophic type. The onset is sudden, often occurs during exertion, and is triggered by bleeding that obstructs and ruptures the small subcortical arterioles in the deep brain. The pathology of the bleeding is not well understood, although some research indicates that it may be precipitated by microaneurysms that cause arteriolar necrosis.
The signs and symptoms of a stroke depend on the site and size of the obstruction. They typically include altered mental status, hemiparesis or hemiplegia, receptive or expressive aphasia, dysarthria, dysphagia, apraxia, hemianopsia, urinary incontinence, and emotional lability. Headache, seizures, stupor, and marked hypertension may also be present.
Coma and death are the most severe consequences of CVA. Permanent neurologic deficits (e.g., paralysis, impaired intellectual capability, speech defects, loss of short-term memory, impaired judgment and problem-solving abilities, reduced impulse control) are common residual complications.
To detect occlusion of large vessels.
Any of the above manifestations, particularly in individuals with identifiable risk factors.
Computed tomography/ magnetic resonance imaging
To identify area of infarct or bleeding.
To identify diminished blood flow in vessels.
Evacuation of hematoma or clot; placement of intracranial pressure monitor; endarterectomy to remove atherosclerotic plaques
Anticoagulants during stroke evolution; antihypertensives to control blood pressure; diuretics to reduce edema in the brain; anticonvulsants to control seizures; long-term aspirin therapy to prevent future stroke
Monitoring and support of vital functions; prevention of decubitus ulcers, thrombosis, and pneumonia; rehabilitation: occupational therapy for adapting activities of daily living, physical therapy to increase strength and endurance; gait training to improve ambulation; cognitive therapy to improve memory and problem solving; speech therapy to improve communication; counseling for poststroke depression and altered sexual functioning; vocational retraining.