Cerebrovascular Accident
(Stroke)
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 ischaemic 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.
Disease
Process
The general
pathophysiology of a CVA involves occlusion of a cerebral vessel, which leads
to ischaemia 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
Thrombotic
strokes account for approximately 40% of ischaemic 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
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
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
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.
Symptoms
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.
Potential
Complications
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.
Diagnostic Tests
Angiography
To detect
occlusion of large vessels.
Clinical
evaluation
Any of the above
manifestations, particularly in individuals with identifiable risk factors.
Computed
tomography/ magnetic resonance imaging
To identify area
of infarct or bleeding.
Ultrasonography
To identify
diminished blood flow in vessels.
Treatments
Surgery
Evacuation of
hematoma or clot; placement of intracranial pressure monitor; endarterectomy to
remove atherosclerotic plaques
Drugs
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
General
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.