Atlas of pathophysiology, 2 Edition
Part II - Disorders
A stroke, also known as a cerebrovascular accident, is a sudden impairment of cerebral circulation in one or more blood vessels. Stroke interrupts or diminishes oxygen supply and commonly causes serious damage or necrosis in the brain tissues.
· Thrombosis of the cerebral arteries supplying the brain or of the intracranial vessels, occluding blood flow
· Embolism from thrombus outside the brain, such as in the heart, aorta, or common carotid artery
· Hemorrhage from an intracranial artery or vein, such as from hypertension, ruptured aneurysm, arteriovenous malformation trauma, hemorrhagic disorder, or septic embolism
Regardless of the cause, the underlying event is deprivation of oxygen and nutrients. Normally, if the arteries become blocked, autoregulatory mechanisms help maintain cerebral circulation until collateral circulation develops to deliver blood to the affected area. If the compensatory mechanisms become overworked, or if cerebral blood flow remains impaired for more than a few minutes, oxygen deprivation leads to infarction of brain tissue.
A thrombotic or embolic stroke causes ischemia. Some of the neurons served by the occluded vessel die from lack of oxygen and nutrients, resulting in cerebral infarction. Injury to surrounding cells disrupts metabolism and leads to changes in ionic transport, localized acidosis, and free radical formation. Calcium, sodium, and water accumulate in injured cells, and excitatory neurotransmitters are released. Consequent continued cellular injury and swelling may cause further damage.
When hemorrhage is the cause of stroke, impaired cerebral perfusion causes infarction, and the blood itself acts as a space-occupying mass. The brain's regulatory mechanisms attempt to maintain equilibrium by increasing blood pressure to maintain cerebral perfusion pressure. The increased intracranial pressure (ICP) forces cerebrospinal fluid (CSF) out, thus restoring the balance. If the hemorrhage is small, this may be enough to keep the patient alive with only minimal neurologic deficits. However, if the bleeding is heavy, ICP increases rapidly and perfusion stops. Even if the pressure returns to normal, many brain cells die.
Signs and symptoms
The clinical features of stroke vary according to the affected artery and the region of the brain it supplies, the severity of damage, and the extent of collateral circulation developed. A stroke in one hemisphere causes signs and symptoms on the opposite side of the body. A stroke that damages cranial nerves affects structures on the same side. Symptoms include:
· hemisensory loss
· altered levels of consciousness
· headache, dizziness, and anxiety
· visual field defects
· ataxia, vertigo, and incoordination
· dysphasia (expressive and receptive)
Diagnostic test results
· Computed tomography (CT) scan identifies an ischemic stroke within the first 72 hours of symptom onset and evidence of a hemorrhagic stroke (lesions larger than 1 cm) immediately.
· Magnetic resonance imaging assists in identifying areas of ischemia or infarction and cerebral swelling.
· Cerebral angiography reveals disruption or displacement of the cerebral circulation by occlusion, such as stenosis or acute thrombus, or by hemorrhage.
· Digital subtraction angiography shows evidence of occlusion of cerebral vessels, lesions, or vascular abnormalities.
· Carotid duplex scan identifies the degree of stenosis.
· Brain scan shows ischemic areas but may not be conclusive for up to 2 weeks after a stroke.
· Single-photon emission CT and positron emission tomography scans identify areas of altered metabolism surrounding lesions not yet able to be detected by other diagnostic tests.
· Transesophageal echocardiogram reveals cardiac disorders—such as atrial thrombi, atrial septal defect, or patent foramen ovale—as causes of thrombotic stroke.
· Lumbar puncture (performed if there are no signs of increased ICP) reveals bloody CSF when stroke is hemorrhagic.
· Ophthalmoscopy identifies signs of hypertension and atherosclerotic changes in retinal arteries.
· EEG helps identify damaged areas of the brain.
· ICP management with monitoring, hyperventilation, osmotic diuretics, and corticosteroids
· Surgery for large cerebellar infarction
· Aneurysm repair
· Percutaneous transluminal angioplasty or stent insertion
· Stool softeners
· Thrombolytic therapy within 3 hours after onset of symptoms
· Anticoagulant therapy
Transient ischemic attacks
· Antiplatelet agents
· Carotid endarterectomy
· Analgesics such as acetaminophen