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INTRODUCTION

  • Stroke involves the abrupt onset of focal neurologic dysfunction that lasts at least 24 hours and is caused by cerebral, spinal, or retinal infarction. Stroke can be either ischemic or hemorrhagic. Transient ischemic attacks (TIAs) are focal ischemic neurologic deficits lasting <24 hours and usually <30 minutes.

PATHOPHYSIOLOGY

Ischemic Stroke

  • Ischemic stroke (87% of all strokes) results from occlusion of a cerebral artery that reduces cerebral blood flow. Ischemic strokes are due either to local thrombus formation or emboli from a distant site. Atherosclerosis of large intracranial or extracranial arteries or small artery disease can result in ischemic stroke. Emboli can arise from the heart in patients with atrial fibrillation, valvular heart disease, or other prothrombotic heart problems and cause about 25% of ischemic strokes. The stroke cause is undetermined in some cases.

  • Decreased cerebral blood flow can lead to infarction of cerebral tissue with a surrounding area that is ischemic but may maintain membrane integrity (the ischemic penumbra). This penumbra is an area of brain tissue that is potentially salvageable with urgent pharmacologic and endovascular treatment interventions.

  • Insufficient oxygen supply in ischemic tissue leads to adenosine triphosphate (ATP) depletion with lactate buildup due to anaerobic metabolism and accumulation of intracellular sodium and water, leading to cytotoxic edema and eventual cell lysis. An influx of calcium intracellularly activates lipases and proteases, resulting in protein degradation and free fatty acid release from cellular membranes. Release of excitatory amino acids (eg, glutamate, aspartate) in ischemic tissue perpetuates neuronal damage and produces damaging prostaglandins, leukotrienes, and reactive oxygen species. These processes occur within 2–3 hours of the onset of ischemia and ultimately lead to cellular apoptosis and necrosis.

  • The most common modifiable risk factors for ischemic stroke include hypertension, cigarette smoking, diabetes, atrial fibrillation, and dyslipidemia.

Hemorrhagic Stroke

  • Hemorrhagic strokes (13% of strokes) include subarachnoid hemorrhage (SAH) and intracerebral hemorrhage (ICH). SAH may result from trauma or rupture of an intracranial aneurysm or arteriovenous malformation (AVM). ICH occurs when bleeding in the brain parenchyma results in hematoma formation.

  • Intracranial hematoma causes mechanical compression of brain parenchyma. Early hematoma expansion often occurs within 3 hours of hemorrhage onset, contributing to worsened functional outcome and increased mortality.

  • Secondary mechanisms of injury are mediated by the subsequent inflammatory response, cerebral edema, and damage from blood product degradation.

CLINICAL PRESENTATION

  • Patients may be unable to provide a reliable history because of cognitive or language deficits. Family members or other witnesses may need to provide this information.

  • Symptoms include unilateral weakness, inability to speak, loss of vision, vertigo, or falling. Ischemic stroke is not usually painful, but some patients complain of headache. Pain and headache are more common and severe in hemorrhagic stroke.

  • Neurologic deficits on physical examination depend on the brain area involved. Hemi- or monoparesis and hemisensory deficits ...

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