Stroke Overview and Ischemic Stroke Pathophysiology
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Questions and Answers

What is the minimum duration for focal neurologic dysfunction to be classified as a stroke?

  • 12 hours
  • 24 hours (correct)
  • 48 hours
  • 1 hour
  • Which of the following best describes the two main types of stroke?

  • Ischemic and hemorrhagic (correct)
  • Transient and permanent
  • Hemorrhagic and embolic
  • Ischemic and thrombotic
  • What characterizes a transient ischemic attack (TIA)?

  • Permanent neurologic deficits
  • Neurologic deficits lasting more than 24 hours
  • Focal ischemic neurologic deficits lasting less than 24 hours (correct)
  • Loss of consciousness for 10 minutes
  • Which of the following scenarios would NOT qualify as a stroke?

    <p>A patient experiences a sudden loss of vision lasting 30 minutes</p> Signup and view all the answers

    Which of the following statements about stroke is accurate?

    <p>Stroke can present with varying neurologic symptoms.</p> Signup and view all the answers

    Study Notes

    Stroke Overview

    • Stroke involves the abrupt onset of focal neurologic dysfunction lasting at least 24 hours.
    • It can be either ischemic or hemorrhagic.
    • Transient ischemic attacks (TIAs) are focal ischemic neurologic deficits lasting less than 24 hours, usually less than 30 minutes.

    Ischemic Stroke Pathophysiology

    • Ischemic stroke (87% of all strokes) occurs due to cerebral artery occlusion.
    • Causes include local thrombus formation or emboli from a distant site.
    • Atherosclerosis of large intracranial or extracranial arteries, or small artery disease can cause ischemic stroke.
    • Emboli originating from the heart (e.g., in patients with atrial fibrillation, valvular heart disease, or other prothrombotic heart problems) account for about 25% of ischemic strokes.

    Ischemic Stroke Pathophysiology (Detailed)

    • Insufficient oxygen supply leads to ATP depletion, lactate buildup, intracellular Na and water accumulation, resulting in cytotoxic edema and eventual cell lysis.
    • Calcium influx triggers activation of lipases and proteases.
    • Release of excitatory amino acids (e.g., glutamate, aspartate) causes neuronal damage and produces damaging substances like prostaglandins, leukotrienes, and reactive oxygen species (ROS).
    • These processes occur within 2-3 hours of ischemia onset, leading to cellular apoptosis and necrosis.

    Ischemic Stroke Pathophysiology (Penumbra)

    • Decreased cerebral blood flow can cause cerebral tissue infarction.
    • The ischemic penumbra is surrounding tissue that's ischemic but maintains membrane integrity.
    • This tissue is potentially salvageable with urgent pharmacologic and endovascular interventions.

    Hemorrhagic Stroke Pathophysiology

    • Hemorrhagic strokes comprise 13% of strokes.
    • Types include subarachnoid hemorrhage (SAH) and intracerebral hemorrhage (ICH).
    • Early hematoma expansion, often within 3 hours of onset, worsens functional outcome and increases mortality.
    • Secondary injury mechanisms involve the inflammatory response, cerebral edema, and damage from blood product degradation.

    Clinical Presentation of Stroke

    • Symptoms include unilateral weakness, aphasia (difficulty speaking), vision loss, vertigo, and falls.
    • Ischemic stroke is typically not painful, but some patients experience a headache.
    • Headaches are more common and severe in hemorrhagic stroke.
    • Neurological deficits (e.g., hemiparesis, hemisensory deficits, vertigo, diplopia, aphasia, altered consciousness) depend on the affected brain area.

    Stroke Diagnosis

    • General blood glucose, platelet count, and coagulation parameters.
    • Computed tomography (CT) and magnetic resonance imaging (MRI) scans reveal hemorrhage and infarction areas.
    • Computed tomography angiography (CTA), carotid Doppler, electrocardiography (ECG), transthoracic echocardiography (TTE), and transcranial Doppler (TCD) studies provide diagnostic information.

    Stroke Treatment Goals

    • Reduce ongoing neurologic injury acutely to minimize mortality and long-term disability.
    • Prevent complications due to immobility and neurologic dysfunction.
    • Prevent stroke recurrence.

    Non-Pharmacological Treatment (Ischemic Stroke)

    • Endovascular intervention and thrombectomy with retrievable stents are strongly recommended for patients with anterior circulation occlusion within 6 hours of symptom onset.
    • Benefits of mechanical thrombectomy are less clear in posterior circulation occlusions and should be considered on a case-by-case basis.

    Non-Pharmacological Treatment (Ischemic Stroke) - Additional

    • Decompressive hemicraniectomy (brain surgery) can reduce mortality and improve functional outcome in select patients.
    • Carotid endarterectomy removes plaque buildup in stenotic carotid arteries, effectively reducing stroke incidence and recurrence.

    Non-Pharmacological Treatment (Hemorrhagic Stroke)

    • Early intervention with surgical clipping or endovascular coiling of vascular abnormalities reduces mortality from rebleeding.
    • Early surgical intervention and hematoma removal are recommended for patients with cerebellar hemorrhage, neurologic deterioration, brainstem compression, or hydrocephalus due to ventricular obstruction.

    Temperature Management

    • Fever worsens outcomes in patients with both hemorrhagic and ischemic strokes.
    • Identification of the source and pharmacologic/nonpharmacologic management are needed to maintain normothermia.

    Pharmacologic Therapy (Ischemic Stroke)

    • Adherence to guideline-recommended protocols is essential for positive outcomes.
    • Activate the stroke team and obtain a CT scan to rule out hemorrhage.
    • Treatment should occur as early as possible (within 4.5 hours).
    • Administer alteplase (0.9 mg/kg IV, maximum 90 mg total), with a 10% initial bolus.
    • Avoid anticoagulants and antiplatelets for 24 hours after alteplase.
    • Monitor blood pressure (BP), neurologic status, and for hemorrhage.

    Pharmacologic Therapy (Ischemic Stroke) - Specific Medications

    • Aspirin (160-325 mg/day) started within 24-48 hours (and 24 hours after alteplase) reduces long-term disability.
    • Alternate antiplatelet agents may be considered for patients with aspirin allergies.
    • Maintain BP <185/110 mm Hg prior to thrombolytic administration; BP <160 mm Hg for SAH.

    Pharmacologic Therapy (Ischemic Stroke) - Prevention

    • Long-term antithrombotic therapy includes antiplatelet agents (e.g., aspirin, extended-release dipyridamole, clopidogrel).
    • In patients with atrial fibrillation or presumed cardiac embolism source, oral anticoagulants (e.g., warfarin, apixaban, dabigatran, edoxaban, or rivaroxaban) are recommended.
    • Statin therapy is recommended regardless of baseline lipid levels to prevent stroke recurrence in all ischemic stroke patients.

    Pharmacologic Therapy (Hemorrhagic Stroke)

    • Pharmacotherapy has limited use in spontaneous ICH.
    • Aggressive blood pressure lowering (using continuous intravenous infusion) is reasonable for patients with systolic BP >220 mmHg.
    • Lowering systolic BP to 140 mmHg may improve functional outcome.
    • In SAH (due to aneurysm rupture), maintaining systolic blood pressure (SBP) less than 160 mmHg is generally reasonable.

    Evaluation (Stroke)

    • Monitoring for bleeding is crucial in patients receiving alteplase.
    • Neurologic examination and blood pressure (BP) should be monitored every 15 minutes for the first hour, then every 30 minutes for six hours, and hourly for 17 hours, then once per shift thereafter.
    • For patients on anticoagulants, monitor for bleeding daily, and check PT/INR and hemoglobin/hematocrit in patients on warfarin.

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    Description

    This quiz covers the essential concepts of stroke, including its types, causes, and underlying mechanisms. Participants will explore the differences between ischemic and hemorrhagic strokes, as well as the pathophysiology of ischemic stroke. Gain a deeper understanding of transient ischemic attacks and the physiological impact of stroke on the brain.

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