Stroke Overview and Ischemic Pathophysiology

Stroke Overview

• Stroke involves a sudden onset of focal neurological dysfunction lasting at least 24 hours.
• Strokes can be ischemic or hemorrhagic.
• Transient ischemic attacks (TIAs) are focal ischemic neurological deficits lasting less than 24 hours and usually less than 30 minutes.
• Ischemic stroke (87% of all strokes) results from occlusion of a cerebral artery.
• Ischemic strokes can be caused by 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, contributing to about 25% of ischemic strokes.

Pathophysiology of Ischemic Stroke

• Insufficient oxygen supply leads to ATP depletion, lactate buildup, intracellular sodium and water accumulation, ultimately causing cytotoxic edema and cell lysis.
• Calcium influx activates lipases and proteases.
• Release of excitatory amino acids (e.g., glutamate, aspartate) damages neurons, producing damaging molecules like prostaglandins, leukotrienes, and reactive oxygen species (ROS).
• These processes occur within 2-3 hours of ischemia, resulting in cellular apoptosis and necrosis.

Pathophysiology of Hemorrhagic Stroke

• Hemorrhagic strokes (13% of strokes) include subarachnoid hemorrhage (SAH) and intracerebral hemorrhage (ICH).
• Early hematoma expansion after hemorrhage onset worsens functional outcomes and increases mortality.
• Secondary injury mechanisms are inflammation, cerebral edema, and damage from blood product degradation.

Clinical Presentation of Stroke

• Symptoms include unilateral weakness, inability to speak, loss of vision, vertigo, or falling.
• Ischemic stroke is not usually painful, although some patients may complain of headache.
• Pain and headache are more common and severe in hemorrhagic stroke.
• Neurologic deficits on physical examination depend on the affected brain area.
• Common deficits include hemi- or monoparesis, hemisensory deficits, vertigo, and diplopia (in posterior circulation involvement). Anterior circulation strokes can cause aphasia.
• Patients may also experience altered levels of consciousness.

Stroke Diagnosis

• General blood glucose, platelet count, and coagulation parameters are assessed.
• Computed tomography (CT) and magnetic resonance imaging (MRI) scans identify hemorrhage and infarction areas.
• Computed tomography angiography (CTA) is recommended for patients needing endovascular treatment.
• Carotid Doppler (CD), electrocardiogram (ECG), transthoracic echocardiogram (TTE), and transcranial Doppler (TCD) provide diagnostic data.

Stroke Treatment Goals

• Reduce ongoing neurologic injury in the acute phase to lower mortality and long-term disability.
• Prevent complications related to immobility and neurological dysfunction.
• Prevent future stroke occurrences.

Non-Pharmacological Treatment of Ischemic Stroke

• Endovascular intervention and thrombectomy with retrievable stents: Strong recommendation for anterior circulation occlusion within 6 hours of symptom onset. Consideration within 6-24 hours. Benefit is less clear for posterior circulation occlusions.
• Decompressive hemicraniectomy: Brain surgery to remove part of the skull can reduce mortality and improve functional outcome in select patients.
• Carotid endarterectomy: Surgery to remove plaque buildup in the carotid artery can reduce stroke incidence and recurrence in appropriate patients.

Non-Pharmacological Treatment of Hemorrhagic Stroke

• SAH early intervention (surgical clipping or endovascular coiling): Reduces mortality from rebleeding.
• Early surgical intervention and hematoma removal: Recommended for patients with cerebellar hemorrhage, neurologic deterioration, brainstem compression, or hydrocephalus from ventricular obstruction.

Temperature Management

• Fever worsens outcomes in patients with both hemorrhagic and ischemic stroke.
• Source identification and pharmacologic or non-pharmacologic management are needed to maintain normothermia.

Pharmacologic Treatment of Ischemic Stroke

• Adherence to a guideline-recommended protocol is essential.
• Activate the stroke team; Obtain CT scan; Treat as early as possible within 4.5 hours of symptom onset; Meet inclusion criteria without contraindications; Administer alteplase; Avoid anticoagulants and antiplatelets for 24 hours after alteplase.
• Monitor patient closely for elevated blood pressure (BP), neurological status, and hemorrhage.
• Aspirin (160-325 mg/day) started within 24-48 hours reduces long-term death and disability. Consider alternate antiplatelet agents for allergies.
• For patients with raised BP and eligible for alteplase, manage BP to a goal of 185/110 mmHg before thrombolytic administration.
• BP can be high (220/120) for up to 48-72 hours after alteplase.

Pharmacologic Treatment of Hemorrhagic Stroke

• The usefulness of pharmacotherapy for spontaneous intracerebral haemorrhage (ICH) is limited.
• Aggressive BP reduction with continuous IV medications is reasonable for systolic blood pressure (BP)>220 mmHg. Achieving 140 mmHg systolic BP is safe and can improve functional outcome.
• For aneurysm rupture-caused subarachnoid haemorrhage (SAH) control systolic BP to <160 mmHg from symptom onset to aneurysm obliteration is reasonable.
• Use of reversal agents when anticoagulants trigger intracranial hemorrhage is recommended.

Evaluation of Therapeutic Outcomes

• Patients receiving alteplase need bleeding monitoring: every 15 minutes for 1 hour, then every 30 minutes for 6 hours, then every hour for 17 hours, followed by periodic checks. 
• Monitor patients receiving aspirin, clopidogrel, extended-release dipyridamole plus aspirin, warfarin, and other oral anticoagulants for bleeding daily. 
• Regularly check INR and hemoglobin/hematocrit in warfarin patients.

This quiz covers the critical aspects of stroke, focusing on its overview and the pathophysiology of ischemic strokes. It delves into types of strokes, their causes, and the biological mechanisms at play. Understanding these factors is essential for recognizing and responding to stroke events effectively.