Stroke Overview and Ischemic Pathophysiology

Stroke involves a sudden onset of focal neurologic dysfunction lasting at least 24 hours.
Strokes can be ischemic or hemorrhagic.
Transient ischemic attacks (TIAs) are focal ischemic neurologic deficits lasting less than 24 hours, usually less than 30 minutes.

Accounts for 87% of all strokes.
Results from the occlusion of a cerebral artery.
Causes include:
- Local thrombus formation
- Embolism from a distant site (e.g., heart).
Atherosclerosis in large intracranial or extracranial arteries can contribute to ischemic stroke.
Small artery disease can also contribute significantly.
Emboli originating from the heart (e.g., in patients with atrial fibrillation, valvular heart disease, or other prothrombotic heart conditions) are responsible for approximately 25% of ischemic strokes.

Insufficient oxygen supply leads to ATP depletion, lactate buildup, intracellular Na+ and water accumulation.
This results in cytotoxic edema and eventual cell lysis.
Influx of calcium activates lipases and proteases.
Excitatory amino acids (e.g., glutamate, aspartate) are released leading to neuronal damage and damaging PG, leukotrienes, and ROS.
These processes occur within 2-3 hours of ischemia, leading to cellular apoptosis and necrosis.

Accounts for 13% of all strokes.
Includes subarachnoid hemorrhage (SAH) and intracerebral hemorrhage (ICH).
Early hematoma expansion within 3 hours of onset often worsens the functional outcome and increases mortality.
Mechanisms of continued injury include inflammatory response, cerebral edema, and damage from blood product degradation.
The causes of hemorrhagic stroke are often related to vessel abnormalities, rupture of aneurysms, and other vascular disorders.

Symptoms include unilateral weakness, loss of speech/vision, vertigo, and/or falling.
Ischemic stroke is not typically painful, although headache can occur in some patients.
Hemorrhagic strokes often present with pain and headache.
Neurological deficits observed on physical examination depend on the specific brain area affected.
Examples include hemiparesis or monoparesis, or hemisensory disorders.
Posterior circulation strokes may cause vertigo and diplopia.
Anterior circulation strokes frequently result in aphasia.
Patients might have altered levels of consciousness.

General blood glucose, platelet count, and coagulation parameters are assessed.
CT and MRI scans detect hemorrhage and infarction areas.
Computed tomography angiography (CTA) is critical for patients needing endovascular treatment.
Carotid Doppler (CD), ECG, transthoracic echocardiogram (TTE), and transcranial Doppler (TCD) generate valuable diagnostic information.

Reduce ongoing neurologic injury to decrease mortality and long-term disability.
Prevent complications of immobility and neurologic dysfunction.
Prevent stroke recurrence.

Endovascular intervention and thrombectomy using retrievable stents are often a critical step.
Ideally performed within 6 hours of symptom onset in anterior circulation occlusions.
The benefit of this approach is less clear in posterior circulation occlusions.
Decompressive hemicraniectomy (brain surgery) may be critical in certain cases to manage the neurological damage.
Carotid endarterectomy may be used in patients with severe carotid artery stenosis.

In subarachnoid hemorrhage (SAH), early intervention with surgical clipping or endovascular coiling of the vascular anomaly is vital to reduce rebleeding.
Early surgical intervention and hematoma removal are critical in patients with cerebellar hemorrhage, brainstem compression, or hydrocephalus from ventricular obstruction.

Fever worsens stroke outcomes in both ischemic and hemorrhagic stroke.
Identification of the fever source and management is vital for maintaining normothermia.

Adherence to a guideline-recommended protocol for ischemic strokes is crucial.
CT scan to exclude hemorrhage.
Treatment is administered as early as possible (within 4.5 hours of symptom onset) if appropriate criteria are met.
Alteplase (tPA) is often administered.
Anticoagulant and antiplatelet therapy is avoided for 24 hours following alteplase administration.
Patients are carefully monitored for elevated blood pressure, neurologic status, and hemorrhage.

Includes factors like age, clinical diagnosis, and time from onset of symptoms.
Various contraindications exist (e.g., past stroke, history of hemorrhagic stroke, active internal bleeding).

Long-term antithrombotic therapy is vital for secondary prevention.
Antiplatelet agents such as aspirin, extended-release dipyridamole plus aspirin, and clopidogrel are commonly used in non-cardioembolic strokes.
Warfarin or other oral anticoagulants are often utilized in patients with atrial fibrillation and presumed cardiac sources of embolism.
Statins are recommended for all patients, regardless of baseline lipid levels.

Treatment in spontaneous intracerebral hemorrhage (ICH) is often less effective.
Lowering blood pressure (BP) in patients with systolic BP above 220 mm Hg with continuous IV infusion medications may be beneficial.
The goal in patients with subarachnoid hemorrhage (SAH) due to an aneurysm rupture is usually considered a systolic BP under 160 mmHg.
Reversal agents may need to be administered if anticoagulants are involved.

Close monitoring of patients who've received alteplase, as well as anticoagulants or other medications is required.
Bleeding assessments, neurologic checks, and blood pressure monitoring is a significant part of treatment.
Depending on the specific medications, evaluations are performed daily to ensure safety and assess response to the treatment plan. This depends on drug regimens employed.