Stroke Classification and Types

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

Ischemic stroke (87% of all strokes) results from cerebral artery occlusion.
Occlusion can be due to 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 (atrial fibrillation, valvular heart disease, or other prothrombotic heart problems) account for approximately 25% of ischemic strokes.

Insufficient oxygen supply leads to ATP depletion, lactate buildup, intracellular sodium and water accumulation, culminating in cytotoxic edema and eventual cell lysis.
Calcium influx activates 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 typically occur within 2-3 hours of ischemia, leading to cellular apoptosis and necrosis.

Decreased cerebral blood flow can lead to cerebral infarction with a surrounding ischemic area that potentially maintains membrane integrity (ischemic penumbra).
This area can be salvaged with timely pharmacologic or endovascular interventions.

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

Symptoms in stroke include unilateral weakness, inability to speak, vision loss, vertigo, or falling.
Ischemic stroke is often not painful, though some patients report headaches.
Pain and headaches are more common and severe in hemorrhagic stroke.
Neurologic deficits on physical examination vary depending on the affected brain area. Hemi- or monoparesis and hemisensory deficits are common. Patients with posterior circulation involvement might exhibit vertigo and diplopia. Anterior circulation strokes often result in aphasia. Patients can experience altered levels of consciousness.

General blood glucose, platelet count, and coagulation parameters should be assessed.
CT and MRI head scans can identify areas of hemorrhage and infarction.
Computed tomography angiography (CTA), carotid Doppler (CD), ECG, transthoracic echocardiogram (TTE), and transcranial Doppler (TCD) studies aid in diagnosis, especially in patients requiring endovascular treatment.

Goals of stroke treatment include:
- Reducing ongoing neurologic injury acutely to lower mortality and long-term disability.
- Preventing complications from immobility and neurologic dysfunction.
- Preventing stroke recurrence.

Endovascular intervention and thrombectomy with retrievable stents are strongly recommended within 6 hours of symptom onset for anterior circulation occlusions.
Endovascular interventions for posterior circulation occlusions are less clear-cut and must be considered on a case-by-case basis, maybe up to 6-24 hours of symptom onset.
Decompressive hemicraniectomy, brain surgery to remove a portion of the skull, can reduce mortality and improve function in specific patients.
Carotid endarterectomy, surgery to remove plaque buildup in stenotic carotid arteries, effectively reduces stroke incidence and recurrence in suitable patients.

Early intervention with either surgical clipping or endovascular coiling of the affected vascular abnormality in SAH (subarachnoid hemorrhage) minimizes mortality associated with rebleeding.
For patients with cerebellar hemorrhage, neurologic deterioration, brainstem compression, or hydrocephalus secondary to ventricular obstruction, early surgical intervention and hematoma removal are advised.

Fever worsens outcomes in both hemorrhagic and ischemic stroke patients.
Identifying the source of fever and implementing appropriate pharmacologic and/or nonpharmacologic management is crucial for maintaining normothermia.

Adhere to a guideline-recommended protocol is essential for achieving positive outcomes in ischemic stroke management.
ACTIVATE stroke team, CT scan to rule out hemorrhage, ideally treated within 4.5 hours of symptom onset, meet all inclusion criteria and no contraindications, administer alteplase within guidelines, avoid anticoagulants and antiplatelets for 24 hours post-alteplase, closely monitor vital signs, neurologic status, and signs of hemorrhage.
Aspirin (160-325mg/day) is started within 24-48 hrs of onset to reduce long-term death and disability.
An alternate antiplatelet agent may be considered for aspirin allergy or contraindications.
Elevated BP should be treated to <185/110 mm Hg in patients eligible for alteplase before thrombolytic administration.
In those not taking alteplase, BP is allowed to rise as high as 220/120 mmHg (first 48-72 hours). This is critical because early BP reduction may be ineffective.

The usefulness of pharmacotherapy is limited in spontaneous intracerebral hemorrhage (ICH).
In general, aggressive blood pressure lowering with continuous intravenous infusions may be warranted in patients with systolic blood pressure (BP) above 220mmHg to improve functional outcome and minimize complications.
Aiming for a systolic BP goal of 140 mmHg is safe and can possibly improve functional outcomes.
In subarachnoid hemorrhage (SAH) due to aneurysm rupture, BP control should aim for a systolic BP below 160mmHg, ideally from symptom onset to aneurysm obliteration.
Use of reversal agents is considered when intracranial hemorrhage occurs in patients on anticoagulants, correcting medication-induced coagulopathy or overdoses.

For patients receiving alteplase therapy, closely monitor for bleeding using neurologic examination and blood pressure at specific intervals
Daily monitoring of bleeding is essential for aspirin, clopidogrel, extended-release dipyridamole plus aspirin, warfarin, and other oral anticoagulants.
Daily PT/INR and haemoglobin/haematocrit checks are important for warfarin recipients.