Circle of Willis Anatomy and Stroke Types | Blood Supply to the Brain

Acute stroke diagnosis begins with non-contrast CT to rule out hemorrhage and identify hyperdense artery signs or hypodense infarcts. CT angiography visualizes vessel occlusions and stenoses. MRI with DWI/ADC sequences provides superior sensitivity for acute infarction detection. Echocardiography identifies cardiac sources of embolism (atrial thrombi, valvular vegetations, wall motion abnormalities, EF assessment). Point-of-care glucose testing identifies hypoglycemia (stroke mimic, tPA contraindication). Coagulation studies (INR) assess bleeding risk. CBC evaluates anemia/polycythemia/thrombocytopenia. These studies form the foundation of acute stroke evaluation and guide treatment decisions.

This section covers stroke imaging: non-contrast CT is investigation of choice for acute brain hemorrhage, while diffusion-weighted MRI (DWI) is best for acute brain infarction. For increased intracranial tension, signs differ by age: children show sutural diastasis (open sutures), while adults show erosion of posterior clinoid process (sutures cannot open). This distinction is crucial for exam questions specifying adult patients.

Diffusion weighted imaging detects acute ischemic stroke by identifying diffusion restriction. In stroke, cytotoxic edema causes neuronal swelling that narrows intercellular spaces, limiting water molecule movement. Lesions appear hyperintense on diffusion images but must be confirmed as diffusion-restricted by checking ADC maps (they should be dark on ADC maps).

In acute stroke management, CT scan is the first-line imaging modality. The CT scan must be absolutely normal to indicate viable brain tissue that can be salvaged. For wake-up stroke patients (when onset time is unknown), the standard MRI protocol consists of three sequences: DWI, SWI, and FLAIR. DWI detects restricted diffusion to confirm acute stroke. SWI differentiates hemorrhagic from ischemic stroke. FLAIR determines the time window for thrombolysis, as it changes between 4.5 to 6 hours after stroke onset. The ideal findings for thrombolysis are: DWI showing restriction, SWI showing normal, and FLAIR showing normal. The 'mismatch' concept (DWI bright, FLAIR normal) indicates the stroke is within the therapeutic window.

This segment summarizes the multi-parametric CT protocol for stroke imaging: non-contrast CT and CT angiography within 4.5 hours to identify large vessel occlusions, MRI with diffusion-weighted imaging and FLAIR between 4.5 and 9 hours to assess infarct core and penumbra, and CT or MR perfusion beyond 6 hours but within 24 hours to identify salvageable tissue. The optimal imaging protocol depends on the time window from symptom onset. CT perfusion results must always be interpreted in conjunction with non-contrast CT findings and clinical assessment.

tPA (alteplase) dissolves clots by converting plasminogen to plasmin. Indications include confirmed neurological deficit, absence of hemorrhage on CT, and documented last known well time. Absolute contraindications include active bleeding, recent surgery, trauma, or stroke within 3 months. Relative contraindications include uncontrolled hypertension (>185/110 mmHg during infusion), severe uncontrolled diabetes, and recent major bleeding. Mechanical thrombectomy removes large vessel occlusions using aspiration devices or stent retrievers, with treatment window extending to 24 hours for patients demonstrating salvageable penumbra. Blood pressure management is critical: <185/110 mmHg during tPA infusion and for 24 hours afterward; <220 systolic for non-tPA patients.

Thrombolysis with alteplase (tPA) is the standard treatment for acute ischemic stroke. The protocol is 0.9 mg/kg (maximum 90 mg), with 10% given as an IV bolus and the remaining 90% infused over 60 minutes. Absolute contraindications include: history of hemorrhagic stroke within 3 months, platelet count less than 100,000/μL, INR greater than 1.7, use of DOACs within 48 hours, active internal bleeding, suspected subarachnoid hemorrhage, intracranial neoplasm, and recent neurosurgery. Mechanical thrombectomy is indicated for patients with large vessel occlusion (LVO) in the anterior circulation (M1 segment of middle cerebral artery or internal carotid artery). The classic criteria are: NIHSS score ≥6, symptom duration ≤6 hours, and occlusion of M1 or internal carotid artery. Posterior circulation thrombectomy is not currently recommended. The DAWN and DEFUSE-3 studies demonstrated that selected patients with DWI-perfusion mismatch (small infarct core, large salvageable penumbra) can benefit from mechanical thrombectomy beyond 6 hours (up to 24 hours).

Acute stroke treatment focuses on restoring blood flow. t-PA (tissue plasminogen activator) is a clot-dissolving medication administered intravenously within three hours of symptom onset for ischemic stroke. It activates plasminogen to break down fibrin clots. Mechanical thrombectomy uses devices like the Merci retriever (threaded through a catheter from the femoral artery) to physically remove clots, with FDA approval extending to eight hours. Both treatments require confirming ischemic stroke via brain imaging before administration. Treatment effectiveness depends on time since symptom onset and quality of collateral blood flow.

Acute ischemic stroke management follows a time-critical protocol. The golden window for tPA administration is within 4.5 hours of symptom onset. Between 4.5-9 hours, CT perfusion or MRI can identify salvageable penumbra to extend treatment window. tPA is administered as 10% bolus over 1 minute followed by 90% over 59 minutes. Contraindications include age >80, glucose <1.7 mmol/L, and recent stroke within 3 months. Mechanical thrombectomy is indicated for large vessel occlusion unresponsive to thrombolysis. Ideal candidates have modified Rankin Scale ≤2, age >18, and NIHSS >6. The procedure involves catheter-based clot removal from internal carotid or proximal cerebral vessels.

Acute stroke treatment involves reperfusion strategies: alteplase (tPA) dissolves clots systemically but is limited to 4.5 hours and less effective for large vessel occlusions; mechanical thrombectomy physically removes clots using aspiration or stent retrievers, extending treatment windows to 24 hours in select patients. Initial evaluation requires rapid assessment of symptom onset timing, medical history (especially anticoagulant use), and neurological examination using the NIH Stroke Scale. Head CT rules out hemorrhage (contraindicating tPA) and identifies acute ischemic changes. tPA contraindications include stroke onset >4.5 hours, extensive infarction, recent bleeding, neurosurgery, trauma, severe hypertension, and anticoagulant use. tPA significantly increases hemorrhage risk (10x higher fatal hemorrhage rate) compared to placebo. Treatment effectiveness follows a steep time curve: patients receiving tPA within 60 minutes have twice the chance of good functional outcome. Historical contraindications like seizure at onset or extreme glucose levels are no longer absolute barriers.

Secondary prevention includes antiplatelet therapy, anticoagulation for cardioembolic sources, and risk factor management. Anticoagulation (warfarin, DOACs) is used for atrial fibrillation and other cardioembolic sources, started 4-14 days after stroke. Carotid endarterectomy is performed for symptomatic carotid stenosis greater than 70%, most effective within 2 weeks of stroke. Rehabilitation begins as soon as the patient is medically stable, including physical therapy, occupational therapy, and speech-language pathology.

Secondary prevention focuses on preventing stroke recurrence through antiplatelet therapy (aspirin, clopidogrel) or anticoagulation (warfarin) based on stroke etiology. Risk factor modification includes blood pressure control, diabetes management, lipid-lowering therapy, smoking cessation, and lifestyle changes. Rehabilitation includes physical therapy, occupational therapy, and speech therapy. Prevention of complications includes DVT prophylaxis, urinary catheterization, and monitoring for depression and seizures.

Secondary stroke prevention focuses on preventing recurrence through risk factor modification and antiplatelet/anticoagulant therapy. Aspirin (160-325 mg) should be initiated within 48 hours of stroke onset. For patients with atrial fibrillation, oral anticoagulation (warfarin or DOACs) is indicated rather than antiplatelet therapy. The choice between aspirin and clopidogrel depends on patient factors and clinical judgment. Antiplatelet therapy should be continued indefinitely in most patients, with regular monitoring for bleeding complications. The decision to anticoagulate should be individualized based on stroke severity, bleeding risk, and patient preferences.

Early rehabilitation (day 1) includes: physical therapy; speech-language pathology (for aphasia and dysphagia); occupational therapy; cognitive rehabilitation. Secondary prevention: antiplatelet therapy (aspirin or clopidogrel) for non-cardioembolic stroke; dual antiplatelet therapy (aspirin + clopidogrel) for 21-30 days in minor non-cardioembolic stroke; anticoagulation for cardioembolic stroke (e.g., atrial fibrillation); statins (atorvastatin 40-80 mg or rosuvastatin 20-40 mg) with LDL goal <70 mg/dL or >50% reduction. Anticoagulation (heparin) is NOT used to dissolve acute thrombi - thrombolytics (alteplase) are used for that purpose. Anticoagulation is for secondary prevention in cardioembolic stroke to prevent recurrent embolism.

Secondary stroke prevention focuses on modifiable risk factors. Hypertension is the most significant contributor, with targeting 120/80 mmHg reducing recurrent stroke risk by 50% (from 8-20% to 2-3%). Statins (atorvastatin/rosuvastatin) provide 20-48% relative risk reduction based on SPARCL and JUPITER trials; muscle aches are acceptable if not interfering with quality of life. Antiplatelet therapy (aspirin, clopidogrel, Aggrenox) offers incremental benefit, with dual therapy most effective in early post-stroke period. Anticoagulation is indicated for AF, low EF, dissection, and venous conditions, with NOACs preferred for non-valvular AF due to lower intracranial hemorrhage risk.