Ischemic CVA (Cerebrovascular Accident) - Complete Review

1. Definition

2. Epidemiology

• ~600,000 "first-ever" ischemic strokes per year in the United States
• More common in Blacks and Hispanics vs. non-Hispanic whites
• Risk increases with age, but ~3-4% occur in patients aged 15-45 years (average age of first stroke is trending younger)
• In >1/3 of cases, no clear cause is identified ("cryptogenic stroke")

3. Etiology & Pathophysiology

A. Thrombotic Stroke (~33% of ischemic strokes)

• Caused by large- or small-vessel occlusion
• Large vessels: clot forms at an ulcerated atherosclerotic plaque, typically at vessel bifurcations (especially internal carotid artery distribution)
• Stenosis must exceed 90% of vessel diameter to markedly reduce flow
• Platelets adhere to the ulcerated region; clot either embolizes or occludes the vessel

B. Lacunar (Small-Vessel) Stroke

• Involves small terminal branches of vasculature
• Infarct size: a few mm to 2 cm
• Common locations: basal ganglia, thalamus, pons, internal capsule
• Seen predominantly in patients with diabetes and hypertension (80-90% have hypertension)
• Mechanism: lipohyalinosis (hypertensive cerebral vasculopathy) or small emboli

C. Cardioembolic Stroke (~25%)

• Most common mechanism: mural thrombus from atrial fibrillation (5x increased stroke risk)
• Other cardiac sources: mural thrombus post-MI, valvular disease, cardiomyopathy
• Non-cardiac embolic sources: artery-to-artery embolism from diseased extracranial arteries, aortic atheromas
• Example: Amaurosis fugax - carotid plaque embolizes to ophthalmic artery causing transient monocular blindness

D. Special Causes in Young Patients

E. Ischemic Penumbra

4. Clinical Features by Vascular Territory

Anterior Cerebral Artery (ACA) Stroke

• Contralateral leg weakness > arm weakness (opposite of MCA)
• Sensory loss in contralateral lower limb
• Altered mentation, impaired judgment and insight
• Primitive reflexes (grasp, suck)
• Bowel and bladder incontinence
• Gait apraxia

Middle Cerebral Artery (MCA) Stroke (most common)

• Contralateral motor and sensory loss - face and arm > leg
• Contralateral homonymous hemianopsia
• Dominant hemisphere (usually left): Aphasia (Broca's = expressive; Wernicke's = receptive)
• Non-dominant hemisphere: Hemineglect, agnosia, anosognosia
• Gaze preference toward the side of the lesion (disruption of cortical lateral gaze center)

Posterior Cerebral Artery (PCA) Stroke

• Contralateral homonymous hemianopsia (with macular sparing)
• Visual agnosia, prosopagnosia
• Memory deficits (thalamic involvement)

Vertebrobasilar (Posterior Circulation) Stroke

• Cranial nerve palsies (ipsilateral CN deficit + contralateral hemiplegia = "crossed signs" - hallmark of brainstem stroke)
• Cerebellar signs: ataxia, dysmetria, nystagmus, dysarthria
• Diplopia, vertigo, nausea/vomiting
• Horner syndrome (ptosis, miosis, anhidrosis)
• Drop attacks, sudden loss of consciousness
• Bilateral weakness or sensory loss
• Anterior circulation strokes: rarely lose consciousness
• Posterior strokes: may progress for up to 3 days (vs. 24 hrs for anterior)

Lacunar Syndromes (pure syndromes due to small deep infarcts)

5. Stroke Terminology

6. Diagnosis

Initial Workup

1. Noncontrast CT head - first and immediate step; distinguishes ischemic from hemorrhagic stroke; sensitivity for ischemia limited in first 6-12 hours
2. CTA head and neck - identifies vessel occlusion (LVO), dissection, stenosis; should be done concurrently with CT to triage thrombectomy candidates
3. MRI with DWI + ADC - most sensitive for acute ischemia; detects restriction of diffusion within minutes of onset; superior for posterior fossa
4. CT Perfusion (CTP) - identifies salvageable penumbra; used for extended time window (6-24 hrs) patient selection for thrombectomy
5. ECG - identify atrial fibrillation, acute MI
6. Blood glucose - immediately (hypo/hyperglycemia mimics stroke)

Early CT Signs of Ischemia (within 3 hours)

• Hyperdense artery sign (clot in MCA or ICA = "hyperdense MCA sign" or "hyperdense dot sign")
• Loss of insular ribbon (early MCA territory ischemia)
• Loss of gray-white junction (sulcal effacement, blurring of deep gray matter)
• Mass effect and acute hypodensity (higher hemorrhagic risk with tPA)

NIHSS (NIH Stroke Scale)

• Standardized 0-42 scale assessing level of consciousness, language, neglect, visual fields, facial palsy, motor and sensory function, coordination, and dysarthria
• Used to assess severity, monitor progression, and determine tPA eligibility
• Patients with "stroke in evolution" should have NIHSS reassessed repeatedly

Stroke Mimics

7. Management

NINDS Time Targets (Door-to-Treatment)

Prehospital

• Airway: intubate only if airway unprotected or brainstem affected
• Oxygen: only if SpO2 <95% (avoid routine supplementation in normoxic patients)
• IV access; avoid dextrose-containing fluids (hyperglycemia worsens ischemic deficit)
• Correct hypoglycemia immediately
• ECG monitoring for arrhythmias/AF
• Document exact last known well (LKW) time
• Use validated prehospital stroke scale (Cincinnati, FAST, LA Prehospital Stroke Screen)

Blood Pressure Management

• Withhold antihypertensives unless SBP >220, DBP >120, or MAP >130 mmHg
• Exceptions: acute MI, aortic dissection, hypertensive encephalopathy, severe LV failure

• Target SBP <185 mmHg, DBP <110 mmHg
• Agents: IV labetalol 10-20 mg over 1-2 min; nicardipine infusion 5 mg/h (max 15 mg/h); clevidipine 1-2 mg/h (max 21 mg/h)
• After tPA: treat hypertension aggressively (SBP <180) for first 24 hours

IV Thrombolysis (tPA - Alteplase)

• Dose: 0.9 mg/kg IV (max 90 mg) - 10% as bolus, rest over 60 min
• Window: 0-3 hours (FDA-approved); 3-4.5 hours (AHA/ASA extended window with additional exclusions)
• Indication: Ischemic stroke with measurable neurologic deficit, no contraindications
• For thrombolysis candidate: advanced imaging (CTP, MRI-DWI) should not delay tPA administration

• Evidence of intracranial hemorrhage on CT
• SBP >185 mmHg or DBP >110 mmHg (unless treatable before tPA)
• Active internal bleeding
• Known intracranial neoplasm, AVM, or aneurysm
• Recent intracranial surgery, serious head trauma, or prior stroke within 3 months
• Symptoms suggesting subarachnoid hemorrhage
• Platelet count <100,000; heparin within 48 h with elevated PTT; current anticoagulant use with INR >1.7

Mechanical Thrombectomy (Endovascular)

• For large vessel occlusion (LVO) - ICA, MCA (M1/M2), vertebrobasilar
• Time window: up to 24 hours from LKW with advanced imaging selection (CTP or MRI DWI-perfusion mismatch - DAWN/DEFUSE-3 trials)
• Stent retriever + aspiration catheter (most common approach)
• CTA confirms LVO and guides patient selection
• tPA should not be withheld while preparing for thrombectomy (combined therapy preferred in eligible patients)
• Recent evidence (2025 meta-analysis [PMID: 40245349]): endovascular thrombectomy benefits patients even with large ischemic core strokes

Antiplatelet Therapy

• Aspirin 325 mg within 24-48 hours of ischemic stroke (if not given tPA, avoid aspirin for 24 h post-tPA)
• Dual antiplatelet (aspirin + clopidogrel) for minor stroke/high-risk TIA for 21 days (POINT/CHANCE trials)
• Long-term: aspirin, clopidogrel, or aspirin + dipyridamole

Anticoagulation

• Not routinely recommended in acute ischemic stroke (increased hemorrhagic transformation)
• Indicated for cardioembolic stroke (AF) after appropriate delay (based on stroke size)
• Patent foramen ovale (PFO): ESO 2024 guidelines support PFO closure in cryptogenic stroke in patients <60 years

Glucose Management

• Target normoglycemia (70-180 mg/dL)
• Hyperglycemia worsens ischemic deficit - treat with insulin
• Hypoglycemia must be corrected immediately (common stroke mimic)

Stroke Unit Care

• All stroke patients admitted to dedicated stroke unit (reduces mortality and dependency by 20% over general ward)
• DVT prophylaxis (early mobilization + compression stockings; LMWH after 24-48 h)
• Dysphagia screening before oral intake (nil by mouth until assessed)
• Urinary catheter avoidance when possible (infection risk)
• Head of bed: flat for first 24 hours in large hemispheric strokes (optimizes CPP); elevate 30° if risk of aspiration or raised ICP

8. Secondary Prevention

9. Complications

10. Prognosis & Rehabilitation

• NIHSS score at 24-48 hours is the best predictor of outcome
• Functional recovery aided by neuroplasticity - reorganization of surviving cortical areas
• Mechanisms of recovery: ipsilateral motor pathways, recruitment of contralateral hemisphere (transcallosal mechanisms), modulation of inhibitory circuits
• Rehabilitation started within 24-48 hours (early mobilization)
• Components: physiotherapy, occupational therapy, speech therapy, cognitive rehabilitation
• TMS (transcranial magnetic stimulation) and tDCS under investigation for post-stroke motor recovery