What are the types, pathophysiology, clinical features, and common presentations of Cerebrovascular Accident (CVA) in the outpatient department (OPD)?

Cerebrovascular Accident (CVA): Comprehensive Overview

Definition and Core Concept

CVA is a loss of neurological function caused by an ischemic or hemorrhagic event with residual symptoms lasting at least 24 hours after onset or leading to death. 1 This distinguishes it from transient ischemic attack (TIA), where symptoms resolve within 24 hours but still carry a stroke risk as high as 13% in the first 90 days. 1

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Types of CVA

Ischemic Stroke (80-85% of cases)

Ischemic CVA results from arterial occlusion through five primary mechanisms:

• Thrombotic occlusion from atherosclerotic plaque rupture in extracranial or intracranial vessels 1
• Embolic stroke from thrombus formed on atherosclerotic plaques (most commonly from carotid arteries) 1
• Atheroembolism from cholesterol crystal or plaque debris 1
• Hypoperfusion from severe stenosis or occlusion reducing cerebral blood flow 1
• Arterial dissection with subintimal hematoma compromising the lumen 1

Hemorrhagic Stroke (15-20% of cases)

Hemorrhagic CVA occurs when blood vessel rupture causes:

• Intracerebral hemorrhage within brain parenchyma, basal ganglia, or other deep structures 1
• Subarachnoid hemorrhage in the space surrounding the brain 1

Cerebral Venous Thrombosis (CVT)

CVT is a distinct entity where thrombosis of cerebral veins or sinuses causes venous infarction or hemorrhage. 1 The superior sagittal sinus is most commonly involved (leading to headache, increased intracranial pressure, papilledema), followed by lateral sinus and deep venous system thrombosis. 1

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Pathophysiology

Ischemic Cascade

When cerebral blood flow drops below critical thresholds, a cascade of cellular injury begins within minutes:

• Core infarct develops in areas with blood flow <10-12 mL/100g/min (irreversible damage within minutes) 2
• Penumbra surrounds the core with blood flow 12-20 mL/100g/min (potentially salvageable tissue for 3-6 hours) 2
• Cytotoxic edema from ATP depletion causes cell swelling visible on diffusion-weighted MRI within minutes 2
• Excitotoxicity from glutamate release, calcium influx, and free radical formation propagates injury 2

Hemorrhagic Mechanisms

Hemorrhagic transformation occurs when:

• Hypertension causes lipohyalinosis and microaneurysm formation in penetrating arteries 1
• Reperfusion of ischemic tissue with damaged blood-brain barrier leads to secondary hemorrhage 1
• Venous hypertension from CVT causes venous infarction with hemorrhagic conversion 1

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Clinical Features by Vascular Territory

Anterior Circulation (Carotid Territory)

Middle Cerebral Artery (MCA) - Most Common:

• Contralateral hemiparesis and hemisensory loss (face and arm > leg) 1
• Aphasia if dominant hemisphere (left in 95% of right-handed, 70% of left-handed patients) 1
• Neglect and visuospatial deficits if non-dominant hemisphere 1
• Homonymous hemianopia from optic radiation involvement 1
• Gaze deviation toward the lesion 1

Anterior Cerebral Artery (ACA):

• Contralateral leg weakness and sensory loss > arm 1
• Abulia and executive dysfunction from frontal lobe involvement 1
• Urinary incontinence 1

Internal Carotid Artery:

• Combination of MCA and ACA territory signs 1
• Amaurosis fugax (transient monocular blindness) from retinal artery involvement 1

Posterior Circulation (Vertebrobasilar Territory)

Vertebrobasilar System:

• Vertigo, nausea, vomiting (acute vestibular syndrome) 1
• Diplopia and dysarthria 1
• Ataxia and gait instability 1
• Crossed sensory or motor findings (ipsilateral face, contralateral body) 1
• Altered consciousness if bilateral thalamic or brainstem involvement 1

Posterior Cerebral Artery (PCA):

• Homonymous hemianopia with macular sparing 1
• Visual agnosia and prosopagnosia 1
• Memory impairment if medial temporal involvement 1

Lacunar Syndromes (Small Vessel Disease)

Pure motor hemiparesis from internal capsule or pons lesion 1 Pure sensory stroke from thalamic lesion 1 Ataxic hemiparesis from pons or internal capsule 1 Dysarthria-clumsy hand syndrome from pontine base lesion 1

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Common OPD Presentations

TIA (Transient Ischemic Attack)

TIA patients present with resolved symptoms but face 13% stroke risk in 90 days, with highest risk in first 7 days. 1 Common presentations include:

• Brief episodes of unilateral weakness or numbness (minutes to hours) 1
• Transient aphasia or dysarthria 1
• Monocular vision loss (amaurosis fugax) suggesting carotid disease 1
• Transient diplopia or vertigo suggesting posterior circulation 1

Critical pitfall: Up to 24% of patients with acute retinal artery occlusion have concurrent cerebral infarction on MRI, even without neurological symptoms. 1 These patients require urgent stroke workup.

Subacute Stroke Presentations

In the ISCVT registry, 56% of CVT patients had subacute onset (>48 hours to 30 days), with median delay to diagnosis of 7 days. 1

• Progressive hemiparesis over days to weeks 1
• Isolated severe headache (25% of CVT cases) without focal signs 1
• Headache with papilledema or sixth nerve palsy mimicking idiopathic intracranial hypertension 1
• Seizures (40% of CVT patients, much higher than arterial stroke) 1

Chronic Presentations

Patients may present months after unrecognized stroke with:

• Established hemiparesis or spasticity 3
• Vascular dementia from multiple lacunar infarcts 1
• Post-stroke epilepsy 3
• Depression and cognitive impairment 4

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Diagnostic Approach in OPD

Immediate Assessment

Perform NIHSS (National Institutes of Health Stroke Scale) to quantify severity: 5

• NIHSS <15: optimal candidates for intervention 5
• NIHSS >15 with obtundation: poor outcomes with aggressive intervention 5

Neuroimaging Priority

Non-contrast CT head must be completed within 30 minutes to distinguish ischemic from hemorrhagic stroke. 5 However, CT misses up to 54% of acute ischemic strokes in first 24 hours. 1

MRI with diffusion-weighted imaging (DWI) is superior: 5

• Detects ischemia within minutes (cytotoxic edema) 2
• Identifies 19-25% of patients with retinal artery occlusion who have silent brain infarction 1
• More sensitive than CT for posterior fossa strokes 1

Vascular Imaging

For patients with TIA or minor stroke, urgent carotid evaluation within 1 week is essential because stroke risk is highest in first 7 days. 1

• Carotid duplex ultrasound as initial screening 1
• CTA or MRA if surgery/stenting considered 1
• Up to 70% of symptomatic retinal artery occlusion patients have significant carotid stenosis 1

Laboratory Evaluation

Essential initial tests: 1

• Complete blood count, chemistry panel, PT/aPTT 1
• Troponin and ECG (concurrent MI in 20-24% of retinal artery occlusion) 1
• Lipid panel and HbA1c 4
• D-dimer if CVT suspected (high sensitivity but poor specificity) 1

Thrombophilia screening for CVT: 1

• Protein C, Protein S, Antithrombin III 1
• Factor V Leiden, Prothrombin G20210A mutation 1
• Antiphospholipid antibodies 1
• Screen for underlying inflammatory disease, infection, malignancy 1

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Risk Stratification

CHADS₂ Score for Embolic Risk

In atrial fibrillation ablation patients, periprocedural CVA occurred in: 6

• 0.3% with CHADS₂ score of 0 6
• 1.0% with CHADS₂ score of 1 6
• 4.7% with CHADS₂ score ≥2 6

Prior CVA history increases risk 9.5-fold for recurrent events. 6

High-Risk Populations

Cancer survivors face dramatically elevated CVA risk: 4

• Leukemia survivors: 6× higher risk than siblings 4
• Brain tumor survivors: 29× higher risk 4

• 50 Gy to prepontine cistern: hazard ratio 17.8 for cerebrovascular death 4

• Hodgkin lymphoma with neck/mediastinal radiation: 2.5× higher ischemic CVD risk 4

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Critical Pitfalls to Avoid

Diagnostic Pitfalls

Posterior circulation strokes are frequently missed: 1

• 75-80% of patients with vertebrobasilar infarction causing acute vestibular syndrome have no focal neurological deficits 1
• HINTS examination (Head Impulse, Nystagmus, Test of Skew) by trained practitioners is 100% sensitive vs. 46% for early MRI 1
• CT misses small posterior fossa infarcts; MRI with DWI is essential 1

CVT masquerades as other conditions: 1

• Isolated headache without focal signs in 25% of cases 1
• Bilateral thalamic involvement causes altered consciousness without lateralizing signs 1
• Seizures at presentation (40% of CVT) may mislead toward primary seizure disorder 1

Retinal artery occlusion is a stroke equivalent: 1

• 19-25% have concurrent silent brain infarction on MRI 1
• 3-6% stroke risk in first 1-4 weeks 1
• Only one-third of ophthalmologists currently refer to emergency department 1

Management Pitfalls

Blood pressure management is counterintuitive: 5

• Avoid aggressive lowering unless >220/120 mmHg (permissive hypertension maximizes penumbral flow) 5
• Must be <185/110 mmHg before thrombolysis, then <180/105 mmHg for 24 hours post-treatment 5

Timing errors compromise outcomes: 5

• Door-to-needle time must be ≤30 minutes for rtPA 5
• Aspirin should wait 24 hours after thrombolysis (but start within 48 hours of stroke onset) 5
• CEA benefit diminishes with time; perform within 2 weeks of TIA/minor stroke 1

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Secondary Prevention

Antiplatelet Therapy

Aspirin 160-300 mg within 48 hours of ischemic stroke (after 24 hours if thrombolysis given). 5 For maintenance, aspirin 81-325 mg daily or clopidogrel 75 mg daily. 1

Lipid Management

Initiate high-intensity statin therapy regardless of baseline cholesterol levels. 5, 4 This reduces recurrent stroke risk even in patients with normal lipids. 4

Anticoagulation

For atrial fibrillation, start anticoagulation after ruling out hemorrhagic transformation (typically after 24-48 hours). 5 Direct oral anticoagulants (DOACs) are preferred over warfarin for most patients. 4

For CVT, anticoagulate for 3-6 months: 1

• IV heparin (aPTT 1.5-2.0× control) or LMWH followed by warfarin (INR 2.0-3.0) 1
• Continue despite hemorrhagic transformation (venous hemorrhage improves with anticoagulation) 1

Blood Pressure Control

Start antihypertensive therapy 24-48 hours post-stroke (after acute phase). 5, 4 Target <140/90 mmHg for most patients, <130/80 mmHg for diabetics. 4

Lifestyle Modifications

Evidence-based dietary interventions: 4

• Increase vegetables, fruits, whole grains, and fiber 4
• Use liquid vegetable oils instead of solid fats 4
• Limit added sugars and sodium 4
• Choose low-fat dairy and lean meats 4
• Alcohol: ≤1 drink/day for women, ≤2 drinks/day for men 4

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Prognosis

Even with optimal treatment, many patients with established vascular disease remain at >20-30% 10-year risk of recurrent events, representing an area of unmet medical need. 4 Among CVA survivors, 75% have learning difficulties or intellectual disability, one-third develop epilepsy, and all have associated cerebral palsy when stroke occurs prenatally. 3