Ischemic Stroke Evaluation Guide

Overview

Case discussion of a 61-year-old hypertensive woman with acute right-sided weakness, facial deviation, and speech difficulty. Focus on stroke type differentiation, localization, exam findings, investigations, and management.

Patient Profile and Presentation

• 61-year-old right-handed woman, Ramnagar; lower-middle socioeconomic status; educated to 8th standard.
• Risk factors: Hypertension (8 years, on amlodipine); postmenopausal age; no diabetes, cardiac disease, smoking, or alcohol.
• Chief complaints (5 days): sudden right upper and lower limb weakness, left mouth angle deviation, slurred speech.
• Functional impact: difficulty holding glass, combing hair (distal > proximal suggested), squatting, gripping slippers.
• No: headache, vomiting, LOC, seizures, visual loss, sensory symptoms, imbalance, dysphagia, chest pain, palpitations.

Stroke Typing by History

• Timing: woke with deficits (early morning onset favors thrombotic ischemic stroke).
• Deficit at onset: not maximal; progressed over hours (stepwise progression favors thrombosis).
• Progression mechanism: expanding infarct core; ischemic penumbra injury via reduced flow and excitotoxic edema.

Coagulation and Circadian Concept

• Fibrinolysis control: tissue plasminogen activator activates plasminogen; countered by plasminogen activator inhibitor (PAI).
• Early morning: higher PAI levels reduce fibrinolysis, favoring thrombosis; age-related endothelial injury adds risk.

Focal Deficits and Localization

• Motor: right hemiparesis; UMN pattern (distal weakness appears early in UMN lesions).
• Face: UMN-type right facial weakness (forehead spared), deviation to left; suggests supranuclear lesion.
• Speech: differentiate dysarthria (articulation, facial/tongue/velar muscles) vs aphasia (language, cortical).
  • Facial involvement supports dysarthria (labial sounds affected).
  • True Broca’s aphasia implies dominant frontal cortex; dense internal capsule lesion alone does not cause aphasia.
• Sensory: no deficits reported; favors internal capsule motor pathways if pure motor.

Ecology of Stroke: Key Differentiators

• Thrombotic: early morning, progressive, not maximal at onset; recurrent similar TIAs (low-flow), lacunar patterns.
• Embolic: maximal at onset; spontaneous improvement within 24–48 h as embolus lyses; TIAs varied (“shotgun”).
• Hemorrhagic: often during activity; headache, vomiting, altered sensorium; worsening from edema, mass effect.

TIAs: Anterior vs Posterior

• Anterior (carotid): amaurosis fugax (ophthalmic artery), transient mono-weakness, sensory loss, aphasia.
• Posterior (vertebrobasilar): vertigo, ataxia, dysarthria, dysphagia, ophthalmoplegia, hiccups.
• TIA prognosis: high short-term stroke risk; many within 1 week, most within 3 months.

Hypertension and Stroke Patterns

• Ischemic more common overall; lacunar infarcts typical in HTN.
• Lacunar syndromes: pure motor, pure sensory, ataxic hemiparesis, dysarthria–clumsy hand, mixed.
• Lacunar sites: posterior limb internal capsule (common), corona radiata, basis pontis, thalamus, genu; cerebellum (rare).
• Hypertensive hemorrhage sites: putamen (commonest), pons, cerebellum; lobar hemorrhage uncommon.

Examination Highlights

• Vitals: normal pulse; BP 128/90; afebrile; JVP normal.
• General: BMI 22.7 (nutritional status should align with normal).
• Higher mental functions: oriented; memory intact; reduced fluency; repetition affected; reading/writing not possible; comprehension normal.
• Cranial nerves:
  • II: acuity and fields normal; fundus needed (papilledema, hypertensive changes, subhyaloid hemorrhage).
  • III, IV, VI: full movements; pupils reactive.
  • V: normal; jaw jerk absent (unilateral UMN does not augment jaw jerk).
  • VII: right UMN facial palsy; preserved eye closure, loss of right nasolabial fold; mouth deviates left.
  • IX, X, XII: clinically no dysphagia; articulation may be affected by VII.
• Motor: increased tone (spasticity); right power 3/5; left 5/5.
  • Spasticity features: velocity-dependent; anti-gravity pattern; clasp-knife phenomenon.
• Reflexes: right DTRs exaggerated; right abdominal reflex absent; right plantar extensor; left normal.
• Sensory: intact.
• Cerebellar: not testable on weak side; normal on left.
• Vascular auscultation: no carotid or skull bruits; should assess carotid and vertebral bruits along defined surface anatomy.
• CVS/RS/Abdomen: normal; ensure full documentation (apex, cardiomegaly absent, S3/S4, murmurs).

Bedside Vascular Examination Essentials

• Carotid bruit: along carotid in anterior triangle (palpate then auscultate).
• Vertebral artery: line from medial clavicle (first part subclavian) to mastoid; auscultate along this path.
• Absence of bruit does not exclude severe occlusion (complete occlusion may be silent).

Investigations

• Neuroimaging: non-contrast CT first (exclude hemorrhage); MRI DWI/T2 for infarct; CT/MR angiography for vessel status.
• Cardiac: ECG, echocardiography (cardioembolism, structural disease).
• Vascular: carotid and vertebral Doppler.
• Labs: CBC (Hb, platelets), glucose and HbA1c, lipid profile; coagulation tests mainly if hemorrhage suspected; uric acid as needed.

Management

• Thrombolysis window: within 4.5 hours (alteplase 0.9 mg/kg; 10% bolus, 90% over 60 min).
• Thrombolysis considerations:
  • BP must be ≤185/110 mmHg prior; reduce if needed.
  • Absolute contraindications include thrombocytopenia (<100K), marked hypo/hyperglycemia (<50 or >400), recent heparin (48 h), recent stroke (3 months), recent major surgery (14 days), recent GI bleed (21 days).
• Antithrombotic therapy: dual antiplatelet (aspirin + clopidogrel) in early phase; statin irrespective of baseline lipids (pleiotropic vascular benefits).
• BP management:
  • Ischemic (no thrombolysis): avoid rapid lowering initially; maintain perfusion; gradual reduction over 24 h.
  • Hemorrhagic: reduce BP promptly (first 6–12 h) to limit expansion.
• Supportive care: glucose control; DVT prophylaxis; swallow assessment/feeding; bladder care; pneumonia/UTI prevention; early rehab.
• Rehabilitation: start day 1 if no thrombolysis and hemodynamically stable; after thrombolysis, begin after 24 hours if stable.

Aphasia vs Dysarthria: Clinical Differentiation

• Aphasia: language disorder (comprehension, naming, repetition, reading/writing); cortical localization (dominant hemisphere).
  • Broca’s aphasia: non-fluent, impaired repetition, good comprehension, minimal word output.
• Dysarthria: motor articulation (labials: p/b; linguals: t/d/n; velars: k/g); cranial nerves VII, IX/X, XII; can accompany internal capsule lesions.

Stroke Mimics

• Organic: brain tumors, subdural/epidural hematomas, infections (meningitis with vasculitis), metabolic (hypo/hyperglycemia), post-ictal Todd’s paresis.
• Venous: cerebral venous thrombosis (often with fever).
• Functional: non-organic presentations.

Examination and History Tips

• Always document deficit evolution, hospital delay reasons, and status change after admission.
• Ask for complications: DVT (limb pain/swelling), pneumonia, UTI, bedsores, fever.
• TIA characterization: anterior vs posterior features; pattern similarity (thrombotic) vs variability (embolic).
• Family history: young strokes—prothrombotic disorders (protein C/S deficiency, factor V Leiden), sickle cell, CADASIL, aneurysms, moyamoya.
• Personal history: diet (B12 deficiency; hyperhomocysteinemia), drug use (cocaine), sexual history (HIV/syphilis), OCP only in premenopausal.

Provisional Diagnosis and Localization

• Likely ischemic thrombotic stroke in left MCA territory.
• Pure motor signs with UMN facial palsy favor left internal capsule (posterior limb) if no aphasia.
• If convincing Broca’s aphasia present, lesion localizes to dominant frontal cortex; MCA superior division involvement; dense capsular signs would suggest larger MCA stem involvement.

Key Terms & Definitions

• Ischemic core: irreversibly infarcted tissue.
• Ischemic penumbra: hypoperfused, salvageable tissue around core.
• PAI: plasminogen activator inhibitor; suppresses tPA-mediated fibrinolysis.
• Dysarthria–clumsy hand: lacunar syndrome with articulation deficit and fine motor clumsiness.
• Amaurosis fugax: transient monocular vision loss due to ophthalmic artery ischemia.
• Cushing’s reflex: bradycardia and hypertension with raised intracranial pressure.
• Todd’s paralysis: transient post-ictal focal weakness.

Structured Comparisons

Action Items / Next Steps

• Ensure fundus examination documentation (papilledema, hypertensive retinopathy, subhyaloid hemorrhage).
• Clarify speech disorder as aphasia vs dysarthria using repetition, naming, reading/writing, and articulation tests.
• Document carotid and vertebral bruits with correct surface anatomy.
• Complete systemic exam write-ups (CVS apex/cardiomegaly, RS, abdomen).
• Confirm imaging: MRI DWI and vascular study to localize lesion (internal capsule vs cortical MCA).
• Optimize secondary prevention: dual antiplatelet (initial phase), statin, BP and glucose targets, risk factor modification.
• Initiate/continue early multidisciplinary rehabilitation; monitor for complications (DVT, pneumonia, UTI).