IM18.1-16 | Cerebrovascular Accident — Graded Quiz

Correct. The time of last known well is 10 PM (9 hours ago) — this is beyond both the 4.5-hour thrombolysis window and beyond the standard 6-hour thrombectomy window without advanced imaging selection. Thrombolysis is contraindicated beyond 4.5 hours. The appropriate management is antiplatelet therapy (aspirin 300 mg), admission to a stroke unit, and full aetiological workup. Mechanical thrombectomy beyond 6 hours requires perfusion imaging (CT perfusion or MRI DWI-FLAIR mismatch) to confirm salvageable penumbra before proceeding.

IV alteplase window: onset within 4.5 hours. Standard thrombectomy window: within 6 hours. Beyond 6 hours, thrombectomy requires perfusion imaging (CT-P or DWI-FLAIR mismatch) to identify salvageable penumbra. Wake-up stroke uses last known well as the onset time.

Thrombolysis is contraindicated when the time of last known well exceeds 4.5 hours — this patient has a 9-hour window, ruling out tPA. Thrombectomy beyond 6 hours requires perfusion imaging selection before proceeding. Aspirin and stroke unit admission are appropriate initial management.

Correct. Neurological deterioration during or after alteplase infusion with a rising BP strongly suggests haemorrhagic transformation (symptomatic intracranial haemorrhage — sICH). The immediate actions are: (1) stop the alteplase infusion if still running; (2) urgent NCCT brain; (3) if confirmed — give cryoprecipitate (contains fibrinogen) to reverse fibrinolysis; also consider fresh frozen plasma and platelets if the fibrinogen is critically low. sICH occurs in approximately 6% of thrombolysed patients and is the most feared complication.

Symptomatic ICH complicates ~6% of alteplase cases. Hallmarks: neurological decline during/after infusion, BP surge. Immediate actions: stop infusion, urgent NCCT, cryoprecipitate (fibrinogen source) if confirmed.

Neurological deterioration during alteplase administration = haemorrhagic transformation until proven otherwise. Stop infusion, get urgent NCCT brain. If confirmed, cryoprecipitate to replace fibrinogen is the treatment. This is the most serious complication of thrombolysis.

Correct. IV alteplase is absolutely contraindicated when INR exceeds 1.7, regardless of the indication for anticoagulation. An INR of 2.8 is a hard exclusion criterion for thrombolysis because of the markedly increased risk of haemorrhagic transformation. Mechanical thrombectomy, however, is NOT contraindicated by elevated INR and may still be appropriate if large vessel occlusion is confirmed on CTA.

Contraindications to IV alteplase include: INR >1.7, platelet count <100,000, prior intracranial haemorrhage, active bleeding, recent major surgery within 14 days, blood glucose <50 or >400. Thrombectomy has fewer pharmacological exclusions.

INR >1.7 is an absolute contraindication to IV thrombolysis. Mechanical thrombectomy does NOT carry the same INR exclusion criterion and can still be considered if CTA confirms a large vessel occlusion.

Correct. The lateral medullary syndrome (Wallenberg syndrome) from PICA occlusion includes: ipsilateral Horner syndrome (descending sympathetics), ipsilateral cranial nerve V (facial pain/temperature), ipsilateral IX/X palsy (dysphagia, dysarthria, hoarseness), ipsilateral cerebellar ataxia, and contralateral spinothalamic loss in the limbs (crossed pattern). In a 40-year-old, vertebral artery dissection must be actively excluded with T1 fat-saturation MRI of the neck.

Lateral medullary (Wallenberg) syndrome = PICA territory. Key findings: crossed sensory loss (ipsilateral face, contralateral limbs), ipsilateral Horner, ipsilateral IX/X palsy, ipsilateral ataxia. In young patients, exclude vertebral artery dissection with T1 fat-sat MRI neck.

Wallenberg syndrome (lateral medullary — PICA territory): ipsilateral Horner, ipsilateral IX/X palsy (dysphagia/dysarthria), ipsilateral cerebellar ataxia, contralateral spinothalamic loss in limbs (crossed signs). In young patients, vertebral artery dissection is the most common cause.

Correct. Wernicke's aphasia: fluent speech with paraphasias and neologisms, severely impaired comprehension, and impaired repetition. The lesion is in the posterior superior temporal gyrus (Wernicke's area, Brodmann's area 22) in the dominant (left) hemisphere, supplied by the inferior division of the left MCA. The most dangerous clinical trap is confusing Wernicke's aphasia with delirium or confusion — the key distinction is that comprehension is selectively impaired and speech is fluent (not reduced as in delirium).

Aphasia classification: Broca (non-fluent, comprehension intact, repetition impaired), Wernicke (fluent, comprehension impaired, repetition impaired), Conduction (fluent, comprehension relatively intact, repetition severely impaired). Wernicke's aphasia is commonly mistaken for confusion.

Wernicke's aphasia: fluent, paraphasic, neologistic speech + severely impaired comprehension + impaired repetition = posterior temporal lobe (Wernicke's area). Broca's aphasia is non-fluent with intact comprehension. Conduction aphasia has intact fluency and comprehension but severely impaired repetition.

Correct. Upper motor neuron bladder (suprapontine lesion — e.g. stroke, brain tumour, high cervical myelopathy) causes detrusor hyperreflexia because the inhibitory cortical micturition centres are disrupted, but the sacral micturition reflex arc is intact. This produces urgency, frequency, and urge incontinence. In contrast, a lower motor neuron/peripheral nerve lesion (conus/cauda equina/pelvic nerve) causes detrusor areflexia with urinary retention and overflow.

Bladder dysfunction in neurological disease: UMN lesion (above pons/high cord) = detrusor hyperreflexia = urgency/urge incontinence. LMN lesion (conus/cauda equina/pelvic nerve) = detrusor areflexia = painless retention + overflow. Stroke commonly causes UMN bladder.

Upper motor neuron bladder = suprapontine lesion = detrusor hyperreflexia = urgency, frequency, urge incontinence. Lower motor neuron bladder = conus/cauda equina/peripheral = detrusor areflexia = retention with overflow.

Correct. Early mobilisation — beginning within 24-48 hours of stroke onset if medically stable — is the most evidence-supported principle in stroke rehabilitation. Early movement prevents DVT, aspiration pneumonia, and contractures, and exploits neuroplasticity during the critical early window. Rehabilitation continues for at least 12 months and may extend beyond, as neuroplasticity allows incremental gains. A multidisciplinary team (physiotherapy, occupational therapy, speech therapy, neuropsychology) is essential.

Stroke rehabilitation: begin within 24-48 hours if medically stable. Multidisciplinary (physiotherapy + OT + speech therapy + neuropsychology + dietitian). Continues for 12 months or beyond. Neuroplasticity supports ongoing recovery beyond 3 months.

Stroke rehabilitation begins within 24-48 hours of onset (if medically stable) and continues for 12 months or beyond. Neuroplasticity underpins recovery; early mobilisation is the single most evidence-supported principle. All disciplines — physiotherapy, OT, speech therapy — are equally important and begin simultaneously.

Correct. The ABCD2 score predicts 2-day stroke risk after TIA. Components: Age ≥60 (1), BP ≥140/90 (1), Clinical features — unilateral weakness (2) or speech without weakness (1), Duration 10-59 min (1) or ≥60 min (2), Diabetes (1). A score of 4-7 indicates high risk. Patients with ABCD2 ≥4 should be admitted or seen in a rapid TIA clinic (within 24 hours) with urgent brain imaging, carotid Doppler, and initiation of antiplatelet therapy (aspirin + clopidogrel dual antiplatelet for 21 days in non-cardioembolic TIA).

ABCD2 score for TIA risk stratification: Age ≥60 (1), BP ≥140/90 (1), Clinical (unilateral weakness 2, speech without motor 1), Duration 10-59 min (1) or ≥60 min (2), Diabetes (1). Score ≥4 = high risk = same-day assessment. Dual antiplatelet (aspirin+clopidogrel) for 21 days in non-cardioembolic TIA.

ABCD2 score 4-7 = high 48-hour stroke risk. Patients with ABCD2 ≥4 after TIA need admission or same-day TIA clinic assessment — not outpatient deferral. Dual antiplatelet therapy (aspirin + clopidogrel) for 21 days is now recommended for non-cardioembolic high-risk TIA.

Correct. Cerebellar haemorrhage with clot >3 cm causing fourth ventricular compression or hydrocephalus, with neurological deterioration, is the clearest surgical indication in haemorrhagic stroke. Posterior fossa decompression and clot evacuation can be life-saving and is the standard of care. EVD alone does not address the mass lesion and risks upward herniation. Alteplase is absolutely contraindicated in haemorrhagic stroke.

Surgical indications in ICH: (1) Cerebellar haemorrhage >3 cm + mass effect/deterioration = urgent posterior fossa surgery. (2) Lobar haemorrhage >30 mL within 1 cm of cortex + herniation risk. Basal ganglia and thalamic ICH: generally medical management. Brainstem ICH: surgery rarely beneficial.

Cerebellar haemorrhage >3 cm with mass effect and deteriorating consciousness = urgent surgical indication. Posterior fossa decompression and clot evacuation is the treatment of choice. EVD alone without clot evacuation risks upward transtentorial herniation. Alteplase is absolutely contraindicated.

Correct. Post-stroke counselling on driving and work: Indian Motor Vehicles Act restricts driving after stroke — typically a minimum of 1 month after a first-ever TIA/minor stroke (longer if any residual deficit or seizure). Return to work depends on the nature of the job (cognitive demand, physical demand), presence of residual cognitive or motor deficits, and optimisation of secondary prevention. Neuropsychological assessment may be required before returning to cognitively demanding work. Driving with persistent visual field defects is prohibited regardless of time elapsed.

Post-stroke counselling: driving deferred at least 1 month (Motor Vehicles Act, India); no driving if visual field defect persists. Return to work: assess cognitive and motor residua + job demands. Sexual activity can resume when medically stable (usually within weeks). Secondary prevention adherence is the priority counselling point.

Post-stroke driving restriction: defer for at least 1 month (longer if residual deficits or seizures). Return to work depends on residual deficits, cognitive function, and job demands. Neuropsychological evaluation is important for cognitively demanding roles. Secondary prevention must be optimised before any return to normal activities.

Correct. The 1-3-6-12 day rule for initiating anticoagulation in cardioembolic stroke: TIA = anticoagulate on day 1; mild stroke (NIHSS <8, small infarct) = day 3; moderate stroke (NIHSS 8-15, moderate infarct) = day 6; severe stroke (NIHSS >15, large infarct) = day 12. This balances early recurrence risk against haemorrhagic transformation risk. DOAC (e.g. apixaban, rivaroxaban) is preferred over warfarin for non-valvular AF. Infarct size >1/3 MCA territory increases haemorrhagic risk but is a relative, not absolute, contraindication to anticoagulation — timing is deferred, not permanently withheld.

Cardioembolic stroke anticoagulation timing (1-3-6-12 rule): TIA=day 1, mild NIHSS <8=day 3, moderate NIHSS 8-15=day 6, severe NIHSS >15=day 12. DOAC preferred over warfarin for non-valvular AF. Balance recurrence risk vs haemorrhagic transformation.

The 1-3-6-12 rule governs anticoagulation timing in cardioembolic stroke: TIA day 1, mild stroke day 3, moderate day 6, severe day 12. DOAC is preferred over warfarin for non-valvular AF. Large infarct does not permanently contraindicate anticoagulation — it delays initiation.

Correct. Acute stroke supportive care for oxygenation and glucose: (1) Supplemental oxygen is given ONLY if SpO2 <94% — routine oxygen in non-hypoxic stroke patients does NOT improve outcomes and may be harmful (IST-3, SO2S trials). (2) Blood glucose should be maintained between 4-11 mmol/L — both hyperglycaemia and hypoglycaemia worsen penumbral injury. Tight glucose control below 6 mmol/L risks hypoglycaemia which is independently harmful. These are standard AHA/ASA and ESO guidelines.

Acute stroke supportive care: O2 only if SpO2 <94% (not routinely). Glucose target 4-11 mmol/L. Temperature <37.5 C (treat fever). BP: permissive (up to 220/120) if no thrombolysis; <185/110 if thrombolysis given. Swallowing screen before oral intake.

Acute stroke oxygen: only if SpO2 <94% — routine O2 in non-hypoxic patients does not improve outcomes. Glucose target: 4-11 mmol/L — both hyperglycaemia (worsens penumbra) and hypoglycaemia (neuronal toxicity) must be avoided. Tight glucose <6 mmol/L risks harm from hypoglycaemia.