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Hemiplegia Long Case — Complete History Taking Format

MBBS Final Year Clinical Examination

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I. PATIENT PROFILE (Biodata)

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II. CHIEF COMPLAINTS

• Weakness of right upper and lower limb — X days/months
• Deviation of face to one side — X days
• Difficulty in speaking — X days
• Numbness/tingling of one half of body — X days

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III. HISTORY OF PRESENT ILLNESS (HoPI)

A. Onset — the most critical discriminating question

• Was the patient awake or asleep when symptoms started?
• Did symptoms develop suddenly (seconds/minutes) or gradually (hours/days)?
• Was weakness maximal at the very start, or did it worsen progressively?

B. Site and Distribution of Weakness

• Upper limb: Can you raise your hand above your head? (proximal — shoulder abductors, deltoid) | Can you button your shirt / pick up a coin? (distal — hand function)
• Lower limb: Can you get up from squatting / climb stairs? (proximal — hip flexors) | Any difficulty walking, foot drop? (distal)
• Face: Deviation of angle of mouth; drooling of food/saliva; difficulty chewing → lower facial palsy (UMN = forehead spared)
• UL > LL vs. LL > UL vs. equal: Helps localise the lesion
  • Internal capsule: arm and leg affected equally
  • Cortical: one region predominates

C. Accompanying Symptoms — Localisation Clues

• Speech disturbance — Ask: Is speech slurred (dysarthria)? Or difficulty finding words / understanding (aphasia)? → aphasia = dominant hemisphere cortical lesion
• Seizures at onset — cortical irritation
• Urinary/faecal incontinence — cortical (medial surface, paracentral lobule involvement) or severe acute event
• Confusion, altered consciousness at onset

• Hemisensory loss — tingling, numbness on the same side as weakness → internal capsule/thalamus
• Pain and temperature loss on opposite side from weakness → brainstem (crossed sensory)

• Diplopia (double vision) → oculomotor/abducens nerve involvement
• Vertigo and vomiting
• Dysphagia (difficulty swallowing), dysphonia (hoarse voice) → lower cranial nerves
• Facial sensation loss on ipsilateral side with contralateral limb weakness → crossed signs = brainstem

• Homonymous hemianopia (loss of half the visual field) — optic radiation/occipital cortex involvement
• Amaurosis fugax (transient monocular blindness) → carotid TIA

• Headache preceding or at onset? Thunderclap headache → subarachnoid haemorrhage; severe occipital headache → posterior fossa event
• Vomiting at onset → raised ICP, haemorrhage, posterior fossa
• Fever, neck stiffness → meningitis with vascular complications
• Trauma to head or neck prior to event → subdural haematoma or carotid dissection
• "Lucid interval" (brief recovery then deterioration) → extradural haematoma
• Palpitations / irregular heartbeat before the event → atrial fibrillation → cardioembolic stroke
• Recent cardiac procedure or MI → embolism

D. Progress of the Illness

• Static since onset (deficit maximal at start → embolic)
• Stepwise progression → thrombotic
• Rapid worsening → haemorrhagic
• Fluctuating → TIA or haemodynamic cause
• Gradual improvement → infarct with oedema resolving; or recovery

E. Current Status and Disability

• Can the patient walk independently, with support, or is bed-bound?
• Dominant or non-dominant side affected?
• Any bedsores, contractures (late presentations)?
• Bladder/bowel control?
• Speech — can they communicate?

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IV. PAST HISTORY

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V. DRUG AND TREATMENT HISTORY

• Anticoagulants (warfarin, NOACs) — relevant to haemorrhagic risk
• Oral contraceptive pills → stroke in young women
• Antiplatelets (aspirin, clopidogrel) — compliance?
• Antihypertensives — compliance
• Illicit drugs: cocaine, amphetamines → vasospasm, haemorrhage in young patients
• Thrombolytics given acutely?

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VI. PERSONAL HISTORY

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VII. MENSTRUAL AND OBSTETRIC HISTORY (Female patients)

• OCP use → prothrombotic
• Pregnancy / puerperium → cerebral venous sinus thrombosis (CVST) — presents with headache, focal deficits, seizures
• Pre-eclampsia / eclampsia

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VIII. FAMILY HISTORY

• Stroke or TIA in first-degree relatives (heritable vasculopathies, CADASIL, familial hypercholesterolaemia)
• Hypertension, diabetes, cardiac disease in family
• Hypercoagulable states (Protein C/S deficiency, Factor V Leiden)
• Sickle cell disease

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IX. SOCIOECONOMIC HISTORY

• Who supports the patient? (disability assessment)
• Living conditions (stairs, ground floor — affects rehabilitation)
• Financial capacity for medications and physiotherapy
• Caregiver availability

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X. REVIEW OF SYSTEMS (Systematic Enquiry)

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XI. SUMMARY STATEMENT (for presentation)

"Mr. X, a 58-year-old right-handed male with hypertension and type 2 diabetes, presented with sudden-onset weakness of the right upper and lower limbs associated with deviation of the angle of the mouth to the left and slurring of speech, occurring at 8 AM while at rest, reaching maximum deficit within minutes. There was no preceding headache, vomiting, loss of consciousness, or seizure. He gives a past history of a similar episode 2 years ago that resolved spontaneously in 4 hours. He is a chronic smoker and is non-compliant with his antihypertensives."

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XII. DIFFERENTIAL DIAGNOSIS TO KEEP IN MIND FROM HISTORY

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Key Tips for the Examination Hall

1. Always establish handedness first — determines which hemisphere is "dominant"
2. Onset timing is the single most important discriminator between stroke subtypes
3. Localise from history before examination: cortical (aphasia, seizure), capsular (pure motor), brainstem (crossed signs), cord (bilateral + level)
4. Always ask about TIA — a history of transient episodes that resolved spontaneously is a red flag
5. Risk factor history is examinable — hypertension, DM, AF, smoking, OCP are mandatory points
6. Do not miss Todd's paresis — seizure before weakness in a young patient
7. Social history matters — examiners ask about rehabilitation and disability

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