Create a detail case presentation with detail history and examination for final year MD General Medicine Resident in front of professor with explanation also mention viva questions with answers with standard books . Topic Hemiplegia- CVA and its localisation in detail

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Case Presentation: Hemiplegia due to Cerebrovascular Accident (CVA) — Clinical Localization

Format for MD General Medicine final-year presentation before the Unit Professor

HOW TO OPEN

"Good morning sir, I present a case of a 57-year-old right-handed male, farmer by occupation, resident of [X], admitted with a chief complaint of sudden onset weakness of the right upper and lower limb along with deviation of angle of mouth since 2 days, associated with difficulty in speech."

1. HISTORY

A. Demographic Data

Age, sex, occupation (relevant to functional disability and rehabilitation planning), handedness (crucial — determines hemisphere dominance for language, tested before localizing aphasia).

B. Chief Complaints (in chronological order)

Sudden weakness of right half of body – 2 days
Deviation of angle of mouth to the left – 2 days
Slurring/loss of speech – 2 days
± Headache, vomiting, giddiness, loss of consciousness, seizures

C. History of Presenting Illness

Elicit onset, evolution, and associated symptoms systematically — this is where localization begins.

Feature to ask	Why it matters
Mode of onset — sudden (seconds-minutes) vs stepwise vs gradual	Sudden = embolic/hemorrhagic; stepwise = thrombotic; gradual = tumor/chronic subdural
Activity at onset — sleep, straining, exertion	Hemorrhage often with exertion/straining/BP surge; thrombotic often on waking
Progression — improving, static, worsening	Worsening over hours suggests expanding hematoma or edema
Headache, vomiting, neck stiffness	Suggests hemorrhage/raised ICP/SAH
Loss of consciousness, seizures	Cortical/large lesion, hemorrhage, or herniation
Which side face + limb involved together?	Confirms UMN-type hemiplegia (corticospinal tract)
Speech disturbance — expressive vs receptive	Localizes to dominant hemisphere (Broca vs Wernicke area)
Vision — field defect, diplopia, transient monocular blindness (amaurosis fugax)	Amaurosis fugax localizes to ipsilateral internal carotid artery; homonymous hemianopia to optic radiation/occipital cortex
Vertigo, vomiting, diplopia, dysphagia, ataxia, crossed sensory loss	Suggests brainstem (vertebrobasilar) localization
Bladder/bowel involvement	If present, think of bilateral/parasagittal lesion or spinal cord as alternative
Sensory symptoms — numbness, tingling	Helps confirm sensorimotor stroke vs pure motor
Involuntary movements	Hemiballismus (subthalamic nucleus), tremor (thalamic/rubral)

D. Past History

Similar episodes in the past (recurrent TIA/stroke) with full recovery — suggests embolic source
Hypertension (most important risk factor, especially for deep lacunar and hemorrhagic stroke)
Diabetes mellitus
Ischemic heart disease / atrial fibrillation / valvular heart disease (cardioembolic source)
Smoking, alcohol
Past history of TB, seizure disorder
Drug history — anticoagulants, antiplatelets, oral contraceptives

E. Personal History

Diet, sleep, bowel/bladder, addictions (smoking — pack-years; alcohol quantify)

F. Family History

Stroke, hypertension, diabetes, IHD in first-degree relatives

G. Socioeconomic History

Relevant for rehabilitation, affordability of investigations/thrombolysis, and follow-up

2. GENERAL PHYSICAL EXAMINATION

Vitals: BP in both arms (mandatory — aortic dissection, subclavian steal), pulse (irregularly irregular pulse → AF → cardioembolic stroke), temperature, respiratory rate, SpO2
Pallor, icterus, cyanosis, clubbing, lymphadenopathy, edema
Carotid bruit on auscultation of neck — carotid stenosis
Cardiac auscultation — murmurs (mitral stenosis, endocarditis), arrhythmia
Fundus examination — hypertensive/diabetic retinopathy, papilledema
Look for tongue bite, bladder involvement (incontinence pointing to seizure or bilateral lesion)

3. NEUROLOGICAL EXAMINATION (systematic, as this decides localization)

A. Higher Mental Functions

Consciousness (GCS), orientation, attention
Handedness — establish dominance before assessing speech
Speech and language — fluency, comprehension, naming, repetition, reading, writing
- Nonfluent, effortful, agrammatic speech with intact comprehension but impaired repetition → Broca aphasia (posterior inferior frontal gyrus, dominant hemisphere, superior division MCA territory) — Bradley and Daroff's Neurology in Clinical Practice
- Fluent, paraphasic, meaningless speech with impaired comprehension → Wernicke aphasia (posterior superior temporal gyrus, inferior division MCA)
- Global aphasia (both impaired) → large dominant MCA stem territory infarct
Memory, calculation (Gerstmann syndrome: acalculia + agraphia + finger agnosia + right-left disorientation → dominant parietal/angular gyrus lesion)
Apraxia, agnosia, neglect (nondominant parietal lobe → anosognosia, hemi-inattention)

B. Cranial Nerves

Most important localizing step: look for UMN facial palsy (lower face weak, forehead spared, can close eye and wrinkle forehead) — this confirms the lesion is above the level of the facial nucleus in the pons (i.e., cortex, corona radiata, internal capsule, or cerebral peduncle) as opposed to LMN facial palsy (Bell's palsy) which would affect the whole side of the face.
Look for crossed cranial nerve findings — e.g., ipsilateral III nerve palsy with contralateral hemiplegia (Weber syndrome, midbrain), ipsilateral VI + VII nerve palsy with contralateral hemiplegia (Millard-Gubler/pontine), ipsilateral palatal/vocal cord/sensory loss on face with contralateral body sensory loss and ataxia (Wallenberg/lateral medullary syndrome). A crossed sign (cranial nerve on one side, limb on the other) always means brainstem localization, not hemisphere.
Tongue deviation (towards the weak side in UMN lesion — deviates away in some texts depending on convention; check protrusion direction toward the paretic side due to unopposed action)
Visual fields — homonymous hemianopia (optic radiation/occipital cortex — PCA territory), quadrantanopia (superior = temporal/Meyer's loop; inferior = parietal)

C. Motor System

Component	Finding in acute hemiplegia	Finding after few weeks (established UMN lesion)
Bulk	Normal initially	Mild disuse atrophy
Tone	Flaccid (cerebral shock/diaschisis)	Spasticity (clasp-knife, more in flexors of arm, extensors of leg)
Power	Grade using MRC scale 0-5 in all muscle groups of face, upper limb, lower limb, trunk	Pyramidal pattern weakness — extensors weaker in arm, flexors weaker in leg
Reflexes	Diminished initially	Exaggerated deep tendon reflexes, clonus
Plantar (Babinski)	Extensor plantar response	Extensor persists
Superficial reflexes	Absent abdominal/cremasteric reflex on the affected side	Same
Gait (once ambulant)	—	Hemiplegic/circumduction gait

Test pronator drift, and pyramidal drift of the outstretched arms — earliest and most sensitive sign of mild hemiparesis.

D. Sensory System

Test all modalities (pain, temperature, touch, vibration, proprioception, cortical sensations — two-point discrimination, stereognosis, graphesthesia).

Pure hemisensory loss without weakness → thalamic (posteroventral nucleus, PCA thalamogeniculate territory)
Loss of discriminative sensation with crossed pain/temperature loss → brainstem
Cortical sensory loss (astereognosis, agraphesthesia with primary modalities intact) → parietal cortex

E. Cerebellar signs

Look for ipsilateral ataxia (crossed cerebellar signs with contralateral hemiparesis point to brainstem — e.g., pontine or midbrain lesion affecting cerebellar peduncles/dentatorubrothalamic tract).

F. Autonomic/Others

Horner syndrome (ptosis, miosis, anhidrosis) — if present with crossed body findings, strongly localizes to lateral brainstem (Wallenberg) rather than hemisphere.

G. Neck and vascular examination

Carotid pulsations, bruit, signs of peripheral vascular disease.

4. LOCALIZATION OF HEMIPLEGIA — LEVEL BY LEVEL

(This is the core of the viva — the professor will test this heavily)

As stated in Adams and Victor's Principles of Neurology, 12th ed.: "Hemiplegia is the most frequent form of paralysis. With rare exceptions, this pattern of paralysis is a result of involvement of the corticospinal pathways. The site or level of the lesion — cerebral cortex, corona radiata, capsule, brainstem, or spinal cord — can usually be deduced from the associated neurologic findings." (Adams and Victor's Principles of Neurology, p. 77)

Level	Key distinguishing features
Cerebral cortex	Weakness restricted to face+arm OR leg alone (monoparesis pattern) rather than uniform hemiplegia because the motor homunculus is spread over a large area; associated cortical signs — seizures (focal), aphasia (dominant), neglect (nondominant), cortical sensory loss, gaze deviation toward the lesion
Corona radiata / Internal capsule	Dense, uniform hemiplegia of face, arm and leg equally (fibers are tightly packed in the posterior limb) — "capsular hemiplegia"; no cortical signs (no aphasia, no seizures, no cortical sensory loss) unless capsular genu with pure motor lacunar syndrome; may have associated hemisensory loss if thalamus/posterior limb involved
Brainstem	Crossed findings — ipsilateral cranial nerve palsy + contralateral hemiplegia; internuclear ophthalmoplegia, Horner's, palatal/pharyngeal involvement, nystagmus, ataxia
— Midbrain	Ipsilateral III nerve palsy + contralateral hemiplegia (Weber syndrome — cerebral peduncle) or + contralateral ataxia/tremor (Claude/Benedikt syndrome — red nucleus)
— Pons	Ipsilateral VI and/or VII nerve palsy + contralateral hemiplegia (Millard-Gubler / Foville syndrome); bilateral lesion → locked-in syndrome
— Medulla	Ipsilateral XII nerve palsy (tongue weakness) + contralateral hemiplegia sparing face (medial medullary syndrome); Wallenberg (lateral medullary) syndrome gives crossed sensory loss + ipsilateral ataxia/Horner's but classically no limb weakness
Spinal cord (cervical, above C4)	Hemiplegia (Brown-Séquard pattern) with ipsilateral loss of proprioception/vibration and contralateral loss of pain/temperature a couple of segments below the lesion, sparing the face, often with a sensory/motor level and bladder involvement

5. VASCULAR TERRITORY CORRELATION (arterial localization)

Artery	Clinical Syndrome
MCA (stem/M1)	Dense contralateral hemiplegia + hemianesthesia + homonymous hemianopia + gaze deviation toward the lesion; global aphasia if dominant, hemineglect if non-dominant
MCA superior division	Face and arm weakness > leg; Broca aphasia (dominant); impaired prosody (non-dominant)
MCA inferior division	Wernicke aphasia (dominant); behavioral disturbance (non-dominant); homonymous hemianopia/quadrantanopia
MCA lenticulostriate (deep) branches	Pure motor hemiparesis (internal capsule) — classic lacunar-type picture even from a large-vessel source
ACA	Contralateral leg weakness > arm (face spared), urinary incontinence, abulia/apathy (frontal), grasp/sucking reflexes; if bilateral — akinetic mutism
PCA	Contralateral homonymous hemianopia with macular sparing (occipital cortex); thalamic syndrome (contralateral hemisensory loss ± later severe dysesthetic pain — Déjérine-Roussy syndrome) if thalamoperforators involved; Weber syndrome if P1 perforators to midbrain
Basilar artery / vertebrobasilar	Bilateral long tract signs, cranial nerve findings, locked-in syndrome, coma, "crossed" brainstem syndromes
Lacunar (small penetrating vessels, usually hypertensive)	Pure motor hemiparesis, pure sensory stroke, sensorimotor stroke, ataxic hemiparesis, dysarthria-clumsy hand syndrome — no cortical signs (Harrison's Principles of Internal Medicine, 22e; Adams and Victor's Principles of Neurology, 12e)

Harrison's summarizes: "A careful history and neurologic examination can often localize the region of brain dysfunction; if this region corresponds to an arterial distribution, the possible causes responsible for the syndrome can be narrowed." (Harrison's Principles of Internal Medicine, 22e, Ch. 437 — Stroke Syndromes)

6. CLINICAL DIAGNOSIS FORMULATION (as presented to the professor)

"Sir, based on the history of sudden onset of dense right-sided hemiplegia with UMN facial palsy, non-fluent (Broca-type) aphasia with preserved comprehension, and no cortical sensory/visual field deficit, I localize the lesion to the left internal capsule / left MCA (superior division) territory, most likely ischemic in nature given the stepwise onset without severe headache or loss of consciousness, in a patient with long-standing hypertension. I would like to confirm this with a non-contrast CT brain followed by MRI with diffusion-weighted imaging, and evaluate for cardioembolic and large-vessel sources with ECG, echocardiography, and carotid Doppler."

7. INVESTIGATIONS TO BE PRESENTED

NCCT brain — rule out hemorrhage first (mandatory before thrombolysis)
MRI brain with DWI/ADC — most sensitive for acute infarct localization
MR/CT angiography — vessel occlusion, stenosis
Carotid Doppler
ECG, 24-hour Holter — atrial fibrillation
2D-Echo — cardioembolic source, valvular disease, LV clot
Blood sugar, lipid profile, renal function, coagulation profile, HbA1c
NIHSS score at admission — used for severity grading and thrombolysis decision (Bradley and Daroff's Neurology in Clinical Practice, Box 54.1: components include level of consciousness, gaze, visual fields, facial palsy, motor arm/leg, ataxia, sensory, language, dysarthria, neglect; score 0-1 normal, ≥21 severe stroke)

8. VIVA QUESTIONS WITH ANSWERS (Standard Textbook References)

Q1. Define hemiplegia. What is the difference between hemiplegia, hemiparesis, and paraplegia? A. Hemiplegia is complete paralysis of one half of the body (face, arm, and leg on the same side) due to a corticospinal tract lesion; hemiparesis is partial/incomplete weakness of the same distribution. Paraplegia refers to paralysis of both lower limbs, typically from a spinal cord lesion. — Adams and Victor's Principles of Neurology, 12th ed.

Q2. What are the causes of hemiplegia? A. Vascular (infarct, hemorrhage — commonest), space-occupying lesion (tumor, abscess), trauma, demyelination (MS), infective (encephalitis, tuberculoma), and, rarely, psychogenic/hysterical hemiplegia (which shows non-organic patterns like give-way weakness, Hoover's sign positive, normal reflexes). — Bradley and Daroff's Neurology in Clinical Practice (chapter on pitfalls in differential diagnosis of hemiplegia)

Q3. How do you clinically differentiate an UMN facial palsy from LMN facial palsy? A. In UMN lesions, the forehead and orbicularis oculi are spared (bilateral cortical innervation to the upper face) so the patient can wrinkle the forehead and close the eye, while the lower face is weak. In LMN (Bell's) palsy, the entire half of the face including the forehead is weak.

Q4. How will you localize whether the lesion is cortical, capsular, or brainstem in a patient with hemiplegia? A.

Cortical: unequal involvement of face/arm/leg, cortical signs (aphasia, seizure, cortical sensory loss, neglect)
Capsular: dense, equal involvement of face, arm and leg; no cortical signs
Brainstem: crossed sign — ipsilateral cranial nerve palsy with contralateral hemiplegia (Adams and Victor's Principles of Neurology, 12th ed.)

Q5. What is a lacunar stroke and name the classic lacunar syndromes. A. Small-vessel occlusive infarcts (usually <1.5-2 cm) in the deep penetrating branches (lenticulostriate, thalamoperforate, pontine perforators), typically due to chronic hypertension/lipohyalinosis or small-vessel atherosclerosis. Classic syndromes: pure motor hemiparesis (internal capsule/pons), pure sensory stroke (thalamus), sensorimotor stroke, ataxic hemiparesis, and dysarthria-clumsy hand syndrome. No cortical signs. — Harrison's Principles of Internal Medicine, 22e, Table "Lacunar Syndromes"; Adams and Victor's Principles of Neurology, 12th ed.

Q6. What is Weber syndrome? Where is the lesion? A. Ipsilateral third cranial nerve palsy with contralateral hemiplegia, due to a lesion in the midbrain cerebral peduncle involving the exiting fascicles of CN III and the corticospinal tract (typically due to occlusion of the paramedian branches of the posterior cerebral artery/P1 segment). — Harrison's Principles of Internal Medicine, 22e; Bradley and Daroff's Neurology in Clinical Practice

Q7. What is Millard-Gubler syndrome? A. Ipsilateral VI and VII cranial nerve palsy with contralateral hemiplegia due to a ventral pontine lesion involving the abducens and facial nerve fascicles along with the corticospinal tract, usually from basilar artery perforator occlusion.

Q8. What is Wallenberg syndrome (lateral medullary syndrome)? Does it cause hemiplegia? A. Occlusion of the posterior inferior cerebellar artery (PICA) causes ipsilateral facial pain/temperature loss, ipsilateral Horner syndrome, ipsilateral ataxia, dysphagia, and hoarseness (IX, X involvement), with contralateral loss of pain and temperature over the body. Classically it spares the corticospinal tract, so there is no hemiplegia — this is an important distinguishing point in viva. — Bradley and Daroff's Neurology in Clinical Practice, Ch. 21

Q9. What is locked-in syndrome? A. Bilateral lesion of the ventral pons (basis pontis), usually due to basilar artery thrombosis, causing quadriplegia and loss of speech/facial movement with preserved consciousness and vertical eye movements/blinking because the reticular activating system is spared. — Bradley and Daroff's Neurology in Clinical Practice

Q10. Differentiate Broca's aphasia from Wernicke's aphasia. How does this help localize a stroke? A. Broca aphasia: non-fluent, effortful, telegraphic speech, impaired repetition, but relatively preserved comprehension; localizes to the posterior inferior frontal gyrus (dominant hemisphere), typically superior division MCA territory, and is usually associated with right hemiparesis. Wernicke aphasia: fluent but paraphasic/meaningless speech with impaired comprehension and repetition; localizes to posterior superior temporal gyrus, inferior division MCA territory, often without hemiparesis. — Bradley and Daroff's Neurology in Clinical Practice, Ch. 13 (Aphasia)

Q11. What is Gerstmann syndrome? A. Finger agnosia, acalculia, right-left disorientation, and agraphia — seen with lesions of the dominant parietal lobe (angular gyrus), typically in the territory of the inferior division of the MCA. — Harrison's Principles of Internal Medicine, 22e

Q12. What is the difference between anterior and posterior circulation stroke clinically? A. Anterior circulation (ICA, MCA, ACA) — hemiplegia, hemisensory loss, aphasia/neglect, homonymous hemianopia, monocular symptoms (amaurosis fugax). Posterior circulation (vertebrobasilar, PCA) — vertigo, diplopia, dysarthria, dysphagia, ataxia, bilateral or crossed signs, cortical blindness, drop attacks.

Q13. What is the ABCD2/NIHSS score and its clinical use? A. NIHSS (National Institutes of Health Stroke Scale) grades stroke severity from 0 (normal) to >20 (severe) based on 11 domains — consciousness, gaze, visual fields, facial palsy, motor arm/leg, limb ataxia, sensory, language, dysarthria, and neglect. It guides thrombolysis eligibility and prognosis. — Bradley and Daroff's Neurology in Clinical Practice, Box 54.1

Q14. What is the golden window for thrombolysis in acute ischemic stroke? A. IV recombinant tissue plasminogen activator (rtPA/alteplase) within 4.5 hours of symptom onset (extendable in select cases); mechanical thrombectomy for large vessel occlusion up to 24 hours in selected patients based on perfusion imaging. — Harrison's Principles of Internal Medicine, 22e

Q15. Why is CT scan preferred over MRI as the first imaging in acute stroke? A. CT is rapid, widely available, and most importantly is highly sensitive for detecting acute hemorrhage, which must be excluded before giving thrombolytics; MRI-DWI is more sensitive for early ischemic changes but is slower and less universally available in the acute emergency setting. — Harrison's Principles of Internal Medicine, 22e

Q16. What is pseudobulbar palsy and how does it differ from bulbar palsy? A. Pseudobulbar palsy results from bilateral upper motor neuron (corticobulbar) lesions above the medulla, causing dysarthria, dysphagia, bilateral facial weakness, and emotional lability (pathological laughing/crying), with exaggerated jaw jerk and gag reflex. Bulbar palsy is due to lower motor neuron involvement of cranial nerve nuclei (IX-XII) in the medulla itself, with wasted, fasciculating tongue and absent/reduced reflexes. — Bradley and Daroff's Neurology in Clinical Practice

Q17. What is stroke recrudescence? A. Re-emergence of a prior stroke's focal deficit (e.g., old hemiparesis) triggered by a systemic metabolic stressor such as infection, fever, or hypoglycemia, without a new vascular event; it resolves once the underlying trigger is treated. — Harrison's Principles of Internal Medicine, 22e

Q18. How would you clinically differentiate an organic from a psychogenic (hysterical) hemiplegia? A. Psychogenic hemiplegia shows inconsistent/give-way weakness, normal tone and reflexes, no true Babinski sign, positive Hoover's sign (weak hip extension on the "paralyzed" side normalizes when the patient is asked to flex the contralateral hip against resistance), and no anatomical pattern corresponding to a vascular territory. — Bradley and Daroff's Neurology in Clinical Practice

Q19. What is the significance of amaurosis fugax? A. Transient monocular visual loss (often curtain-like) lasting 1-5 minutes, due to transient ischemia of the retina/optic nerve; localizes to the ipsilateral internal carotid artery and indicates significant carotid disease as a stroke risk factor. — Bradley and Daroff's Neurology in Clinical Practice, Ch. 65

Q20. What secondary prevention would you advise after ischemic stroke? A. Antiplatelet therapy (aspirin/clopidogrel), statins, strict BP and glycemic control, anticoagulation if cardioembolic source (e.g., AF), carotid endarterectomy/stenting if significant symptomatic carotid stenosis, lifestyle modification (smoking cessation), and structured physiotherapy/rehabilitation.

Key Standard Textbooks to Cite/Carry for This Case

Harrison's Principles of Internal Medicine, 22nd ed. — Chapter on Stroke Syndromes (primary for general medicine viva)
Adams and Victor's Principles of Neurology, 12th ed. — Chapter on Hemiplegia/Monoplegia and MCA Stroke Syndromes
Bradley and Daroff's Neurology in Clinical Practice — Chapters on Aphasia, Brainstem Stroke Syndromes, NIHSS
Localization in Clinical Neurology (Brazis), 8th ed. — Vascular anatomy and localization correlation
Hutchison's Clinical Methods — for detailed bedside history and examination technique (standard for undergraduate/postgraduate clinical exams in India)

If you'd like, I can convert this into a formatted Word document (.docx) or PowerPoint slide deck (.pptx) with tables/diagrams for your actual presentation before the professor — just let me know which format you prefer.

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