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Neuroscience-III — Clinical Long & Short Cases Copy

FINAL YEAR MBBS  |  KMU CURRICULUM  |  AIM CLINICAL LEARNING
🩺 AIM LONG CASE 02

Cerebrovascular Accident — Ischemic Stroke

Neuroscience Module | General Medicine

A structured whole-patient approach to acute focal neurological deficits, neurological examination, NIHSS assessment, neuroimaging interpretation, ischemic stroke management and secondary prevention.

01. Long Case Title

Long Case 02 — Evaluation of a Patient Presenting with Acute Hemiparesis and Speech Difficulty

Related AIM Topic: Cerebrovascular Disorders — Ischemic Stroke, Hemorrhagic Stroke & Subarachnoid Hemorrhage

02. Patient Scenario

A 68-year-old right-handed man is brought to the emergency department by his family because of sudden weakness of the right arm and leg associated with difficulty speaking.

His wife reports that he was speaking normally while having breakfast approximately 90 minutes earlier, when he suddenly dropped his cup and became unable to express himself properly.

He has a history of hypertension and type 2 diabetes mellitus. His symptoms have persisted since onset.

03. Student Task

The student should:

  • Obtain a focused history of sudden focal neurological deficits, establishing the exact time last known well.
  • Assess relevant cerebrovascular risk factors and alternative diagnoses.
  • Perform an appropriate general and neurological examination.
  • Assess consciousness using the Glasgow Coma Scale and stroke severity using the NIH Stroke Scale.
  • Recognize hemiparesis and aphasia and identify their likely neurological localization.
  • Interpret relevant CT and MRI brain findings.
  • Formulate differential diagnoses and establish the most likely diagnosis.
  • Discuss emergency and subsequent management of ischemic stroke.
  • Identify important complications and counsel regarding rehabilitation and secondary prevention.

04. Relevant History

A. Presenting Complaints

  • Sudden weakness of the right upper and lower limbs — approximately 90 minutes.
  • Difficulty producing speech — approximately 90 minutes.
  • Deviation of the mouth towards the left, noticed by the family.

B. History of Presenting Illness

The patient was well earlier that morning. At approximately 8:00 AM, while having breakfast, he suddenly lost grip of a cup with his right hand. His wife noticed that his speech became limited and effortful. He subsequently had difficulty standing because of right leg weakness.

There was no preceding trauma, convulsion or loss of consciousness. The neurological deficits were maximal at onset and persisted until arrival at the emergency department at approximately 9:30 AM.

History Clue Clinical Significance
Sudden onset of weakness Strongly suggests an acute vascular neurological event.
Right-sided arm and leg weakness Suggests involvement of left-sided motor pathways above the pyramidal decussation.
Difficulty producing language Suggests involvement of the dominant cerebral hemisphere.
Symptoms lasting longer than one hour and persisting Raises concern for an evolving stroke rather than a fully resolved transient episode.
Exact last-known-well time Essential for assessing eligibility for time-sensitive reperfusion treatment.
Hypertension and diabetes Important vascular risk factors.

C. Important Associated Symptoms and Negative History

  • Headache: No sudden severe headache, which makes subarachnoid hemorrhage less likely, although hemorrhage still requires imaging exclusion.
  • Consciousness: No initial loss of consciousness.
  • Seizures: No witnessed seizure activity or postictal confusion.
  • Vision: No reported sudden blindness or diplopia.
  • Swallowing: Wife reports mild coughing when he attempted to drink water after symptom onset, raising concern for dysphagia.
  • Trauma: No recent head injury.
  • Previous episodes: No known previous stroke or transient ischemic attack.

D. Past Medical and Medication History

He has had hypertension for 12 years and type 2 diabetes for eight years, with inconsistent follow-up. He takes antihypertensive and oral antidiabetic medication but occasionally misses doses.

He has no known history of atrial fibrillation. The student should specifically ask about anticoagulant or antiplatelet use, previous bleeding, recent surgery and other factors affecting acute treatment eligibility.

E. Family and Social History

The patient is a retired shopkeeper who previously managed all personal activities independently. He has a history of cigarette smoking but stopped five years ago. His father had a stroke in older age.

F. Functional and Psychosocial History

Before this event, he walked independently, communicated normally and managed his daily activities without assistance. His family is concerned about whether he will recover movement, speech and independence.

🔎 Clinical Clue

Sudden onset of a persistent focal neurological deficit is a stroke emergency. The exact last-known-well time must be established immediately, as it may determine eligibility for reperfusion therapy.

05. Physical Examination

A. General and Initial Assessment

The patient is conscious, alert and cooperative but struggles to express words. The airway is patent and breathing is spontaneous. Neurological assessment proceeds alongside urgent stabilization and imaging arrangements.

Parameter Representative Finding
Blood pressure 174/96 mmHg
Pulse 88/min, regular
Respiratory rate 18/min
Oxygen saturation 97% on room air
Capillary blood glucose 168 mg/dL
Temperature 36.8°C

B. Glasgow Coma Scale

The patient opens his eyes spontaneously, obeys commands and is alert, but his verbal response is limited by aphasia.

  • Eye opening: E4 — spontaneous.
  • Motor response: M6 — obeys commands.
  • Verbal response: V4 — impaired conversational responses in the setting of aphasia.
  • Documented GCS: E4 V4 M6 = 14/15, with a clear note that aphasia limits verbal assessment.

Important: GCS is not a language assessment. Aphasia may affect the verbal component even in an otherwise alert patient; document the limitation rather than interpreting the total as proof of reduced consciousness.

C. Focused Neurological Examination

  • Higher functions: Alert and oriented by appropriate non-verbal responses; speech is non-fluent, with impaired word production and relatively preserved comprehension of simple commands.
  • Cranial nerves: Right lower facial weakness with preserved forehead movement, suggesting a central facial palsy.
  • Motor system: Right upper limb power 2/5 and right lower limb power 3/5; left-sided power 5/5.
  • Tone: Reduced on the affected side in the acute stage.
  • Reflexes: Right plantar response is extensor; left plantar response is flexor.
  • Sensation: Mild reduction of sensation over the right side.
  • Coordination and gait: Gait is not tested because of acute weakness and fall risk.

D. NIH Stroke Scale — Clinical Severity Assessment

The NIHSS systematically assesses consciousness, gaze, visual fields, facial movement, limb motor function, ataxia, sensation, language, dysarthria and neglect.

NIHSS Component Finding Score
1a–1c. Level of consciousness, questions and commands Alert; answers one orientation question; follows both commands 1
2–3. Gaze and visual fields No abnormality 0
4. Facial palsy Right lower facial weakness 2
5a. Left arm No drift 0
5b. Right arm Some effort against gravity, cannot maintain elevation 2
6a. Left leg No drift 0
6b. Right leg Drift to bed with some antigravity effort 2
7. Limb ataxia No demonstrable ataxia independent of weakness 0
8. Sensory Mild right-sided sensory reduction 1
9. Best language Moderate expressive aphasia 1
10. Dysarthria No separate dysarthria 0
11. Extinction/inattention No neglect 0
TOTAL NIHSS 9

Interpretation: NIHSS 9 indicates a clinically significant stroke with moderate neurological deficits. NIHSS is used to quantify baseline severity and monitor neurological change; the score does not replace imaging or assessment of treatment eligibility.

🩺 Important Examination Finding

Right hemiparesis, right central facial weakness and expressive aphasia suggest a lesion in the dominant left cerebral hemisphere, most likely involving the left middle cerebral artery territory.

06. Clinical Problem Representation

A 68-year-old right-handed man with hypertension and diabetes presents within 90 minutes of sudden-onset, persistent right hemiparesis, right central facial weakness and expressive aphasia. He is alert, has no severe headache or preceding seizure and has an NIHSS score of 9.

Main Clinical Problem

Acute focal neurological deficit strongly suggestive of stroke involving the dominant left cerebral hemisphere, requiring immediate neuroimaging to distinguish ischemic from hemorrhagic stroke and determine reperfusion eligibility.

07. Differential Diagnosis

Differential Supporting Findings Features Against / Distinguishing Tests
Acute ischemic stroke Sudden persistent focal deficit with vascular risk factors and dominant hemisphere signs. No major contradictory feature; confirmation requires clinical assessment and imaging.
Intracerebral hemorrhage Can present with sudden hemiparesis and aphasia, particularly in hypertension. No severe headache or reduced consciousness; urgent non-contrast CT is required to exclude hemorrhage.
Transient ischemic attack Acute focal neurological symptoms of vascular origin. Deficits remain persistent; subsequent imaging can demonstrate infarction.
Postictal Todd paresis Can cause temporary unilateral weakness and speech disturbance after a seizure. No witnessed seizure or postictal state; neuroimaging remains essential.
Hypoglycemia Diabetes treatment can cause stroke-like neurological deficits. Bedside blood glucose is not low.

Clinical priority: Hemorrhagic and ischemic stroke cannot be reliably distinguished on symptoms alone. Urgent non-contrast CT brain is necessary.

08. Investigations and Interpretation

A. Immediate Investigations

Test Why Requested Representative Result / Interpretation
Bedside glucose Exclude hypoglycemia, an important stroke mimic. 168 mg/dL; hypoglycemia excluded.
Non-contrast CT brain Urgently exclude intracranial hemorrhage and assess early ischemic changes. No acute hemorrhage; subtle loss of left insular cortical definition consistent with early ischemia.
ECG Detect atrial fibrillation, acute cardiac abnormalities or another embolic risk. Sinus rhythm, 88/min; paroxysmal atrial fibrillation is not excluded by one ECG.
Full blood count Assess haemoglobin and platelets before treatment decisions. Platelets 230 × 10⁹/L, Hb 14 g/dL.
PT/INR and aPTT Identify clinically relevant coagulation abnormalities, particularly when anticoagulant use is possible. INR 1.0, aPTT normal.
Renal function/electrolytes Assess general condition and guide contrast imaging and medication selection. No clinically significant abnormality.

B. Neuroimaging and Vascular Assessment

Investigation Reason Case Finding / Meaning
CT angiography of head and neck Identify large-vessel occlusion and evaluate eligibility for thrombectomy. No proximal large-vessel occlusion requiring mechanical thrombectomy; distal left MCA branch disease may be present.
MRI brain with diffusion-weighted imaging Demonstrate acute cerebral infarction when clinically indicated. Restricted diffusion in the left frontal-insular MCA territory confirms acute ischemic infarction.
Carotid vascular imaging Identify relevant extracranial carotid stenosis as a potential cause. No severe symptomatic carotid stenosis.

Imaging interpretation: An early CT may be normal or show subtle ischemic changes. Acute ischemia is often more conspicuous on diffusion-weighted MRI. In a patient within a reperfusion window, MRI must not unnecessarily delay treatment. CT angiography identifies large-vessel occlusion and informs endovascular treatment decisions.

C. Underlying Cause and Secondary Prevention Assessment

  • Lipid profile: LDL cholesterol 145 mg/dL — supports the need for intensive lipid management.
  • HbA1c: 8.1% — indicates suboptimal longer-term diabetes control.
  • Cardiac rhythm monitoring: Used to detect intermittent atrial fibrillation not identified on the initial ECG.
  • Echocardiography: Considered where a cardiac embolic source is suspected or where the result would affect management.
💡 Clinical Reasoning

Sudden right hemiparesis with expressive aphasia localizes to the dominant left cerebral hemisphere. Absence of hemorrhage on CT, together with subsequent restricted diffusion in the left MCA territory, supports acute ischemic stroke. Early neuroimaging determines safe reperfusion decisions.

09. Final Diagnosis

Acute Ischemic Stroke — Dominant Left Middle Cerebral Artery Territory

Presenting with right hemiparesis, right central facial weakness, expressive aphasia and clinically significant neurological impairment (NIHSS 9), in a patient with hypertension and diabetes mellitus.

The clinical diagnosis is supported by acute focal neurological findings and corresponding neuroimaging. The precise stroke mechanism requires etiological evaluation.

10. Management

A. Immediate Priorities — Acute Stroke Pathway

  • Activate the acute stroke team/pathway immediately.
  • Assess airway, breathing, circulation, oxygen saturation, consciousness and capillary blood glucose.
  • Establish exact time last known well and determine neurological deficit severity.
  • Obtain urgent non-contrast CT brain to exclude intracranial hemorrhage.
  • Perform vascular imaging where indicated to assess for large-vessel occlusion.
  • Establish IV access, review medications and evaluate contraindications to reperfusion treatment.

B. Reperfusion Treatment

Intravenous thrombolysis: In eligible patients with disabling ischemic stroke presenting within the appropriate treatment window, urgent IV thrombolysis may improve functional recovery. Treatment eligibility depends on imaging, time since onset, blood pressure, bleeding risk, anticoagulant exposure and other clinical criteria.

In this case, the patient presents approximately 90 minutes after onset, with disabling aphasia and hemiparesis, no hemorrhage on CT and blood pressure below the usual pre-thrombolysis threshold. He is therefore a candidate for urgent formal thrombolysis eligibility assessment.

Mechanical thrombectomy: Consider for selected patients with an appropriate intracranial large-vessel occlusion, with eligibility determined by vascular imaging, timing and clinical assessment. This patient’s CTA does not demonstrate a suitable proximal target.

⚠️ Critical Reperfusion Safety

Do not administer thrombolytic treatment until intracranial hemorrhage and important contraindications have been excluded. Blood pressure and neurological status must be closely monitored. Antiplatelet therapy is generally withheld for the first 24 hours after IV thrombolysis, pending follow-up imaging to exclude hemorrhage.

C. Supportive Management

  • Stroke unit care: Admit to an organized stroke unit for neurological and medical monitoring.
  • Oxygen: Provide supplemental oxygen if hypoxemic; routine oxygen is unnecessary with normal saturation.
  • Blood pressure: Follow the appropriate acute stroke treatment pathway; avoid unnecessary rapid reduction because cerebral perfusion may be compromised.
  • Glucose: Avoid hypoglycemia and marked hyperglycemia.
  • Temperature: Identify and treat fever and infection.
  • Swallowing: Keep the patient nil by mouth until an appropriate swallowing screen is completed.
  • Hydration: Maintain appropriate fluid balance and avoid dehydration.

D. Antithrombotic and Vascular Prevention

Antiplatelet therapy: Aspirin is generally initiated after hemorrhage has been excluded in patients not receiving IV thrombolysis. For patients receiving thrombolysis, antiplatelets are deferred until appropriate follow-up imaging, usually after 24 hours, confirms no intracranial hemorrhage.

Statin treatment: High-intensity statin therapy is generally appropriate for secondary prevention in atherosclerotic ischemic stroke, with treatment individualized to the stroke mechanism and patient.

Anticoagulation: If atrial fibrillation or another cardioembolic indication is subsequently confirmed, long-term anticoagulation may be required. It is not started automatically for every ischemic stroke, and timing depends on infarct characteristics and bleeding risk.

E. Treatment of Underlying Risk Factors

  • Optimize long-term blood pressure control after the acute phase.
  • Improve diabetes management and follow-up.
  • Treat dyslipidemia and assess atherosclerotic risk.
  • Maintain smoking cessation and address physical inactivity.
  • Investigate potential atrial fibrillation or significant carotid disease when indicated.

F. Rehabilitation

  • Physiotherapy: Improve muscle strength, posture, transfers and walking.
  • Occupational therapy: Restore functional independence and adapt daily activities.
  • Speech and language therapy: Address aphasia and communication difficulties.
  • Swallowing rehabilitation: Reduce aspiration risk and support safe nutrition.
  • Psychological support: Identify depression, frustration and adjustment difficulties after stroke.

G. Monitoring and Prevention of Complications

Monitor neurological status, consciousness, blood pressure, glucose and evidence of hemorrhagic transformation or cerebral swelling. Prevent aspiration, pressure injury, falls, venous thromboembolism and complications of immobility through appropriate stroke-unit care.

H. Follow-Up

Arrange stroke and rehabilitation follow-up to review neurological recovery, swallowing and speech, functional independence, antithrombotic treatment, vascular risk control, medication adherence and caregiver needs.

11. Complications and Red Flags

Important Complications

  • Cerebral edema: Can produce neurological deterioration and raised intracranial pressure, particularly with a large infarction.
  • Hemorrhagic transformation: Bleeding into an ischemic infarct may cause deterioration.
  • Aspiration pneumonia: May develop due to impaired swallowing.
  • Deep vein thrombosis: Increased risk with immobility.
  • Pressure injuries and contractures: Related to prolonged immobility.
  • Post-stroke seizures: May occur, particularly with cortical involvement.
  • Persistent disability: Hemiparesis, aphasia and impaired activities of daily living.
  • Post-stroke depression: Can interfere with rehabilitation and quality of life.
  • Recurrent stroke: Risk remains elevated without secondary prevention.
⚠️ RED FLAGS — IMMEDIATE REASSESSMENT

  • Sudden deterioration in neurological deficits.
  • Reduced consciousness or new severe headache and vomiting.
  • New seizures.
  • Respiratory distress or suspected aspiration.
  • New focal deficits suggesting recurrent stroke.
  • Clinical deterioration following thrombolysis suggesting intracranial hemorrhage.

Urgent clinical evaluation and repeat brain imaging may be necessary to identify hemorrhage, edema, recurrent ischemia or another acute complication.

12. Patient Counselling and Follow-Up

A. Explanation of the Condition

Explain that the patient has experienced an ischemic stroke caused by interruption of blood supply to part of the brain. The resulting injury explains his right-sided weakness and difficulty producing language.

B. Recovery and Prognosis

Explain that recovery varies according to the location and extent of the stroke, initial neurological severity, complications and response to rehabilitation. Improvement may occur over weeks and months, but complete recovery cannot be guaranteed.

C. Medication Adherence

Emphasize regular use of prescribed antithrombotic therapy, statins and medication for hypertension or diabetes, according to the final stroke mechanism and discharge plan. Advise against independently stopping or changing medication.

D. Lifestyle and Secondary Prevention

  • Maintain regular blood pressure and diabetes follow-up.
  • Continue smoking cessation and avoid tobacco exposure.
  • Adopt a balanced diet with appropriate salt reduction.
  • Gradually increase physical activity within rehabilitation recommendations.
  • Address excess weight, dyslipidemia and other vascular risk factors.
  • Attend recommended cardiac or vascular investigations.

E. Rehabilitation and Family Support

Explain the importance of physiotherapy, occupational therapy and speech-language rehabilitation. Encourage the family to communicate slowly, use short sentences and allow additional time for responses without assuming that expressive aphasia means loss of understanding.

F. Recognizing Recurrent Stroke

Educate the family to recognize sudden facial weakness, arm weakness, speech difficulty, visual symptoms or other acute neurological deficits. Any suspected recurrence requires emergency medical services, even if symptoms improve.

G. Long-Term Follow-Up

Follow-up should address recovery, walking and communication, mood, swallowing, recurrent symptoms, medication adherence, cardiovascular risk management and the need for additional home support.

13. Long Case Presentation to the Examiner

“I have assessed a 68-year-old right-handed man with hypertension and diabetes who presented approximately 90 minutes after sudden-onset right-sided weakness and difficulty producing speech. The neurological deficits were persistent from onset. There was no preceding seizure, major trauma or severe headache. He was previously independent in daily activities.”

“On examination, he is alert with right central facial weakness, right hemiparesis more pronounced in the upper limb, mild right-sided sensory impairment and expressive aphasia. His NIHSS is 9. The findings localize to the dominant left MCA territory. Urgent non-contrast CT excludes hemorrhage, and subsequent MRI demonstrates acute left frontal-insular ischemic infarction. My diagnosis is acute left MCA territory ischemic stroke. My priorities are urgent reperfusion assessment, organized stroke-unit care, prevention of complications, secondary prevention and multidisciplinary rehabilitation.”

14. Examiner Discussion / Viva Preparation

Q1. What clinical features suggest acute ischemic stroke in this patient?

Answer: Sudden onset of persistent focal neurological deficits, including hemiparesis and aphasia, with vascular risk factors strongly suggests stroke. Ischemic and hemorrhagic causes must be distinguished by urgent imaging.

Q2. Where is the most likely neurological lesion?

Answer: The dominant left cerebral hemisphere, particularly the left middle cerebral artery territory. Right hemiparesis indicates contralateral motor pathway involvement, while expressive aphasia suggests dominant frontal language-network dysfunction.

Q3. Why is non-contrast CT brain the urgent initial imaging investigation?

Answer: It rapidly identifies or excludes intracranial hemorrhage and may demonstrate early ischemic changes. Excluding hemorrhage is essential before administering intravenous thrombolysis.

Q4. What is the purpose of the NIH Stroke Scale?

Answer: NIHSS provides a standardized assessment of stroke-related neurological deficits, helps quantify clinical severity and enables monitoring for improvement or deterioration. It does not independently diagnose stroke subtype or establish eligibility for a specific intervention.

Q5. Which factors are important before intravenous thrombolysis?

Answer: Exact time last known well, presence of a disabling ischemic deficit, brain imaging excluding hemorrhage, blood pressure, bleeding risk, relevant anticoagulant use and other treatment contraindications. Urgent stroke-team assessment is essential.

Q6. Why should swallowing be assessed before oral feeding?

Answer: Stroke may cause oropharyngeal dysphagia and impaired airway protection. A swallowing screen identifies patients at risk of aspiration, choking and aspiration pneumonia.

Q7. What complications require particular vigilance during acute stroke care?

Answer: Hemorrhagic transformation, cerebral edema, aspiration pneumonia, recurrent stroke, seizures, venous thromboembolism and complications of immobility. Sudden neurological deterioration warrants urgent reassessment.

Q8. What are the essential elements of secondary stroke prevention?

Answer: Appropriate antithrombotic treatment based on stroke mechanism, lipid management, control of hypertension and diabetes, smoking cessation, physical activity, assessment for atrial fibrillation or symptomatic carotid disease where indicated, and long-term treatment adherence.

15. ⭐ AIM Long Case — High-Yield Review

  1. Sudden focal neurological deficit is stroke until urgently evaluated.
  2. Last-known-well time is essential for reperfusion assessment.
  3. Right hemiparesis with expressive aphasia suggests dominant left hemisphere involvement, commonly in the MCA territory.
  4. NIHSS measures stroke severity and helps monitor neurological changes.
  5. GCS assesses consciousness; aphasia can complicate interpretation of its verbal component.
  6. Non-contrast CT brain is essential to exclude hemorrhage before thrombolysis.
  7. Diffusion-weighted MRI can demonstrate acute ischemia but must not unnecessarily delay reperfusion treatment.
  8. Eligible patients with disabling ischemic stroke require urgent consideration of reperfusion therapy.
  9. Keep the patient nil by mouth until swallowing safety is established.
  10. Sudden neurological deterioration may indicate hemorrhagic transformation, edema or recurrent stroke.
  11. Secondary prevention requires cause-directed antithrombotic therapy and control of vascular risk factors.
  12. Early organized rehabilitation and family counselling are essential for recovery and long-term independence.

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Final Year MBBS | KMU-Aligned Neuroscience | Clinical Long Case Learning
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