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Medical diagram showing the left middle cerebral artery (MCA) territory infarct in the brain. Axial cross-section of the brain with clearly labeled: left MCA territory highlighted in red/orange showing ischemic zone, surrounding brain tissue in normal gray, labeled structures including frontal lobe, parietal lobe, temporal lobe, internal capsule, basal ganglia, thalamus, and the MCA branches (M1, M2, M3). Clean clinical neurology teaching diagram with annotations showing clinical deficits: right-sided hemiplegia, aphasia (Broca + Wernicke zones marked), right facial droop, right hemisensory loss. White background, professional medical illustration style.

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Medical teaching diagram showing two panels side by side: Left panel - DWI MRI (diffusion-weighted imaging) of acute ischemic stroke showing bright white hyperintense signal in left MCA territory (frontal and parietal lobes), dark background, labeled "DWI - Restricted Diffusion (Acute Infarct)". Right panel - CT scan of head showing no hemorrhage in same territory, hyperdense MCA sign on left side labeled, normal appearing brain parenchyma. Both panels labeled with clinical annotations. Clean clinical radiology teaching style, black background for MRI, grayscale for CT, with color-coded labels.

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Clinical neurology flowchart diagram for acute ischemic stroke management algorithm. Flowchart starting with "Acute Stroke Symptoms" at top, branching to: CT Head (rule out hemorrhage) -> two branches: 1) Hemorrhagic Stroke (no thrombolysis) and 2) Ischemic Stroke. Ischemic branch leads to: check time window, NIHSS score, contraindications. Then branches to: IV tPA/Alteplase (within 4.5 hours, 0.9 mg/kg max 90mg), AND Mechanical Thrombectomy (large vessel occlusion, within 24hrs, ASPECTS score). Post-treatment: ICU monitoring, BP control, anticoagulation for AF, statin, antiplatelets. Secondary prevention branch. Clean clinical decision tree, color-coded boxes (red for hemorrhage, blue for ischemic, green for treatment), professional medical flowchart style.


Clinical Case: Acute Ischemic Stroke


PATIENT PRESENTATION

Patient: Mr. Arjun Mehta, 67-year-old right-handed male Presented via: Emergency Department, brought by family at 09:15 AM Last known well: 08:00 AM (1 hour 15 minutes prior to arrival)

CHIEF COMPLAINT

"He suddenly couldn't speak and his right arm went limp."

HISTORY OF PRESENTING ILLNESS

Mr. Mehta was having breakfast when his wife noticed he suddenly stopped mid-sentence, dropped his cup with his right hand, and was unable to form words. He did not lose consciousness. He had no preceding headache, visual changes, or trauma. He was brought immediately to the ED.
PMH:
  • Hypertension (on amlodipine 5 mg OD) - poorly controlled
  • Type 2 Diabetes Mellitus (on metformin 1g BD)
  • Paroxysmal atrial fibrillation - NOT on anticoagulation (patient refused warfarin 6 months ago)
  • Hyperlipidemia (on atorvastatin 20 mg)
  • Non-smoker; occasional alcohol
Family History: Father died of stroke at age 72.
Medications: Amlodipine, Metformin, Atorvastatin, Aspirin 75 mg (self-discontinued 2 weeks ago)
Allergies: NKDA

PHYSICAL EXAMINATION

Vitals:
ParameterValue
BP188/106 mmHg
HR98 bpm, irregularly irregular
RR18/min
SpO₂97% on room air
Temperature36.8°C
Blood glucose9.2 mmol/L
GCSE4 V2 M6 = 12/15
Cardiovascular: Irregularly irregular rhythm; no murmurs. Respiratory: Clear bilaterally.

NEUROLOGICAL EXAMINATION

DomainFinding
Level of consciousnessAlert but confused
SpeechSevere non-fluent (Broca's) aphasia; cannot repeat or follow complex commands
Cranial NervesRight lower facial droop (UMN pattern); gaze deviation to the LEFT
MotorRight arm: 0/5 power; Right leg: 2/5 power; Left side: 5/5
SensoryRight hemisensory loss (pinprick and light touch)
ReflexesRight hyperreflexia; right Babinski positive
CoordinationUnable to assess right side; left side normal
NeglectRight-sided visual and tactile neglect absent (left hemisphere dominant)
NIHSS Score Calculated:
NIHSS ItemScore
1a. LOC1
1b. LOC questions2
1c. LOC commands1
2. Best gaze1
3. Visual fields0
4. Facial palsy2
5a. Motor arm (right)4
5b. Motor arm (left)0
6a. Motor leg (right)3
6b. Motor leg (left)0
8. Sensory1
9. Best language2
10. Dysarthria1
TOTAL NIHSS18 (Severe stroke)

INVESTIGATIONS

Bedside / Urgent:
  • Blood glucose: 9.2 mmol/L (hypoglycemia excluded)
  • ECG: Atrial fibrillation with rapid ventricular response (~110 bpm)
  • CBC: Normal; platelets 240 x 10⁹/L
  • PT/aPTT: Normal; INR 1.0
  • Renal/liver function: Normal
  • Troponin I: Mildly elevated (0.08 ng/mL) - likely demand ischemia, no STEMI morphology on ECG
Imaging:
Non-contrast CT Head (performed at T+30 min):
  • No intracranial hemorrhage
  • Hyperdense left MCA sign present (clot visible in left M1 segment)
  • ASPECTS score: 8/10 (early ischemic changes in left putamen and internal capsule)
  • No midline shift
CT Angiography (CTA) Head and Neck (T+45 min):
  • Left M1 segment occlusion confirmed
  • Mild atherosclerosis at left carotid bifurcation; no significant stenosis (45%)
  • Contralateral vessels patent
MRI Brain (DWI/ADC) - ordered to follow:
  • Expected: Bright DWI signal + dark ADC map in left MCA territory (restricted diffusion = cytotoxic edema, confirms infarct core)

DIAGRAM 1: Left MCA Territory Infarct - Brain Anatomy

Left MCA Territory Infarct - Axial Brain Section showing ischemic zone with clinical deficits
This diagram illustrates the left MCA territory (highlighted), the zones of Broca's and Wernicke's areas, right-sided hemiplegia distribution, and key structures at risk including the internal capsule and basal ganglia.

DIAGRAM 2: Neuroimaging - CT vs MRI Findings

CT Head showing hyperdense MCA sign alongside DWI MRI showing acute restricted diffusion in left MCA territory
Left panel shows the CT hyperdense MCA sign (early infarct marker). Right panel shows DWI-MRI with bright white signal confirming cytotoxic edema in the acute infarct core.

CLINICAL DIAGNOSIS

Primary Diagnosis:

Acute Left MCA (M1) Territory Ischemic Stroke
  • Etiology: Cardioembolic - secondary to non-anticoagulated paroxysmal atrial fibrillation
  • Territory: Left middle cerebral artery, M1 occlusion
  • Syndrome: Left hemisphere dominant stroke with Broca's aphasia, right hemiplegia, right hemisensory loss, right lower facial droop, contralateral gaze deviation
Pathophysiology: Paroxysmal AF leads to stagnant blood flow in the left atrial appendage, forming a mural thrombus. Embolization to the left M1 segment occludes blood flow to the entire left MCA territory. Disruption of perfusion to Broca's area (left inferior frontal gyrus, BA 44/45) produces expressive aphasia. Corticospinal tract involvement at the posterior limb of the internal capsule causes right hemiplegia - the face and upper limb more affected than lower limb (classic MCA pattern, as the ACA supplies the leg area of the motor homunculus). As noted in Tintinalli's Emergency Medicine, "the middle cerebral artery is the vessel most commonly involved in stroke, and clinical findings can be quite variable, depending on exactly where the lesion is located and which brain hemisphere is dominant."

DIFFERENTIAL DIAGNOSIS

PriorityDiagnosisSupporting FeaturesAgainst
1stAcute Ischemic Stroke (left MCA)Sudden onset, AF, cortical deficits, hyperdense MCA sign, NIHSS 18-
2ndIntracerebral HemorrhageSudden onset, hypertension (BP 188/106)CT shows no hemorrhage; no headache
3rdTodd's Paralysis (post-ictal)Focal weakness, confusionNo witnessed seizure; aphasia persists; hyperdense MCA sign
4thHypoglycemic HemiplegiaCan exactly mimic strokeBlood glucose 9.2 mmol/L - excluded
5thHypertensive EncephalopathySevere hypertension presentFocal cortical deficits localizing to MCA - not diffuse; no papilledema
6thBrain Tumour (glioblastoma)Can cause focal deficits and aphasiaAcute onset (minutes); no prior symptoms; no ring enhancement on CT
7thComplex Migraine with AuraCan cause aphasia and motor deficitsNo prior migraine history; age 67; AF present; CT hyperdense MCA
8thCerebral Venous Sinus ThrombosisCan mimic strokeNo headache; no papilledema; arterial pattern on imaging
9thDemyelinating Disease (MS)Can cause focal deficitsAge 67, acute abrupt onset, vascular risk factors, AF
10thWernicke's EncephalopathyConfusion, gaze palsyNo alcoholism; no ophthalmoplegia-ataxia triad
As detailed in Rosen's Emergency Medicine, other conditions that may mimic stroke include "complex migraines, seizure followed by Todd postictal paralysis, Bell palsy, labyrinthitis, vestibular neuronitis, peripheral nerve palsy, and demyelinating diseases." Metabolic causes like hypoglycemia must always be excluded first at the bedside.

TREATMENT PLAN

Phase 1: Hyperacute Management (0-4.5 Hours)

Step 1 - Secure Airway, Breathing, Circulation
  • IV access (2 large-bore cannulas)
  • Continuous cardiac monitoring + pulse oximetry
  • NPO (nil per os) until formal swallow assessment - risk of aspiration
Step 2 - IV Thrombolysis (tPA/Alteplase) Indications met: Ischemic stroke confirmed on CT, time from last known well = 75 min, NIHSS 18, BP controllable, no contraindications, INR normal, platelets adequate.
Alteplase 0.9 mg/kg IV (max 90 mg)
  • 10% as IV bolus over 1 minute
  • Remaining 90% as infusion over 60 minutes
  • Target BP < 185/110 before and during infusion
As confirmed in Adams and Victor's Principles of Neurology 12th Ed: "treatment within 3 h of the onset of symptoms led to a 30 percent increase in the number of patients who remained with little or no neurologic deficit 3 months after the stroke." The window has since been extended to 4.5 hours in selected patients.
Step 3 - Mechanical Thrombectomy (Concurrent Evaluation) CTA confirms left M1 occlusion. ASPECTS 8 (≥6 eligible). NIHSS 18 (≥6). Time within 24 hours from last known well. Transfer to catheterization suite for:
Stent-retriever mechanical thrombectomy - Target: TICI 2b/3 reperfusion Multiple 2015 pivotal trials (MR CLEAN, ESCAPE, SWIFT-PRIME, EXTEND-IA, THRACE) confirmed benefit of intra-arterial thrombectomy for large-vessel occlusion, as documented in Tintinalli's EM.
BP Management During Thrombolysis:
  • Target: ≤185/110 mmHg before tPA; ≤180/105 during infusion
  • Agent: Labetalol 10-20 mg IV bolus; or Nicardipine infusion if resistant

Phase 2: Acute Management (First 24-72 Hours)

InterventionDetails
ICU/Stroke unit admissionClose neurological monitoring q2h; watch for cerebral edema, hemorrhagic transformation
BP ManagementAfter tPA: keep <180/105; After 24h if no thrombolysis: permissive hypertension up to 220/120
Glucose controlTarget 7.8-10 mmol/L; avoid hypoglycemia (worsens penumbra)
TemperatureTreat fever aggressively - hyperthermia worsens outcome; paracetamol
DVT prophylaxisCompression stockings; anticoagulation held 24h post-tPA
Swallow assessmentFormal SLT assessment before oral intake
NutritionNG feeding if unsafe swallow
Aspirin300 mg loading after 24h (if no hemorrhagic transformation on repeat CT)
StatinContinue atorvastatin; uptitrate to 80 mg (high-intensity)
Anti-edemaMonitor for malignant MCA syndrome; ICP management if needed

Phase 3: Secondary Prevention (After Stabilization)

Anticoagulation for AF (the key intervention):
The underlying cause is cardioembolic AF. AF carries a 3-5% annual stroke risk without anticoagulation, reduced to ~1-1.5% with anticoagulation (Fuster and Hurst's The Heart, 15th Ed).
After 2-4 weeks post-infarct (depending on stroke size and hemorrhagic risk): DOAC therapy - Apixaban 5 mg BD (first-line for non-valvular AF, superior bleeding profile vs warfarin) CHA₂DS₂-VASc score for Mr. Mehta: C=0, H=1, A₂=2, D=1, S₂=2 (prior stroke = 2), V=0, A=0, Sc=0 → Score = 6 (very high risk - anticoagulation strongly indicated)
Additional Secondary Prevention:
DrugDoseIndication
Apixaban5 mg BDAF-related cardioembolic prevention
Atorvastatin80 mg ODLDL-C target <1.8 mmol/L
Amlodipine10 mg OD (uptitrate)Hypertension - target BP <130/80
AspirinDiscontinue once on DOACDOAC alone sufficient; combination increases bleeding
Rehabilitation:
  • Early mobilization (within 24h if neurologically stable post-procedure)
  • Physiotherapy (upper and lower limb rehabilitation)
  • Occupational therapy (ADL independence)
  • Speech and Language Therapy (aphasia rehabilitation - Broca's aphasia recovery is variable but often partial)
  • Cognitive rehabilitation
  • Driving cessation counseling
  • Cardiac monitoring: 72h continuous + 30-day Holter to confirm AF burden

DIAGRAM 3: Acute Stroke Management Algorithm

Acute ischemic stroke management flowchart showing decision tree from CT imaging through IV tPA and mechanical thrombectomy to secondary prevention
This flowchart shows the complete decision algorithm from initial CT assessment, through thrombolysis eligibility, thrombectomy selection, to secondary prevention planning including anticoagulation for AF.

PROGNOSIS & COMPLICATIONS TO WATCH

ComplicationTimeframeMonitoring
Hemorrhagic transformation24-72hRepeat CT at 24h post-tPA
Malignant MCA syndrome2-5 daysProgressive decline → decompressive hemicraniectomy may be life-saving
Aspiration pneumoniaDays 1-7Strict swallow precautions; early chest physio
DVT / PEDay 3 onwardsCompression + early anticoagulation after safe window
Post-stroke depressionWeeks-monthsScreen and treat with SSRI (also may aid motor recovery)
Recurrent stroke (without anticoagulation)High risk (AF)Initiate DOAC as soon as safe
SeizuresFirst yearAnti-epileptics only if clinical seizure occurs
Expected outcome with reperfusion: With successful M1 thrombectomy achieving TICI 2b-3, meaningful neurological recovery is achievable. Broca's aphasia recovery is the most variable - some patients regain functional communication, others retain significant deficit. Right arm recovery is typically worse than leg recovery due to dense corticospinal tract involvement at the internal capsule.

SUMMARY TABLE

DomainFinding
DiagnosisAcute left MCA (M1) ischemic stroke - cardioembolic (AF)
NIHSS18 (severe)
CT findingHyperdense left MCA sign; ASPECTS 8; no hemorrhage
EtiologyNon-anticoagulated paroxysmal AF; CHA₂DS₂-VASc = 6
Acute treatmentIV Alteplase 0.9 mg/kg + left M1 mechanical thrombectomy
Secondary preventionApixaban 5 mg BD; atorvastatin 80 mg; BP control
RehabilitationPT/OT/SLT; aphasia therapy; early mobilization
Key avoidable errorFailure to anticoagulate for known AF - this stroke was preventable

Sources: Tintinalli's Emergency Medicine, A Comprehensive Study; Adams and Victor's Principles of Neurology, 12th Ed; Fuster and Hurst's The Heart, 15th Ed; Rosen's Emergency Medicine; Neuroanatomy through Clinical Cases, 3rd Ed; Bradley and Daroff's Neurology in Clinical Practice; Plum and Posner's Diagnosis and Treatment of Stupor and Coma.
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