1) Core idea

• Right heart pumps deoxygenated blood to lungs
• Lungs oxygenate blood
• Left heart pumps oxygenated blood to body

2) Types of cardiac shunts

A) Left-to-right shunt

• ASD (atrial septal defect)
• VSD (ventricular septal defect)
• PDA (patent ductus arteriosus)

• Increased pulmonary blood flow
• Volume overload of right heart/lungs
• Over time can cause pulmonary hypertension

• Murmur
• Recurrent chest infections/failure to thrive in infants
• Breathlessness on exertion

• Usually no early systemic cyanosis (blood to body still mostly oxygenated)

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B) Right-to-left shunt

• Tetralogy of Fallot
• Eisenmenger physiology (reversal of longstanding L→R shunt)
• Severe pulmonary hypertension with septal defect

• Cyanosis (bluish lips/fingers)
• Clubbing (chronic)
• Polycythemia (compensatory increased RBCs)
• Risk of paradoxical emboli/brain abscess in some conditions

3) Why shunt direction matters

• Pressure difference between the two sides
• Resistance in pulmonary vs systemic circulation
• Size of the defect

4) Qp:Qs (important exam/hemodynamic concept)

• Qp = pulmonary blood flow
• Qs = systemic blood flow

• Qp:Qs > 1 → left-to-right shunt
• Qp:Qs < 1 → right-to-left shunt
• Higher ratio means larger L→R shunt burden

5) Clinical progression (classic)

1. Pulmonary overcirculation
2. Pulmonary vascular remodeling
3. Pulmonary hypertension
4. Shunt reversal to R→L (Eisenmenger syndrome)
   At this stage, many defects are no longer safely correctable.

6) Diagnosis

• Clinical exam (murmurs, cyanosis, signs of heart failure)
• ECG, chest X-ray
• Echocardiography (key test)
• Bubble study in selected cases
• Cardiac MRI/CT or catheterization for complex anatomy/hemodynamics

7) Management principles

• Observation for small, hemodynamically insignificant defects
• Medical therapy for heart failure symptoms (when present)
• Catheter device closure (selected ASD/PDA/VSD)
• Surgical repair for unsuitable/large/complex lesions
• Pulmonary hypertension-specific therapy in Eisenmenger
• Endocarditis prophylaxis only in selected high-risk scenarios (not all defects)

8) Non-cardiac use of “shunt” (also important)

• VP shunt (ventriculoperitoneal shunt) for hydrocephalus
• Portosystemic shunts in liver disease (natural or TIPS procedure)

1. a table comparing ASD vs VSD vs PDA, or
2. a simple flowchart to remember shunt physiology for exams.

1) What is a shunting procedure

• Neurosurgery: CSF shunts for hydrocephalus
• Cardiology/cardiac surgery: systemic-pulmonary shunts, intracardiac shunt closure, etc.
• Hepatology/interventional radiology: portosystemic shunt (TIPS)

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2) CSF shunting (Hydrocephalus) in detail

A) Principle

B) Types

1. VP shunt (ventriculoperitoneal)
   Ventricle → peritoneal cavity (most common)
2. VA shunt (ventriculoatrial)
   Ventricle → right atrium (when peritoneum unsuitable)
3. VPL shunt (ventriculopleural)
   Ventricle → pleural space (selected cases)
4. LP shunt (lumboperitoneal)
   Lumbar subarachnoid → peritoneum (often communicating hydrocephalus/IIH selected cases)

C) Components

• Proximal ventricular catheter
• Valve/reservoir (fixed or programmable pressure)
• Distal catheter to target cavity

D) Indications for CSF shunting (high-yield)

Absolute/strong indications

• Symptomatic hydrocephalus with raised ICP signs:
  • headache, vomiting, papilledema, drowsiness, sixth nerve palsy
• Progressive ventricular enlargement on imaging with symptoms
• Congenital hydrocephalus (for example aqueductal stenosis, myelomeningocele-associated)
• Post-hemorrhagic hydrocephalus (IVH in neonates/adults) not resolving
• Post-infectious hydrocephalus after acute infection controlled
• Normal pressure hydrocephalus (NPH) with clinical triad and supportive testing, usually VP shunt
• Failed or unsuitable endoscopic third ventriculostomy (ETV)

Relative/context-based indications

• Progressive macrocephaly in infants with imaging evidence
• Recurrent CSF pressure symptoms in communicating hydrocephalus
• Idiopathic intracranial hypertension in select refractory cases (usually LP shunt or VP in specialized settings)

E) Contraindications / caution

• Active untreated CNS or systemic infection (delay permanent shunt if possible)
• Abdominal contraindications for VP (extensive adhesions, peritonitis, major abdominal pathology)
• Cardiac/venous issues for VA shunt (endocarditis risk, venous thrombosis concerns)
• Very high protein/bloody CSF can increase early obstruction risk (sometimes temporary drainage first)

F) Pre-op workup

• Clinical neuro exam, fundus if possible
• CT/MRI brain (ventricular size, etiology, obstruction level)
• CSF/infection assessment if concern
• Choose shunt type and valve setting (programmable often preferred)
• Baseline head circumference in children

G) Procedure steps (typical VP shunt)

1. General anesthesia, sterile prep
2. Burr hole and ventricular catheter insertion (frontal or parietal entry)
3. Confirm CSF flow
4. Valve connected to proximal catheter
5. Subcutaneous tunneling to abdomen
6. Distal catheter introduced into peritoneal cavity
7. System connected, tested, wounds closed
8. Post-op imaging/check function

H) Complications (very important)

Early

• Hemorrhage, malposition
• Infection (wound, shunt, ventriculitis, peritonitis)
• Overdrainage (headache, slit ventricle, subdural hygroma/hematoma)
• Seizure (less common)

Late

• Mechanical obstruction (most common failure)
• Catheter fracture/disconnection/migration
• Valve malfunction
• Abdominal pseudocyst (VP)
• Shunt nephritis/endocarditis/thromboembolism (VA)
• Repeated revisions needed in children as they grow

I) Follow-up and revision indications

• Return of hydrocephalus symptoms
• Redness/tenderness along tract, fever
• Imaging: enlarged ventricles or catheter issue
• Need for valve pressure adjustment
• Any confirmed infection usually requires externalization/removal + antibiotics + re-shunt later

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3) Common clinical signs of shunt malfunction/infection (exam pearl)

• Headache, vomiting, confusion, visual symptoms

• Irritability, poor feeding, bulging fontanelle, increasing head size, sunset eyes, developmental regression

• Fever, lethargy, wound erythema, abdominal pain (VP), meningitic signs

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4) Other important “shunting procedures” and indications

A) Modified Blalock-Taussig shunt (cardiac)

• What: systemic-to-pulmonary arterial shunt (subclavian to pulmonary artery using graft)
• Indications: cyanotic congenital heart disease with reduced pulmonary blood flow as palliative step (for example TOF with severe cyanosis, pulmonary atresia) before definitive repair.

B) TIPS (Transjugular Intrahepatic Portosystemic Shunt)

• What: tract between portal vein and hepatic vein to decompress portal system
• Indications:
  • refractory variceal bleeding
  • refractory ascites
  • selected hepatic hydrothorax/Budd-Chiari situations
• Major caution: can worsen hepatic encephalopathy.

C) Portocaval/surgical portosystemic shunts

• Less common now due to TIPS/transplant strategies; used in selected portal hypertension contexts.

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5) Quick indication summary table

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1. ETV vs VP shunt (when to choose which), or
2. A complication management algorithm (what to do when shunt stops working).

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Endarterectomy — Complete Detailed Guide

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1) What is Endarterectomy?

• Most commonly performed at the carotid artery (CEA — Carotid Endarterectomy)
• Also done at femoral, iliac, renal, mesenteric arteries (less commonly)

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2) Anatomy Relevant to CEA

• Common carotid artery (CCA) bifurcates into internal carotid artery (ICA) and external carotid artery (ECA) at the level of C3-C4 vertebra
• Atherosclerotic plaque accumulates most at the carotid bifurcation and proximal ICA
• Plaque causes either:
  • Thromboembolism → stroke/TIA
  • Hemodynamic compromise → reduced flow to brain

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3) Pathophysiology (Why the Operation Matters)

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4) INDICATIONS for Carotid Endarterectomy

A) Symptomatic Carotid Stenosis (most important)

• Ipsilateral amaurosis fugax (transient monocular blindness)
• Contralateral facial paralysis or paraesthesia
• Arm/leg paralysis or paraesthesia (hemiparesis/hemiplegia)
• Hemianopia
• Dysphasia (dominant hemisphere)
• Sensory or visual inattention/neglect

NASCET trial (North American Symptomatic Carotid Endarterectomy Trial) established these thresholds. Absolute risk reduction for stroke was 17% for 70-99% stenosis.

ECST trial (European Carotid Surgery Trial) confirmed CEA benefit for high-grade symptomatic stenosis.

• Ideally within 2 weeks of the symptomatic event (greatest risk of recurrent stroke is in the first 2 weeks — up to 10-20%)
• Do not delay unnecessarily after TIA with high-grade stenosis

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B) Asymptomatic Carotid Stenosis

• ≥60–70% stenosis in patients with:
  • Low surgical risk (fit, young-elderly patients)
  • High-risk plaque features (ulceration, rapid progression, contralateral occlusion)
  • Long life expectancy (to realize long-term benefit)
  • Centre with <3% perioperative stroke/death rate
  • Patient preference after informed discussion

• ACAS (Asymptomatic Carotid Atherosclerosis Study): 5-year stroke risk reduced from 11% to 5% with CEA in >60% asymptomatic stenosis
• ACST (Asymptomatic Carotid Surgery Trial): confirmed benefit in <75 year-olds with ≥70% stenosis and fit for surgery

In asymptomatic patients, the absolute benefit is smaller than symptomatic patients. Modern best medical therapy (BMT) is very good, so this remains an area of ongoing debate (CREST-2 trial ongoing).

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C) Other Situations Where CEA Is Indicated

• Recurrent TIA on antiplatelet therapy with significant ipsilateral stenosis
• Pre-operative before major cardiac surgery (CABG) with severe bilateral carotid disease in selected high-risk patients (controversial, individualized)
• Contralateral ICA occlusion with symptomatic ipsilateral stenosis ≥50%
• Crescendo TIAs (multiple TIAs in short period) — semi-urgent CEA often performed

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D) CONTRAINDICATIONS to CEA

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5) Pre-Operative Assessment

• Duplex ultrasound of carotid arteries (primary imaging, assesses stenosis, plaque morphology)
• CT angiography or MRA for confirmation and anatomy planning
• CT/MRI brain — assess extent of prior infarction; determine if deficit is disabling
• Cardiology assessment — optimize cardiac status (ECG, echo if needed)
• Blood pressure control, statin therapy optimization
• Antiplatelet therapy (aspirin typically continued; clopidogrel sometimes)
• Blood glucose control in diabetics
• Anaesthetic assessment — CEA can be done under General Anaesthesia (GA) or Local Regional Anaesthesia (LRA/cervical block)

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6) Surgical Steps of CEA

1. Patient positioned — neck extended, head turned to opposite side
2. Incision along anterior border of sternocleidomastoid
3. Dissection to expose CCA, ICA, ECA, superior thyroid artery
4. Systemic heparin administered
5. Clamps applied on CCA, ICA, ECA
6. Arteriotomy (longitudinal cut in artery)
7. Plaque carefully dissected out from the intima/inner media
8. Distal end-point checked and tacked if needed
9. Arteriotomy closed:
   • Primary closure, or
   • Patch angioplasty (vein or synthetic patch — reduces risk of restenosis)
10. Clamps released, flow restored, hemostasis achieved
11. Wound closed in layers

• Cerebral function (EEG, transcranial Doppler, stump pressure measurement)
• If cerebral ischemia detected during clamping → shunt inserted to maintain flow during surgery
• Under LRA: awake patient — can directly monitor neurological function (gold standard for detecting ischemia)

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7) COMPLICATIONS of Endarterectomy — In Detail

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A) Neurological Complications

1. Intra-operative Stroke

• Most serious complication
• Caused by:
  • Embolisation from plaque during manipulation (most common — ~80%)
  • Thromboembolism at flow restoration (from thrombus accumulating on endarterectomy zone)
  • Haemodynamic — from clamping or shunt malfunction (~20%)
• Features: hemiplegia, homonymous hemianopia, higher cortical dysfunction on recovery from GA
• Management: immediate imaging, neurosurgical/neurointerventional involvement

2. Post-operative Stroke

• Early (within 24-48 hrs): usually thrombosis at operative site
• Management: urgent duplex/CTA — if thrombosis, return to theatre for re-exploration
• Can also be due to hyperperfusion

3. Transient Ischaemic Attack (TIA)

• New TIA post-op requires urgent investigation of the operative artery

4. Cerebral Hyperperfusion Syndrome

• Occurs in 0.2–1% of CEA
• Mechanism: chronically hypoperfused brain suddenly receives high-pressure flow after stenosis removal → loss of cerebral autoregulation
• Features: severe ipsilateral headache, focal neurological deficit, seizures, intracerebral haemorrhage
• High risk: severe bilateral disease, poor collaterals, severe hypertension post-op
• Management: strict blood pressure control post-op (target SBP <140 mmHg), anticonvulsants if seizures

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B) Cardiac Complications

• Myocardial infarction — most common cause of death after CEA (not stroke!)
• Most patients with carotid atherosclerosis have coexistent coronary artery disease
• Requires post-op troponin monitoring in high-risk patients, ECG surveillance

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C) Cranial Nerve Injuries (very high-yield in exams)

Most cranial nerve injuries are neuropraxia (stretch/retraction) and resolve spontaneously within weeks-months. Transection is rare.

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D) Wound Complications

Expanding neck haematoma is a surgical emergency — can cause airway obstruction. Management: immediate re-exploration at bedside or theatre, secure airway first.

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E) Arterial Complications

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F) Systemic Complications

• Deep vein thrombosis / pulmonary embolism
• Aspiration pneumonia (especially if cranial nerve injury affecting swallowing)
• Haemodynamic instability — carotid sinus manipulation can cause intraoperative hypotension/bradycardia

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8) CEA vs Carotid Artery Stenting (CAS)

CREST trial: CEA had lower stroke rates; CAS had lower MI rates. Both are acceptable in experienced centres.

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9) Summary of Outcomes

• Perioperative stroke/death rate should be:
  • <3% for asymptomatic patients
  • <6% for symptomatic patients (If a centre's rates exceed these, benefit of operation is negated)
• 5-year stroke prevention: CEA for symptomatic 70–99% stenosis reduces 5-year stroke risk from ~26% to ~9%
• Long-term: lifelong antiplatelet therapy, statin, blood pressure, diabetes control, smoking cessation essential

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10) Quick Exam Summary Table

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1. Pulmonary endarterectomy (for chronic thromboembolic pulmonary hypertension), or
2. Femoral/peripheral endarterectomy indications and technique?

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HYDROCEPHALUS — Complete Detailed Guide

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1) DEFINITION

• It is NOT simply "water on the brain" — it reflects a dynamic imbalance between CSF production, circulation, and absorption
• Can be congenital or acquired
• Can affect any age group — neonates to elderly
• Normal CSF volume: 150 mL (50 mL in ventricles, 100 mL in subarachnoid space)
• CSF production rate: 0.3–0.35 mL/min (~500 mL/day); entirely replaced ~3 times/day

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2) CSF CIRCULATION — Normal Physiology (Essential to Understand Hydrocephalus)

Choroid plexus (lateral ventricles)
         ↓ CSF produced
Lateral ventricles
         ↓ via Foramen of Monro
Third ventricle
         ↓ via Aqueduct of Sylvius (cerebral aqueduct)
Fourth ventricle
         ↓ via Foramina of Luschka (lateral) + Magendie (midline)
Subarachnoid space (basal cisterns → cortex)
         ↓ absorbed
Arachnoid granulations → Dural venous sinuses → Venous blood

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3) CLASSIFICATION

A) Based on Mechanism (Most Important)

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B) Based on Age of Onset

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C) Based on Pressure

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D) Based on Onset

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4) CAUSES

A) Congenital Causes

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B) Acquired Causes

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5) PATHOPHYSIOLOGY

Step-by-Step Mechanism:

• Physical block in CSF pathway (obstructive), OR
• Impaired arachnoid granulation function (communicating), OR
• Rarely, CSF overproduction (choroid plexus papilloma)

• CSF continues to be produced at 0.35 mL/min but cannot drain adequately
• Ventricular system dilates — starts at the site of obstruction

• Ventricles expand, compressing periventricular white matter
• Transependymal CSF flow — fluid crosses ependymal lining into white matter (visible as periventricular lucency on CT/MRI)
• ICP rises progressively

• Stretching of cortical veins, bridging veins
• Compression of periventricular long white matter tracts (especially legs of corona radiata — explains gait disturbance in NPH)
• Compression of thalamus, hypothalamus, brainstem (late)
• Cerebral blood flow reduced → ischemia

• Skull sutures not fused → head enlarges rather than ICP rising acutely
• Stretching of cortex → "setting sun" sign (eyes deviated downward due to pretectal compression)
• Fontanelle bulging

• Pressure rises acutely → progressive herniation risk
• Cushing's triad (hypertension + bradycardia + irregular breathing) — late, pre-terminal sign

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Specific Pathophysiology in NPH:

• Communicating hydrocephalus but ICP normal on LP (intermittent pressure waves may occur at night)
• Exact mechanism debated: reduced CSF absorption in arachnoid villi due to aging/fibrosis
• Disproportionate enlargement of ventricles compresses:
  • Periventricular motor tracts for legs → gait apraxia (magnetic gait)
  • Frontal lobe connections → cognitive decline
  • Bladder control pathways → urinary incontinence

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6) CLINICAL FEATURES

A) In Infants (Sutures Not Fused — Age <2 Years)

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B) In Older Children and Adults

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C) Normal Pressure Hydrocephalus (NPH) — Classic Triad (Hakim-Adams Triad)

Memory aid: "Wet, Wobbly, and Wacky" (incontinence, gait, cognition)

Harrison's (p. 778): "Other features of the diagnostic triad (mental changes, incontinence) may be absent in a substantial number of patients."

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7) INVESTIGATIONS

A) Imaging

1. CT Brain (First-line Investigation)

• Best first investigation — rapid, widely available
• Findings:
  • Ventricular dilation (all four or specific ventricles depending on level of block)
  • Periventricular lucency (transependymal CSF seepage — low density rim around ventricles)
  • Sulcal effacement (in raised ICP)
  • Cause may be visible (tumor, hemorrhage, cyst)
  • In NPH: "disproportionate sulcal enlargement" — ventricles enlarged more than sulci

2. MRI Brain (Best for Cause and Detail)

• Identifies etiology more precisely (tumor, aqueduct stenosis, Chiari, etc.)
• T2/FLAIR: periventricular white matter hyperintensity
• Phase-contrast MRI: CSF flow studies through aqueduct
• In NPH: "flow void" at aqueduct (pulsatile CSF flow), high convexity tightness
• Better posterior fossa visualization than CT

3. Cranial Ultrasound (Neonates and Infants)

• Investigation of choice in neonates — fontanelle provides acoustic window
• Bedside, no radiation, serial monitoring
• Shows ventricular size, IVH, cysts

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B) Lumbar Puncture (LP)

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C) Other Investigations

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8) MEDICAL MANAGEMENT

Medical treatment is generally temporizing, not curative for most hydrocephalus. Used to buy time or manage specific situations.

A) Carbonic Anhydrase Inhibitors

• Acetazolamide (main agent)
  • Reduces CSF production by ~50%
  • Dose: 25 mg/kg/day in children; 250–1000 mg/day in adults
  • Side effects: metabolic acidosis, electrolyte disturbance, renal stones, paraesthesia
  • Used in: post-hemorrhagic hydrocephalus of prematurity (short-term), IIH
• Furosemide (sometimes combined with acetazolamide)
  • Reduces CSF production
  • Risk of electrolyte imbalance

B) Osmotic Agents (Acute Rise in ICP)

• Mannitol 20% — 0.25–1 g/kg IV bolus; reduces ICP acutely by osmotic effect
• Hypertonic saline (3%) — used in ICU settings for acute intracranial hypertension
• These are bridge therapies pending definitive surgery

C) Corticosteroids

• Dexamethasone — reduces cerebral edema around tumors causing obstructive hydrocephalus
• Does NOT treat hydrocephalus itself; reduces peritumoural edema

D) Management of Idiopathic Intracranial Hypertension (IIH)

• Weight loss (most important — target 10% body weight)
• Acetazolamide (first-line drug)
• Topiramate (weight loss + carbonic anhydrase inhibition)
• Serial therapeutic LPs (temporary relief)
• Surgical options if refractory (see surgical section)

E) Specific Medical Management

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9) SURGICAL MANAGEMENT

A) External Ventricular Drain (EVD)

• Temporary catheter inserted into lateral ventricle, drained to external bag
• Emergency temporizing measure

• Acute hydrocephalus (hemorrhage, post-op, meningitis)
• Pre-operative stabilization
• Measurement of ICP
• Intraventricular drug delivery (e.g., antibiotics, fibrinolytics for IVH)

• Infection (ventriculitis) — risk increases after 5–7 days
• Hemorrhage during insertion
• Catheter displacement
• Over-drainage

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B) Ventriculoperitoneal (VP) Shunt — MOST COMMON PROCEDURE

• Proximal ventricular catheter
• One-way pressure valve (fixed or programmable)
• Distal peritoneal catheter

• Communicating and obstructive hydrocephalus (most types)
• NPH
• Post-hemorrhagic, post-infectious hydrocephalus

• Fixed differential pressure (low, medium, high settings)
• Programmable (adjustable non-invasively — Codman, Medtronic Strata)
• Anti-siphon devices (prevent overdrainage on standing)

• Large absorptive surface (peritoneum)
• Distal catheter can be left long in children (grows into it)

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C) Ventriculoatrial (VA) Shunt

• When peritoneum is unsuitable (adhesions, peritonitis, abdominal malignancy, previous abdominal surgery)

• Shunt nephritis (immune complex deposition → membranoproliferative GN)
• Infective endocarditis
• Pulmonary embolism
• Arrhythmia (catheter in right heart)
• Catheter does NOT grow with child → multiple revisions

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D) Endoscopic Third Ventriculostomy (ETV) — Key Procedure

• Endoscope inserted into lateral ventricle → third ventricle
• A stoma (hole) created in the floor of third ventricle
• CSF bypasses the obstruction and flows directly into basal cisterns
• Avoids need for shunt hardware entirely

• Obstructive hydrocephalus — aqueductal stenosis (ideal indication)
• Tectal/midbrain tumors, pineal tumors obstructing aqueduct
• Dandy-Walker, third ventricular cysts
• Post-hemorrhagic or post-infectious hydrocephalus (if aqueduct blocked)
• Shunt failure — ETV can replace shunt in suitable anatomy

• Communicating hydrocephalus (ETV will not work — absorption is the problem, not flow)
• Very young infants (<6 months) — lower success rates
• Scarred basal cisterns (post-meningitis)

• No implanted hardware → no shunt infection/obstruction risk
• Eliminates shunt dependency
• Single procedure if successful

• Age of patient
• Cause of hydrocephalus
• Previous shunt

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E) Other Surgical Options

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10) SPECIAL SITUATIONS

A) Hydrocephalus in Premature Neonates (Post-IVH)

• Most common acquired cause in neonates
• Serial cranial USS monitoring
• Temporizing: serial LP, reservoir tap, EVD
• Acetazolamide used short-term
• VP shunt when infant is large enough (usually >2 kg) and CSF protein is low enough for shunt to function

B) Normal Pressure Hydrocephalus

• Diagnosis by clinical triad + imaging + tap test
• Gait improvement after large-volume LP = best predictor of shunt success
• Treatment: VP shunt (programmable valve preferred)
• Gait improves most reliably; cognition and incontinence less predictable
• Up to 70–80% improve with shunt if patient selection is good

C) Idiopathic Intracranial Hypertension (IIH / Pseudotumor Cerebri)

• Young obese women predominantly
• Normal or small ventricles on imaging
• Raised ICP on LP (>25 cmH₂O)
• Treatment: weight loss, acetazolamide, serial LP, LP shunt or VP shunt if refractory, optic nerve sheath fenestration for visual threat

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11) PROGNOSIS

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12) QUICK REVISION SUMMARY TABLE

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1. Dandy-Walker malformation in detail, or
2. ICP monitoring and management in detail, or
3. Shunt complications and their management step-by-step?

1. MMSE (Mini-Mental State Examination)?
2. MSc (Master of Science)?
3. A specific medical topic or abbreviation?

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Mini-Mental State Examination (MMSE)

A 30-point cognitive screening tool. Each correct answer = 1 point. (Harrison's Principles of Internal Medicine, 21st Ed., p. 845)

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DOMAIN 1 — ORIENTATION (10 points)

Time Orientation (5 points)

Place Orientation (5 points)

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DOMAIN 2 — REGISTRATION (3 points)

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DOMAIN 3 — ATTENTION AND CALCULATION (5 points)

Option A — Serial 7s

Option B — Spelling "WORLD" Backwards

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DOMAIN 4 — RECALL (3 points)

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DOMAIN 5 — LANGUAGE (8 points)

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DOMAIN 6 — VISUOSPATIAL / CONSTRUCTION (1 point)

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TOTAL SCORE SUMMARY

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INTERPRETATION OF SCORES

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IMPORTANT CLINICAL NOTES

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MMSE vs MoCA — Quick Comparison

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