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CNS Clinical Medicine — Medical Student Exam Guide

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1. RAISED INTRACRANIAL PRESSURE (RICP)

Definition & Normal Values

• Normal ICP: 5–15 mmHg (adults). Sustained >20 mmHg is pathological.

Causes (Mnemonic: VITAMIN C)

Clinical Features

• High-pressure headache: worse on coughing, bending forward, lying down (worse in morning)
• Nausea & vomiting (projectile)
• Blurred/double vision (CN VI palsy — false localising sign)
• Papilloedema on fundoscopy (takes time to develop — may be absent acutely)
• Altered consciousness → coma

In infants (before skull suture closure):

• Increased head circumference
• Tense bulging fontanelle
• Prominent scalp veins
• Sunsetting sign (Parinaud's syndrome — loss of upgaze due to dorsal midbrain compression)

Cushing's Triad (late/dangerous sign of herniation):

• Hypertension
• Bradycardia
• Irregular respiration

Investigations

1. CT head (first-line) — identifies mass lesions, haemorrhage, hydrocephalus, cerebral oedema
2. MRI — better for anatomy, planning surgical treatment (third ventriculostomy)
3. Invasive ICP monitoring (gold standard) — external ventricular drain or intraparenchymal pressure monitor

Management

1. Head-of-bed elevation 30°
2. Osmotherapy: IV mannitol 20% or hypertonic saline 3% (reduces cerebral oedema)
3. Avoid hypoxia, hypercapnia (keep PaCO₂ 35–40 mmHg)
4. Treat underlying cause (e.g., neurosurgery for mass/haematoma)
5. Dexamethasone — for vasogenic oedema (tumour/abscess, NOT cytotoxic oedema)

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2. STROKE (Cerebrovascular Accident)

Definition

Classification

Ischaemic Stroke — Aetiology (TOAST Classification)

1. Large artery atherosclerosis (e.g., carotid stenosis)
2. Cardioembolism (AF is most common cardiac cause)
3. Small vessel/lacunar (HTN, DM → lipohyalinosis)
4. Other determined (dissection, vasculitis, hypercoagulable)
5. Undetermined

FAST + BE-FAST Recognition

• Balance loss, Eyes (vision loss), Face droop, Arm weakness, Speech difficulty, Time to call

Arterial Territory Syndromes

Investigations

1. Non-contrast CT head — immediately (excludes haemorrhage before thrombolysis)
2. CT/MR angiography — identifies large vessel occlusion
3. MRI DWI — gold standard for early ischaemic infarct
4. ECG (AF), Echo, Carotid Doppler, FBC, coagulation, glucose, lipids

Management — Acute Ischaemic Stroke

Secondary Prevention

• AF → anticoagulation (DOAC/warfarin)
• Atherosclerosis → antiplatelet (clopidogrel) + statin + antihypertensive
• Carotid endarterectomy if symptomatic stenosis 70–99%

Haemorrhagic Stroke / SAH

• SAH: "Worst headache of life" (thunderclap) ± neck stiffness, photophobia
• CT head within 6 h: sensitivity approaching 99%
• If CT negative and suspicion high: LP for xanthochromia (≥12 h post-onset)
• Management: neurosurgical clipping or endovascular coiling; nimodipine (prevents vasospasm)

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3. EPILEPSY & SEIZURES

Definition

• Seizure: paroxysmal, hypersynchronous, excessive discharge of cerebral cortical neurons
• Epilepsy: ≥2 unprovoked seizures >24 h apart, OR 1 unprovoked seizure with high recurrence risk (≥60%)
• Prevalence: ~2 million in the USA; ~1% by age 20; bimodal incidence (childhood & >60 years)

2017 ILAE Classification

By Onset:

1. Focal (partial) — from one hemisphere region
   • Focal aware (simple partial — no LOC)
   • Focal impaired awareness (complex partial — impaired consciousness)
   • Focal to bilateral tonic-clonic
2. Generalised — both hemispheres from outset
3. Unknown onset

Generalised Seizure Types:

Common Epilepsy Syndromes

Status Epilepticus

• Definition: Seizure lasting >5 min OR ≥2 seizures without recovery
• Management (stepwise, time-critical):
  1. 0–5 min: Airway, Oxygen, IV access, glucose check
  2. 5–20 min (Early SE): Lorazepam 0.1 mg/kg IV or Diazepam PR/IV
  3. 20–40 min (Established SE): Levetiracetam IV / Phenytoin / Valproate / Phenobarbital IV
  4. >40 min (Refractory SE): ICU + General anaesthesia (propofol, thiopental, midazolam infusion)

Postictal Features (Help distinguish from other causes of LOC):

• Todd's paresis (transient focal weakness)
• Confusion, drowsiness
• Headache, muscle ache
• Tongue biting, urinary incontinence

Investigations

• EEG (supports diagnosis; normal EEG does not exclude epilepsy)
• MRI brain (structural cause; preferred over CT)
• Metabolic screen (glucose, Na, Ca, Mg, LFTs)

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4. MENINGITIS & ENCEPHALITIS

Key Clinical Triad of Meningitis

Meningism Signs

• Kernig's sign: Resistance/pain on knee extension with hip flexed 90°
• Brudzinski's sign: Passive neck flexion causes involuntary hip/knee flexion
• Photophobia, phonophobia, severe headache ("worst of life")

Aetiology by Age

Meningococcal Meningitis — Red Flags

• Non-blanching petechial/purpuric rash → Meningococcal septicaemia (medical emergency)
• Waterhouse-Friderichsen syndrome (bilateral adrenal haemorrhage → Addisonian crisis)

Investigations

1. Blood cultures (before antibiotics if possible)
2. CT head before LP if: focal neurology, papilloedema, GCS <13, new seizure, immunocompromised
3. Lumbar puncture (LP) — CSF analysis

CSF Analysis

Management — Bacterial Meningitis

1. Do NOT delay antibiotics if LP is delayed
2. Ceftriaxone IV 2g BD (adults) — empirical first-line
3. Add Dexamethasone 0.15 mg/kg IV QDS × 4 days (reduces hearing loss & inflammation in S. pneumoniae)
4. Add Ampicillin if age >55 or immunocompromised (Listeria cover)
5. Viral (HSV encephalitis) → Aciclovir IV 10 mg/kg TDS × 14–21 days

Encephalitis vs Meningitis

• Meningitis: inflammation of meninges → meningism, headache, fever; consciousness usually preserved initially
• Encephalitis: inflammation of brain parenchyma → altered consciousness, behaviour change, focal neurology, seizures
• HSV encephalitis: temporal lobe predilection → temporal lobe seizures, personality change; MRI shows temporal signal change; treat empirically with aciclovir

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5. MULTIPLE SCLEROSIS (MS)

Definition

Epidemiology

• Incidence: 1.5–11 per 100,000/year
• 2nd most common cause of neurological disability in young adults (after trauma)
• Female > Male (~3:1); peak onset 20–40 years
• Higher prevalence farther from the equator (latitude effect)

Types of MS

Common Presentations (Dissemination in Space & Time)

McDonald Diagnostic Criteria (2017)

• Dissemination in space (DIS): ≥2 separate CNS areas affected
• Dissemination in time (DIT): ≥2 episodes at different times OR MRI shows simultaneous gadolinium-enhancing and non-enhancing lesions

Investigations

1. MRI brain & spine — periventricular, juxtacortical, infratentorial, spinal cord lesions (T2 bright, T1 black holes); gadolinium-enhancing = active
2. CSF: Oligoclonal IgG bands (not in serum) in >90%; lymphocytic pleocytosis
3. Visual/auditory evoked potentials — prolonged latencies
4. Exclude mimics: ANA, ANCA, AQP4-IgG (NMOSD), MOG-IgG

Management

Acute Relapse:

• Methylprednisolone IV 1g/day × 3–5 days — shortens duration, does not improve long-term outcome

Disease-Modifying Therapies (DMTs):

Symptomatic:

• Spasticity: Baclofen, tizanidine
• Fatigue: Amantadine, modafinil
• Neuropathic pain: Amitriptyline, gabapentin
• Bladder: Oxybutynin, self-catheterisation

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6. CNS TUMOURS

Classification

Presenting Features

• Focal neurological deficit (depends on location)
• Raised ICP (headache, vomiting, papilloedema)
• Seizures (especially cortical tumours)
• Personality/cognitive change (frontal lobe)

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7. PARKINSON'S DISEASE

Pathology

Cardinal Motor Features (TRAP)

• Tremor: resting ("pill-rolling"), 4–6 Hz, asymmetric, lessens with action
• Rigidity: "lead-pipe" or "cogwheel" (when tremor superimposed)
• Akinesia/Bradykinesia: slow movement, micrographia, hypomimia (mask-like face), shuffling gait
• Postural instability: late feature; falls

Non-Motor Features

• Autonomic: constipation, orthostatic hypotension, urinary dysfunction
• Cognitive: dementia (late)
• Anosmia (often precedes motor symptoms)
• REM sleep behaviour disorder
• Depression

Investigations (clinical diagnosis — investigations mainly to exclude mimics)

• DaTscan (dopamine transporter SPECT): confirms dopaminergic deficiency (differentiates from essential tremor)
• MRI (normal in PD; abnormal in PSP/MSA)

Management

Motor Complications of Long-term Levodopa:

• Wearing off: benefit shortens between doses
• On-off fluctuations: unpredictable motor switching
• Dyskinesias: involuntary movements at peak dose

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8. DEMENTIA

Definition

Common Causes

Management of Alzheimer's

• AChEIs (Donepezil, Rivastigmine, Galantamine): symptomatic; mild-moderate
• Memantine (NMDA antagonist): moderate-severe
• Newest: Lecanemab/Donanemab (anti-amyloid mAbs) — FDA-approved, slow disease progression in early AD (2023–2024)

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9. NEUROLOGICAL EXAMINATION — KEY SIGNS

UMN vs LMN Summary

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10. CSF FINDINGS SUMMARY (Exam Favourite)

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Quick Exam Mnemonics

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CNS CLINICAL MEDICINE — COMPREHENSIVE DEEP DIVE

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SECTION 1: STROKE (CEREBROVASCULAR DISEASE)

1.1 Pathophysiology

• Penumbra concept: Central core of irreversibly infarcted tissue surrounded by a penumbra of viable but at-risk tissue. The penumbra is the target of acute reperfusion therapy.
• Mechanism: Excitotoxicity → glutamate release → calcium influx → mitochondrial failure → cell death within minutes
• "Time is brain": 1.9 million neurons die every minute without treatment

• Intracerebral haemorrhage (ICH): usually hypertensive (putamen > thalamus > pons > cerebellum > subcortical white matter)
• Subarachnoid haemorrhage (SAH): 85% from ruptured saccular (berry) aneurysm; commonly at Circle of Willis bifurcations

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1.2 Risk Factors

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1.3 Stroke Syndromes — Full Localisation

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1.4 TIA — Key Points

• Definition: Focal neurological deficit resolving within 24 h with no infarct on DWI-MRI (some older definitions allow up to 24 h)
• ABCD² Score (predicts 2-day stroke risk):
  • A ge ≥60 (1 pt)
  • B P ≥140/90 (1 pt)
  • C linical features: unilateral weakness (2 pt), speech disturbance without weakness (1 pt)
  • D uration ≥60 min (2 pt), 10–59 min (1 pt)
  • D iabetes (1 pt)
  • Score ≥4 = high risk → admit and investigate urgently

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1.5 Investigations

1. Non-contrast CT head: First test — excludes haemorrhage; ischaemic changes may not appear for 6–12 h (early signs: loss of grey-white differentiation, hyperdense MCA sign)
2. MRI DWI/ADC: Detects ischaemia within minutes; gold standard; restricted diffusion = cytotoxic oedema
3. CT angiography / MR angiography: Identifies LVO for thrombectomy eligibility
4. ECG: AF (most common cardiac embolism cause)
5. Echocardiography: Cardiac thrombus, PFO, valvular disease
6. Carotid Doppler / CT-A: Carotid stenosis for endarterectomy decision
7. Bloods: FBC (polycythaemia, thrombocytosis), coagulation (thrombophilia screen), fasting glucose/HbA1c, lipids, ESR (vasculitis)

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1.6 Acute Management — Ischaemic Stroke

IV Thrombolysis — Alteplase

• Dose: 0.9 mg/kg IV (max 90 mg); 10% as bolus, rest over 60 min
• Time window: ≤4.5 hours from onset (NNT ~8 for good outcome)
• Contraindications (absolute): haemorrhage on CT, BP >185/110 (uncontrolled), recent surgery/trauma, anticoagulation with INR >1.7, platelets <100, prior stroke within 3 months, blood glucose <2.8 or >22.2

Mechanical Thrombectomy

• Indication: LVO (M1, M2 segment MCA, ICA, basilar), NIHSS ≥6
• Time window: ≤6 h routine; ≤24 h in selected patients (DAWN/DEFUSE-3 criteria: mismatch imaging)
• Can be combined with IV thrombolysis or standalone ("direct MT")
• Technique: Stent retriever or aspiration catheter via transfemoral approach

Supportive Care (all patients)

• Aspirin 300 mg within 24 h (if no thrombolysis, delay 24 h post-thrombolysis)
• Admit to stroke unit (reduces mortality by ~20% vs general ward)
• Permissive hypertension: do NOT treat BP acutely unless >220/120 (or >185/110 pre-thrombolysis)
• Maintain normoglycaemia (hypoglycaemia worsens outcome; hyperglycaemia also harmful)
• Swallowing assessment before oral intake (risk of aspiration pneumonia)
• DVT prophylaxis; early mobilisation

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1.7 Secondary Prevention

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1.8 SAH Management

• Confirm: Non-contrast CT → if negative after 6 h onset → LP (xanthochromia)
• Aneurysm treatment: Endovascular coiling preferred over surgical clipping (ISAT trial)
• Nimodipine (calcium channel blocker) 60 mg PO q4h × 21 days: reduces delayed cerebral ischaemia/vasospasm (NOT to acutely lower BP)
• Complications: Re-bleeding (peak day 1), vasospasm (days 4–14), hydrocephalus, hyponatraemia (SIADH or cerebral salt wasting)

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SECTION 2: EPILEPSY & SEIZURES (DEEP)

2.1 Pathophysiology

• Abnormal, hypersynchronous discharge of cortical neurons
• Focal seizures: arise from one area; may spread (Jacksonian march) or generalise
• Generalised seizures: simultaneously involve both hemispheres
• Underlying mechanisms: Reduced GABAergic inhibition, increased glutamatergic excitation, or channelopathies (Na⁺, K⁺, Ca²⁺ channels)

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2.2 ILAE 2017 Classification in Detail

Focal Seizures

• Focal aware (formerly simple partial): consciousness preserved; motor, sensory, autonomic, psychic features
• Focal impaired awareness (formerly complex partial): consciousness impaired; most common type in adults → temporal lobe epilepsy; automatisms (lip smacking, fumbling, chewing)
• Focal to bilateral tonic-clonic: secondary generalisation

• Most common symptomatic epilepsy in adults
• Aura: rising epigastric sensation, déjà vu/jamais vu, olfactory hallucinations (uncinate fits)
• Postictal confusion prominent
• Cause: hippocampal sclerosis (MRI: hippocampal atrophy, T2 signal change)
• Treatment: carbamazepine/lamotrigine; surgery (temporal lobectomy) if drug-resistant — 60–70% seizure free

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2.3 Generalised Tonic-Clonic Seizure — Phases (from Adams & Victor)

1. Prodrome: hours before — irritability, headache (inconsistent)
2. Tonic phase (10–20 s): sudden LOC, cry (forced air through closed cords), limb extension, cyanosis, tongue biting, pupils dilated, bladder may empty
3. Clonic phase (~30 s): rhythmic flexor spasms, 8→4/s, autonomic surge (tachycardia, ↑BP, salivation, sweating)
4. Postictal phase: deep coma → confusion → drowsiness → sleep; Todd's paresis (transient focal weakness); headache, myalgia
5. EEG correlates: 10 Hz spikes (tonic) → polyspike-and-wave (clonic) → near-isoelectric (postictal)

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2.4 Absence Seizures (Petit Mal)

• Classic absence: 3 Hz generalised spike-and-wave; brief (5–30 s) abrupt staring; no postictal phase; multiple per day; onset 4–12 years
• Juvenile absence: 3.5–4 Hz; older onset; may have associated generalised tonic-clonic
• Hyperventilation or photic stimulation provokes absence on EEG
• Treatment: Ethosuximide (first-line for absence-only), Valproate (if associated GTCS), Lamotrigine

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2.5 Juvenile Myoclonic Epilepsy (JME)

• Most common generalised epilepsy in adolescents
• Triad: myoclonic jerks (early morning, on waking), GTCS, absence
• EEG: 4–6 Hz polyspike-wave
• Precipitants: sleep deprivation, alcohol, photosensitivity
• Treatment: Sodium valproate (most effective); lifelong therapy usually needed
• Avoid: carbamazepine, phenytoin (worsen myoclonus/absence)

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2.6 Status Epilepticus — Time-Critical Protocol

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2.7 Antiepileptic Drug (AED) Guide

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SECTION 3: MENINGITIS & ENCEPHALITIS (DEEP)

3.1 Clinical Approach

• Photophobia, phonophobia
• Kernig's sign: With hip flexed 90°, pain/resistance on passive knee extension (hamstring meningism)
• Brudzinski's sign: Passive neck flexion → involuntary bilateral hip and knee flexion
• Jolt accentuation: 2–3 Hz horizontal head rotation worsens headache (sensitive early sign)

3.2 Differential Diagnosis of Acute Headache + Fever + Neck Stiffness

• Bacterial meningitis
• Viral meningitis
• SAH (fever can develop later)
• Viral encephalitis (HSV)
• Brain abscess
• Cerebral venous sinus thrombosis

3.3 When to Do CT Before LP

• GCS <13 or falling
• New focal neurological deficit
• Papilloedema
• New-onset seizure
• Immunocompromised
• History of CNS disease

3.4 CSF Interpretation (Detailed)

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3.5 Bacterial Meningitis Treatment Protocol

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3.6 Viral Encephalitis — HSV

• Tropism for temporal and frontal lobes (limbic encephalitis)
• Clinical: fever, headache, behavioural change (personality/psychosis), temporal lobe seizures, aphasia, olfactory hallucinations
• MRI: T2/FLAIR hyperintensity in medial temporal lobes, insular cortex, cingulate ± haemorrhagic change
• EEG: periodic lateralising epileptiform discharges (PLEDs) over temporal lobes
• CSF: lymphocytic pleocytosis, mild protein ↑, normal glucose; HSV PCR (sensitivity >95%)
• Treatment: Aciclovir 10 mg/kg IV TDS × 14–21 days — start empirically; mortality 70% untreated → 20–30% with treatment
• Complications: Amnesia (hippocampal damage), epilepsy, personality change; anti-NMDAR encephalitis can be triggered by HSV (autoimmune post-infectious)

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SECTION 4: MULTIPLE SCLEROSIS (DEEP)

4.1 Pathology

• Plaque: area of focal demyelination with perivenular inflammation, T-lymphocyte and macrophage infiltration, reactive gliosis
• Axonal loss: key substrate of permanent disability (not just demyelination)
• Oligodendrocytes (myelin-forming cells in CNS) are the primary target
• Histology: Shadow plaques (remyelination), chronic silent plaques, cortical grey matter lesions

4.2 Characteristic MRI Lesions

• Periventricular (perpendicular to ventricles — "Dawson's fingers" on sagittal FLAIR)
• Juxtacortical (touching cortex)
• Infratentorial (cerebellum, brainstem)
• Spinal cord (cervical most common; <2 vertebral segments — distinguishes from NMOSD)
• Gadolinium-enhancing = active lesion (breakdown of blood-brain barrier)
• T1 black holes = axonal loss/permanent damage

4.3 McDonald Criteria 2017 (DIS + DIT)

1. Periventricular
2. Cortical/juxtacortical
3. Infratentorial
4. Spinal cord

• New T2 or Gd-enhancing lesion on follow-up MRI
• Simultaneous presence of Gd-enhancing AND non-enhancing T2 lesions
• CSF-specific oligoclonal bands (allows DIT diagnosis without second MRI)

4.4 Key Clinical Syndromes in MS

• Painful, unilateral visual loss; colour desaturation ("washed out")
• Relative Afferent Pupillary Defect (RAPD/Marcus Gunn pupil): swinging torch test — affected eye has less constriction
• Recovery common but residual Uhthoff's phenomenon persists
• 50% develop MS within 10 years after isolated ON

• Lesion: Medial Longitudinal Fasciculus (MLF)
• Ipsilateral eye fails to adduct (III palsy-like) on lateral gaze; contralateral eye has nystagmus
• Bilateral INO in young adult = MS until proven otherwise

• Incomplete (partial) cord syndrome → distinguishes from NMOSD (which is complete)
• Lhermitte's sign, spastic paraparesis, sensory level, bladder dysfunction

• Intention tremor, Nystagmus, Scanning/staccato dysarthria

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4.5 Disease-Modifying Therapies (Full Table)

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SECTION 5: PARKINSON'S DISEASE (DEEP)

5.1 Pathology in Detail

• Braak staging (Braak H et al., 2003): α-synuclein pathology begins in the olfactory bulb and dorsal motor nucleus of vagus (Stage 1), ascends through brainstem (Stage 2–3: locus coeruleus, SN), reaches cortex (Stage 5–6: prefrontal, sensorimotor cortex)
• This explains why anosmia and constipation precede motor symptoms by years (prodromal PD)
• Lewy body: intracytoplasmic eosinophilic inclusion containing α-synuclein + ubiquitin
• Lewy neurites: abnormal α-synuclein in axons

5.2 Differentiating Parkinsonism

5.3 Levodopa Complications (Long-term)

5.4 Surgical Treatment

• Deep Brain Stimulation (DBS): Electrode in subthalamic nucleus (STN) or globus pallidus interna (GPi); reduces "off" time and dyskinesias; does not slow disease progression; best response in tremor and motor fluctuations

5.5 Non-Motor Management

• Orthostatic hypotension: fludrocortisone, midodrine
• Constipation: macrogol laxatives
• Psychosis/hallucinations: reduce AED polypharmacy; Clozapine (low dose), Quetiapine — avoid typical antipsychotics
• Depression: SSRIs; avoid TCAs in elderly
• Dementia in PD: Rivastigmine (only licensed acetylcholinesterase inhibitor for PDD)
• REM sleep disorder: clonazepam, melatonin

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SECTION 6: DEMENTIA (DEEP)

6.1 Alzheimer's Disease (AD)

• Amyloid plaques (extracellular Aβ 42 aggregates — "senile plaques")
• Neurofibrillary tangles (intracellular hyperphosphorylated tau — "NFTs")
• Basal nucleus of Meynert (cholinergic neurons) → cholinergic deficit → memory impairment
• Genetic: Early-onset familial AD: mutations in APP, PSEN1, PSEN2; Late-onset: APOE ε4 allele (biggest genetic risk factor)
• Biomarkers: CSF Aβ42 ↓, CSF tau ↑, phospho-tau ↑; amyloid PET positive

1. Mild: Episodic memory, word-finding difficulty, normal daily function
2. Moderate: Visuospatial deficits, disorientation, needs help with ADLs
3. Severe: Mutism, incontinence, bed-bound, dysphagia

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6.2 Vascular Dementia

• Stepwise (not gradual) deterioration; may plateau between events
• Multiple lacunar infarcts, white matter ischaemia (Binswanger disease)
• Treat vascular risk factors (BP, statin, antiplatelet, glycaemic control)
• No specific disease-modifying therapy approved

6.3 Lewy Body Dementia (DLB)

1. Fluctuating cognition
2. Recurrent complex visual hallucinations (well-formed, detailed — people/animals)
3. REM sleep behaviour disorder (acts out dreams)
4. Parkinsonism

• Treatment: Rivastigmine (cognitive), levodopa (motor — low dose), avoid antipsychotics

6.4 Frontotemporal Dementia (FTD)

• Behavioural variant (bvFTD): disinhibition, apathy, hyperorality, executive dysfunction, relative memory preservation; frontotemporal atrophy
• Progressive non-fluent aphasia (PNFA): effortful speech, agrammatism; left inferior frontal atrophy
• Semantic dementia: fluent but empty speech, loss of word meaning; bilateral anterior temporal atrophy
• Pathology: TDP-43, tau, or FUS inclusions
• Genetics: C9orf72 expansion (also ALS-FTD), GRN, MAPT mutations
• No specific treatment; manage behavioural symptoms (SSRIs for disinhibition)

6.5 Normal Pressure Hydrocephalus (NPH)

1. Gait apraxia ("magnetic gait" — feet appear stuck to floor; wide-based, small steps)
2. Urinary incontinence (urgency → incontinence)
3. Dementia (frontal-subcortical pattern)

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SECTION 7: RAISED ICP & BRAIN HERNIATION

7.1 Monroe-Kellie Doctrine

7.2 Herniation Syndromes

7.3 Grades of Consciousness — Glasgow Coma Scale

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SECTION 8: CNS TUMOURS (DEEP)

8.1 WHO Classification of Brain Tumours (2021)

8.2 Management of GBM

• Surgery: maximal safe resection (extends survival, confirms molecular diagnosis)
• Stupp protocol (standard of care): Temozolomide (oral alkylating agent) concurrent with RT (60 Gy), then 6 cycles adjuvant temozolomide
• MGMT methylation: Promoter methylation → better response to temozolomide (epigenetic silencing of DNA repair enzyme)
• Bevacizumab (anti-VEGF): Used at recurrence; reduces oedema/steroid need
• Prognosis: MGMT methylated GBM ~21 months; unmethylated ~14 months

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SECTION 9: NEUROLOGICAL EXAMINATION & LOCALISATION

9.1 UMN vs LMN Lesions

9.2 Localisation by Pattern

9.3 Cauda Equina Syndrome

• Cause: Central L4/5 disc prolapse (most common), tumour, abscess, haematoma
• Features: Bilateral leg pain/weakness, saddle anaesthesia (S3–S5), urinary retention (painless), bowel incontinence, absent ankle jerks
• Management: MRI spine URGENTLY; emergency surgical decompression within 24–48 h (best within 6 h for bladder recovery)

9.4 Cranial Nerve Examination — High-Yield Lesions

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SECTION 10: GUILLAIN-BARRÉ SYNDROME (GBS)

Pathophysiology

• Post-infectious acute inflammatory demyelinating polyneuropathy (AIDP) — most common subtype in Western world
• Molecular mimicry: antibodies (anti-ganglioside — anti-GQ1b in Miller-Fisher) attack peripheral myelin
• Triggers: Campylobacter jejuni (most common, associated with AMAN — axonal variant), CMV, EBV, HIV, Zika virus, vaccines (rare)

Clinical Features

• Ascending flaccid paralysis: starts in legs, progresses over days–4 weeks
• Areflexia (cardinal sign)
• Autonomic instability (BP fluctuations, arrhythmias, urinary retention) — most dangerous feature
• Cranial nerve involvement (bilateral VII palsy, bulbar palsy)
• Pain (radicular) very common
• Respiratory failure — monitor FVC; intubate if FVC <20 mL/kg or <1 L

Variants

• AIDP (classic): demyelinating; anti-ganglioside antibodies
• AMAN (acute motor axonal neuropathy): axonal; anti-GM1/GD1a; post-Campylobacter; common in Asia
• Miller-Fisher syndrome: anti-GQ1b; triad of ophthalmoplegia, ataxia, areflexia — no limb weakness; generally benign

CSF Finding

Management

1. IVIG 2 g/kg over 5 days (or plasma exchange — equally effective; do NOT combine)
2. Supportive: HDU/ICU monitoring; ventilatory support; DVT prophylaxis; pain management
3. Steroids NOT effective in GBS (worsen outcome)
4. Brighton criteria for case diagnosis

Prognosis

• Most recover fully over weeks–months
• 5–10% permanent disability; 3–5% mortality (respiratory/autonomic complications)
• AIDP better prognosis than AMAN (axons take longer to regenerate)

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QUICK-REFERENCE SUMMARY TABLES

Top 10 Exam Scenarios

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Antiepileptic Drug Contraindications (Exam Favourite)

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