Cerebellar syndrome = complex of signs from cerebellar/cerebellar pathway dysfunction.

• Causes: Alcohol (most common ); MS; cerebellar stroke (PICA → lateral medullary syndrome ); cerebellar tumour (medulloblastoma in children; haemangioblastoma = VHL ); paraneoplastic (anti-Yo — ovarian/breast cancer ); drugs (phenytoin, carbamazepine); hypothyroidism; Friedreich's ataxia (hereditary )
• Localisation: midline/vermis lesions cause truncal and gait ataxia with titubation; cerebellar hemisphere lesions cause IPSILATERAL limb ataxia, intention tremor, dysmetria and dysdiadochokinesia; flocculonodular lesions cause vertigo and nystagmus.
• Causes (expanded): vascular (PICA/SCA stroke), demyelination (MS), toxic/metabolic (alcohol, phenytoin, lithium), tumour (medulloblastoma in children; metastases/haemangioblastoma in adults), hereditary (Friedreich ataxia, spinocerebellar ataxias), paraneoplastic (anti-Yo), hypothyroidism and B12 deficiency.
• Investigations: MRI brain focused on the posterior fossa; B12, TFTs and an alcohol history; autoimmune/paraneoplastic antibodies; genetic testing where a hereditary ataxia is suspected.
• Key point: cerebellar signs are ipsilateral to the lesion; gait is wide-based and speech is a scanning/staccato dysarthria.

Status Epilepticus (SE) = seizure lasting > 5 minutes OR 2 or more seizures without full recovery of consciousness between them. After 5 min, self-termination becomes unlikely; after 30 min → neuronal injury ; after 60 min → systemic complications (hyperthermia, rhabdomyolysis, ARDS, hypoglycaemia).

• Treat underlying cause: Blood glucose (thiamine before glucose in alcoholics); electrolytes; LP if CNS infection; CT/MRI; antibiotics empirically if infection suspected
• Definition detail: convulsive status is a continuous seizure > 5 min or repeated seizures without recovery of consciousness; beyond ~30 min there is risk of permanent neuronal injury; non-convulsive status presents as a prolonged altered conscious state and needs EEG.
• Causes: low AED levels or non-adherence (commonest in known epilepsy), acute brain insult (stroke, CNS infection, trauma, tumour), metabolic derangement (hypoglycaemia, hyponatraemia, hypocalcaemia), drug or alcohol withdrawal, and eclampsia.
• Refractory status: if seizures persist after a benzodiazepine and a second-line agent, induce general anaesthesia (midazolam, propofol or thiopentone infusion) with intubation and continuous EEG monitoring.
• Complications: hypoxia, aspiration pneumonia, rhabdomyolysis with acute kidney injury, hyperthermia, cardiac arrhythmia and lasting neuronal damage.

Migraine = recurrent episodic headache characterised by unilateral, pulsating , moderate-severe intensity, aggravated by physical activity, associated with nausea/vomiting and/or photophobia + phonophobia. Duration 4–72 hours (untreated). Prevalence: 15%; F > M (3:1). Aura (visual — scintillating scotoma; sensory; motor) in 30% (migraine with aura ).

• Clinical phases: prodrome (mood/appetite change), aura (reversible visual or sensory symptoms over 5-60 min), headache (unilateral, throbbing, with nausea, photophobia and phonophobia), and postdrome (fatigue).
• Types and diagnosis: migraine with aura and without aura; diagnosis is clinical (recurrent attacks lasting 4-72 h with the typical features); identify triggers (stress, sleep change, hormones, foods, dehydration).
• Prophylaxis (>= 4 attacks/month): propranolol, amitriptyline, topiramate or sodium valproate (avoid in women of childbearing potential); newer CGRP monoclonal antibodies for refractory cases; manage medication-overuse headache.
• Red flags (exclude secondary cause): thunderclap onset, new headache over 50 years, fever with neck stiffness, focal deficit, papilloedema, or progressive/positional headache.

• Drug-resistant epilepsy = failure of 2 appropriate AEDs → consider epilepsy surgery (temporal lobe epilepsy with hippocampal sclerosis → temporal lobectomy: 60–80% seizure-free ); VNS (vagus nerve stimulation); ketogenic diet (children )
• Classification: seizures are focal (aware/impaired awareness, +/- secondary generalisation) or generalised (tonic-clonic, absence, myoclonic, atonic); epilepsy syndromes are then defined by EEG and clinical pattern.
• Investigations: EEG (supports classification; interictal discharges), MRI brain (structural cause, especially in focal epilepsy), and bloods/glucose/ECG to exclude provoked seizures.
• AED principles: start after a second unprovoked seizure (or after the first if high recurrence risk); monotherapy first, titrated slowly; broad-spectrum agents (valproate, lamotrigine, levetiracetam) for generalised epilepsy.
• Special situations: pregnancy - prefer lamotrigine/levetiracetam, give folate, avoid valproate; counsel on driving rules and sudden unexpected death in epilepsy (SUDEP).

Syncope = transient loss of consciousness (T-LOC) due to global cerebral hypoperfusion , characterised by rapid onset, short duration, and complete spontaneous recovery. Must distinguish from seizure, cardiac arrest, TIA, metabolic (hypoglycaemia).

• Red flags for cardiac syncope: syncope on exertion or when supine, palpitations preceding the event, no prodrome, family history of sudden death, and structural heart disease or an abnormal ECG.
• Investigations: 12-lead ECG in all (arrhythmia, long QT, Brugada, ischaemia); lying/standing BP (orthostatic drop); echocardiogram if structural disease suspected; ambulatory ECG/Holter or loop recorder for arrhythmia; tilt-table testing for recurrent reflex syncope.
• Management: treat the cause; reflex syncope - reassurance, avoid triggers, counter-pressure manoeuvres; orthostatic - review drugs, fluids/salt, compression stockings; cardiac - treat arrhythmia (pacing/ICD) or structural disease.

GBS = acute immune-mediated polyradiculoneuropathy causing ascending flaccid paralysis. Precipitated by infection (1–3 weeks prior) — *Campylobacter jejuni* (#1), CMV, EBV, HIV, COVID-19.

• Pathogenesis: Molecular mimicry → antibodies cross-react with peripheral nerve gangliosides (anti-GQ1b = Miller Fisher; anti-GM1 = AMAN )
• Clinical features: Ascending flaccid weakness (legs → arms); areflexia (even in initially strong muscles); autonomic dysfunction (arrhythmias, BP lability, urinary retention — most dangerous feature ); respiratory failure (monitor VC — intubate if VC < 15–20 mL/kg or NIF < -25 cmH2O)
• CSF: Albumino-cytological dissociation (↑ protein > 0.55 g/L with < 10 cells/μL — pathognomonic ); peaks 1–2 weeks after onset
• NCS: Slowed conduction velocity + prolonged distal latency + conduction block (AIDP ); reduced/absent CMAP (AMAN/AMSAN )

▶ IVIg 2 g/kg over 5 days OR Plasmapheresis × 5 exchanges over 2 weeks — EQUALLY effective; do NOT combine (no additive benefit); steroids NOT beneficial in GBS (unlike most autoimmune neuropathies)

• Respiratory monitoring — 20/30/40 rule: VC < 20 mL/kg OR MIP < 30 cmH2O OR MEP < 40 cmH2O → intubate ; ICU monitoring; anticoagulation (DVT risk from immobility)

• Variants: AIDP (commonest, demyelinating), AMAN/AMSAN (axonal, anti-GM1, Campylobacter-associated), and Miller Fisher syndrome (ophthalmoplegia, ataxia, areflexia; anti-GQ1b).
• Complications: neuromuscular respiratory failure, autonomic instability (arrhythmia, labile BP), aspiration, venous thromboembolism, and pain.
• Poor prognostic factors: older age, rapid onset, preceding Campylobacter/diarrhoeal illness, axonal subtype, and the need for ventilation.

Bell's palsy = idiopathic unilateral LMN facial palsy (CN VII); most common cause of acute facial nerve palsy (70% of all cases). Presumed cause: VZV/HSV reactivation (herpes simplex virus-1 most likely) causing inflammation + oedema within the facial canal (stylomastoid foramen).

• Clinical features: Acute onset (< 72 hrs) unilateral facial weakness; COMPLETE ipsilateral facial weakness — both upper AND lower face affected (LMN ); cannot wrinkle forehead (distinguishes from UMN/central lesion where forehead sparing )
• UMN vs LMN facial palsy:

• LMN (Bell's): Upper + lower face affected; cannot wrinkle forehead; cannot close eye (Bell's phenomenon — eye rolls upward ); taste loss (anterior 2/3 tongue — chorda tympani ); hyperacusis (stapedius branch)
• UMN (Stroke/tumour): SPARES FOREHEAD (bilateral cortical representation of forehead); lower face mainly affected

• House-Brackmann scale — grades severity I (normal) to VI (complete paralysis)

▶ Prednisolone 50 mg OD × 10 days (start within 72 hours ) — improves recovery rate (NNT 11); reduces incomplete recovery by ~60%

▶ Aciclovir 400 mg 5×/day × 7 days — if Ramsay Hunt suspected or severe palsy; evidence weak for Bell's alone (added to steroids in some guidelines)

• Eye care — CRITICAL; patch at night; lubricating eye drops; if cannot close eye → tape shut at night (prevent corneal exposure keratopathy )
• Prognosis: 85% complete recovery without treatment; 95%+ with steroids; poor signs: complete paralysis from onset, elderly, HTN, DM, no recovery at 3 weeks
• Differential diagnosis: exclude a UMN (forehead-sparing) lesion such as stroke or tumour; consider Ramsay Hunt syndrome (herpes zoster - vesicles, severe pain), Lyme disease (bilateral), otitis media/cholesteatoma, parotid tumour, and sarcoidosis.
• Investigations: Bell palsy is a clinical diagnosis; investigate (serology, imaging, nerve conduction studies) only for atypical features - bilateral palsy, slow onset, recurrence, or other cranial nerve involvement.
• Complications: exposure keratopathy (the key risk - hence eye protection), aberrant reinnervation (synkinesis), crocodile tears, and contracture.

AFP (Acute Flaccid Paralysis) = sudden onset flaccid paralysis of limbs in a child < 15 years OR any age — NOTIFIABLE condition (WHO — all AFP must be investigated to exclude poliomyelitis).

• WHO AFP surveillance: 2 stool samples at least 24 hours apart within 14 days of onset — isolation of poliovirus confirms polio; ≥ 60 days follow-up for residual paralysis
• Approach: rapidly distinguish the cause by tempo and pattern - asymmetric paralysis with fever and meningism suggests polio; ascending symmetrical weakness with areflexia suggests GBS; a sensory level suggests transverse myelitis.
• Investigations: two stool samples for poliovirus 24-48 h apart; nerve conduction studies and CSF (albuminocytological dissociation in GBS); MRI spine (myelitis, compression); serum potassium (periodic paralysis) and creatine kinase.
• Management: supportive care with airway and respiratory monitoring; GBS - IVIG or plasmapheresis; transverse myelitis - high-dose steroids; notify and investigate every case as possible polio.
• Poliomyelitis features: asymmetric, predominantly lower limb flaccid paralysis; fever at onset; CSF shows mild pleocytosis; asymmetry is characteristic (unlike GBS); diagnosed by stool viral culture for poliovirus; eradication ongoing - India certified polio-free 2014.
• Investigation algorithm: two stool samples 24-48 h apart for poliovirus culture (within 14 days of onset); if stools negative and GBS suspected - nerve conduction studies and CSF; if transverse myelitis suspected - urgent MRI spine; classify each AFP case within 60 days.

TIA = transient episode of neurological dysfunction due to focal brain, spinal cord or retinal ischaemia without acute infarction , symptoms lasting < 24 hours (usually < 1 hour). Medical emergency — risk of stroke highest in first 48 hours.

• Symptoms: Transient hemiplegia; aphasia; hemisensory loss; amaurosis fugax (transient monocular visual loss — 'curtain descending' — ophthalmic artery/retinal embolism)
• ABCD² score — risk stratification for stroke after TIA:

▶ Immediate dual antiplatelet: Aspirin 300 mg STAT + Clopidogrel 300 mg loading → then 75 mg/75 mg OD × 21 days (POINT/CHANCE trial ) → then single antiplatelet; statin 80 mg; BP management; cardiology review (ECG + echo)

• Admit for > 48 hrs if ABCD² ≥ 4 OR crescendo TIAs OR AF found
• Causes: cardioembolic (atrial fibrillation, valve disease), large-artery atherosclerosis (carotid stenosis), and small-vessel disease; consider rarer causes (dissection, vasculitis) in younger patients.
• Investigations: urgent brain imaging (MRI-DWI preferred), carotid Doppler (for carotid territory symptoms), ECG and ambulatory monitoring for paroxysmal AF, and bloods (glucose, lipids, FBC).
• Secondary prevention: long-term antiplatelet (clopidogrel) or anticoagulation if AF; high-intensity statin; treat hypertension and diabetes; carotid endarterectomy for symptomatic 70-99% stenosis.
• Mimics to exclude: hypoglycaemia, focal seizure with Todd paresis, migraine with aura, and syncope.
• Express TIA clinic: rapid specialist review within 24 h reduces stroke risk by 80% (FASTER/EXPRESS trials); brain imaging (MRI-DWI preferred), ECG, carotid Doppler, and bloods; admit if ABCD2 >= 4, crescendo TIAs, or AF detected.
• DWI-positive TIA: up to 50% of clinical TIAs show an acute diffuse-weighted lesion on MRI; these are now termed TIA with infarct and carry a higher recurrence risk; management is the same.

Bacterial (Pyogenic) Meningitis = acute inflammation of meninges by pyogenic bacteria — medical emergency with mortality 5–30%.

• Clinical features: Fever + Headache + Neck stiffness (meningism); Kernig's sign (inability to extend knee with hip flexed — 135°); Brudzinski's sign (neck flexion → involuntary hip flexion); Photophobia + Phonophobia; Altered sensorium; Petechial/purpuric rash (meningococcaemia — emergency )
• CSF: Turbid; opening pressure ↑↑; PMN (usually > 1000); protein ↑↑; glucose ↓↓↓ (< 50% blood glucose )

▶ Empirical antibiotics IMMEDIATELY (before CT if no papilloedema/no focal signs):
Ceftriaxone 2 g IV BD + Ampicillin 2 g IV q4h (if > 50 yrs or immunocomp — Listeria cover)
+ Dexamethasone 0.15 mg/kg IV q6h × 4 days (give WITH or BEFORE first dose of antibiotic — reduces mortality + hearing loss in S. pneumoniae meningitis )

• Contact prophylaxis (meningococcal): Close contacts → Rifampicin 600 mg BD × 2 days (adults) OR Ciprofloxacin 500 mg single dose OR Ceftriaxone 250 mg IM single dose
• Investigations: blood cultures and bloods before antibiotics where possible; CT head before LP only if reduced GCS, focal signs, papilloedema or immunocompromise; lumbar puncture for CSF (cell count, protein, glucose, Gram stain, culture, meningococcal/pneumococcal PCR).
• Adjunctive steroids: dexamethasone with or just before the first antibiotic dose reduces hearing loss and mortality in pneumococcal meningitis.
• Complications: septic shock and DIC, raised intracranial pressure, seizures, SIADH with hyponatraemia, sensorineural deafness, hydrocephalus, and cerebral abscess.

• Components: Eye opening (1-4), Verbal response (1-5) and best Motor response (1-6); best total 15, worst 3; always report the three components separately (e.g. E3 V4 M5).
• Interpretation: mild head injury 13-15, moderate 9-12, severe <= 8; GCS <= 8 means the airway cannot be protected (indication to intubate); a fall of >= 2 points indicates deterioration.
• Uses and limitations: used in trauma, coma and serial neurological observation; limited by intubation (record V as VT), sedation, intoxication, aphasia and eye injury; use the paediatric GCS in young children.
• Head injury grading: mild TBI (GCS 13-15), moderate TBI (9-12), severe TBI (3-8); serial GCS monitoring detects deterioration; a drop of >= 2 points indicates significant deterioration and warrants urgent reassessment and imaging.
• Alternative scales: FOUR score (Full Outline of UnResponsiveness) can assess brainstem reflexes and breathing patterns in intubated patients; AVPU (Alert, Voice, Pain, Unresponsive) is a rapid bedside triage tool.

Coma = state of unresponsiveness (GCS < 8 ) with no purposeful response to stimuli. NOT the same as sleep. Requires dysfunction of both cerebral hemispheres OR brainstem ARAS (reticular activating system).

• AEIOU TIPS mnemonic for coma causes: Alcohol; Epilepsy/Electrolytes; Insulin (glucose); Overdose; Uraemia; Trauma; Infection; Psychogenic; Stroke/Structural
• Management: A = Airway (GCS < 8 → intubate ); B = Breathing; C = Circulation; D = Dextrose 50% 50 mL IV (hypoglycaemia); Thiamine before glucose in alcoholics; naloxone if opioid; flumazenil if benzo; CT head; LP if meningitis suspected (after CT)
• Examination: assess GCS, pupil size and reactivity (pinpoint - opioids/pontine; fixed dilated - herniation), brainstem reflexes (corneal, gag, oculocephalic), respiratory pattern, posturing, and look for meningism, fever and focal signs.
• Investigations: capillary glucose immediately, then U&E, calcium, ABG, ammonia, toxicology and drug levels, FBC and cultures; CT head for a structural cause; lumbar puncture if CNS infection is suspected and imaging permits.
• Localising value: focal signs or asymmetric pupils suggest a structural cause; symmetrical examination with preserved brainstem reflexes suggests a metabolic/toxic cause.

• UMN lesion: lesion above the anterior horn cell (cortex, internal capsule, brainstem, spinal cord); spastic weakness, increased tone (clasp-knife), hyperreflexia, extensor plantar (Babinski), little wasting and no fasciculations; e.g. stroke, MS, cord compression.
• LMN lesion: lesion of the anterior horn cell, nerve root, plexus or peripheral nerve; flaccid weakness, reduced tone, hyporeflexia, marked wasting and fasciculations; e.g. motor neurone disease (LMN component), poliomyelitis, GBS, radiculopathy.
• Mixed UMN + LMN: seen in motor neurone disease (ALS), subacute combined degeneration of the cord (B12 deficiency) and conus medullaris lesions.
• Clinical importance: precise localisation of the UMN vs LMN lesion and its level guides the differential diagnosis and investigation; a C5-6 cord lesion causes UMN signs in the legs and LMN signs at the level of the lesion (wasted deltoids and biceps with brisk knee and ankle jerks).
• Investigations: MRI (brain and spine) to localise structural lesions; nerve conduction studies and EMG to characterise LMN vs myopathy; CSF analysis for inflammatory or infective causes; specific antibodies (anti-AChR for MG, anti-GQ1b for GBS variants).

Parkinson's disease (PD) = neurodegenerative disorder with loss of dopaminergic neurons in substantia nigra → ↓ dopamine in striatum → imbalance (↓ dopamine + relative ↑ acetylcholine) → movement disorder. Lewy bodies (alpha-synuclein inclusions) are pathognomonic.

• Cardinal features — TRAP:

• T = Tremor: Resting tremor (4–6 Hz; 'pill-rolling'; present at rest; absent on intention; worse with stress); earliest feature
• R = Rigidity: Lead-pipe rigidity (cogwheel rigidity with tremor superimposed; felt on passive flexion-extension); throughout range of motion
• A = Akinesia/Bradykinesia: Slowness of initiation + movement; micrographia; hypophonia; expressionless face (hypomimia — 'mask face' )
• P = Postural instability: Retropulsion; festinant gait (shuffling, stooped, short steps); 'pull test' positive

• Non-motor: Constipation; anosmia (earliest pre-motor feature ); depression; dementia; autonomic dysfunction; REM sleep behaviour disorder (predates motor by years)

▶ Levodopa + Carbidopa (Sinemet) — gold standard; most effective; carbidopa inhibits peripheral decarboxylation; dyskinesias (involuntary movements) with long-term use; 'wearing off'

▶ Dopamine agonists (Ropinirole, Pramipexole) — monotherapy in younger patients; fewer dyskinesias; impulse control disorders (gambling, hypersexuality) — important SE

▶ MAO-B inhibitors (Selegiline, Rasagiline) — mild symptomatic + possible neuroprotective effect; adjunctive

• Deep Brain Stimulation (DBS) of STN or GPi — for advanced PD + motor fluctuations/dyskinesias refractory to medical therapy; dramatic improvement in motor function
• Differential (Parkinson-plus and secondary): drug-induced (antipsychotics, metoclopramide), vascular parkinsonism, progressive supranuclear palsy (early falls, vertical gaze palsy), multiple system atrophy (early autonomic failure), and Lewy body dementia.
• Investigations: primarily a clinical diagnosis; MRI to exclude secondary causes; DaTscan (dopamine transporter imaging) where the diagnosis is unclear; a good response to levodopa supports idiopathic PD.
• Treatment complications: long-term levodopa causes motor fluctuations (wearing-off, on-off) and dyskinesias; dopamine agonists can cause impulse-control disorders, hallucinations and somnolence.

MS = chronic inflammatory demyelinating disease of CNS (brain + spinal cord), characterised by dissemination in time and space (different lesions at different times). Autoimmune T-cell mediated attack on myelin. Young adults; F > M (2:1); Northern Europeans; latitude gradient.

• Clinical features (presentations):

• Optic neuritis — MOST COMMON FIRST PRESENTATION; unilateral painful visual loss; afferent pupillary defect (RAPD — Marcus Gunn pupil); pain with eye movement; central scotoma; Uhthoff's phenomenon (worsening with heat/exercise — classic for MS)
• Internuclear ophthalmoplegia (INO) — MLF lesion → ipsilateral adduction failure + contralateral nystagmus; bilateral INO = MS until proven otherwise
• Sensory symptoms (paraesthesia); fatigue (most common overall symptom ); bladder dysfunction; cerebellar signs; Lhermitte's sign (electric shock down spine on neck flexion = posterior column lesion )

• McDonald Criteria (2017) — dissemination in space (DIS) + dissemination in time (DIT) on MRI
• MRI — periventricular white matter lesions (Dawson fingers — plaques perpendicular to ventricles); T2/FLAIR bright; T1 black holes (axonal loss); gadolinium enhancement (active lesions)
• CSF: Oligoclonal bands (OCB) (IgG bands on electrophoresis — > 2 more in CSF than serum = positive ); ↑ IgG index; pleocytosis (mild); VEP (Visual Evoked Potentials) — delayed P100 in optic neuritis

▶ Acute relapse: IV Methylprednisolone 1 g/day × 3–5 days (speeds recovery; does not alter long-term outcome)

▶ Disease-modifying therapy (DMT) ): Interferon-beta or Glatiramer acetate (1st line, RRMS); Natalizumab (JC virus risk → PML ); Ocrelizumab (anti-CD20 — for RRMS and PPMS ); Dimethyl fumarate; Alemtuzumab

• Clinical features: optic neuritis (painful visual loss, central scotoma, RAPD), internuclear ophthalmoplegia (INO - MLF demyelination), Lhermitte phenomenon (electric shock down spine on neck flexion), Uhthoff phenomenon (worsening with heat), bladder urgency and incontinence, fatigue (most common symptom), neuropathic pain, and depression.
• Relapse treatment and MS types: acute relapse - IV methylprednisolone 1 g/day for 3-5 days (speeds recovery, does not alter long-term outcome); MS types - RRMS (relapsing-remitting, most common), SPMS (secondary progressive), PPMS (primary progressive), PRMS; neuroprotection and remyelination therapies are under investigation.

SAH = bleeding into the subarachnoid space, most commonly from ruptured intracranial aneurysm (85% — berry aneurysm at arterial bifurcations; MCA, ACoA, PCoA ) or AVM (5%).

• Clinical features: Thunderclap headache ('worst headache of my life'; sudden onset; maximal at onset — 'hit on the head with a bat'); meningism (neck stiffness, Kernig's positive); photophobia; vomiting; brief LOC; CN III palsy (PCoA aneurysm — painful pupil-involving CN III)
• Warning leak (sentinel headache) — minor bleed days before major rupture; important to recognise and investigate urgently
• Diagnosis: CT head (hyperdense blood in cisterns ) → if CT negative and high clinical suspicion → LP (12 hours after headache onset for xanthochromia — yellow pigment from haemoglobin breakdown); MRA/CTA to localise aneurysm
• Complications: Rebleeding (24–72 hrs); Vasospasm (days 3–14; ischaemic stroke); hydrocephalus; hyponatraemia (SIADH or cerebral salt wasting )

▶ Nimodipine 60 mg q4h oral × 21 days — reduces vasospasm and cerebral infarction (NOT antihypertensive here — improves neurological outcome); first-line for vasospasm prevention

• Aneurysm treatment: Endovascular coiling (preferred; ISAT trial — coiling superior to clipping in eligible patients ) OR surgical clipping; treat within 24–72 hrs to prevent rebleed; triple-H therapy (hypertension + haemodilution + hypervolaemia) for vasospasm (controversial now)
• Grading: clinical severity is graded by the World Federation of Neurosurgeons (WFNS) or Hunt-Hess scales (based on GCS and deficit); the Fisher scale grades the volume of blood on CT and predicts vasospasm risk.
• Investigations: non-contrast CT (very sensitive within 6 h); LP at 12 h showing xanthochromia if CT is negative; CT or catheter angiography to define the aneurysm for treatment.
• Supportive care: bed rest, analgesia, laxatives, and careful blood-pressure control before securing the aneurysm; maintain euvolaemia and treat hyponatraemia; manage hydrocephalus with an external ventricular drain.

Wernicke's encephalopathy (WE) = acute neuropsychiatric syndrome caused by Thiamine (Vitamin B1) deficiency , most commonly in alcoholics but also malnutrition, prolonged vomiting, bariatric surgery, refeeding syndrome, eating disorders.

• Classic triad:

• Ophthalmoplegia — CN VI palsy most common (lateral rectus weakness → diplopia; horizontal gaze palsy); nystagmus
• Ataxia — cerebellar/vestibular; wide-based gait; cannot tandem walk
• Confusional state — disorientation; apathy; altered consciousness; NOT the classic Korsakoff amnesia (that is the chronic phase )

• ALL 3 present in only 33% — diagnosis is clinical; do NOT wait for all 3 features
• Korsakoff psychosis (amnesic syndrome) = chronic consequence; anterograde amnesia (inability to form new memories) + retrograde amnesia + confabulation (fabricating false memories unconsciously); dementia-like; poorly reversible

• Risk factors: chronic alcohol misuse, hyperemesis gravidarum, prolonged vomiting, bariatric surgery, malnutrition and refeeding.
• Investigations: a clinical diagnosis - treat on suspicion; a low red-cell transketolase and a clinical response to thiamine support it; MRI may show mammillary body and periaqueductal changes.
• Treatment: high-dose IV thiamine (e.g. 500 mg three times daily) before any glucose, then oral maintenance; correct magnesium (a cofactor); untreated Wernicke progresses to irreversible Korsakoff amnesic syndrome.
• Thiamine biochemistry: thiamine pyrophosphate (TPP) is a cofactor for pyruvate dehydrogenase, alpha-ketoglutarate dehydrogenase, and transketolase; deficiency impairs aerobic glucose metabolism and leads to lactic acid accumulation and neuronal injury particularly in areas with high metabolic demand.
• MRI findings: hyperintensity on DWI and FLAIR in the periaqueductal grey, mammillary bodies, medial thalami, and tectal plate; mammillary body atrophy on T1-weighted images in chronic Korsakoff syndrome; these findings support the clinical diagnosis.

BROWN-SÉQUARD SYNDROME

Brown-Séquard syndrome = hemisection of spinal cord producing IPSILATERAL UMN signs + proprioception/vibration loss AND CONTRALATERAL pain/temperature loss.

• Causes: Penetrating trauma (knife/gunshot ); MS (most common NON-traumatic cause ); cord compression (tumour); epidural abscess; infarction

CAUDA EQUINA SYNDROME

Cauda Equina Syndrome (CES) = compression of lumbar + sacral nerve roots below L1 (where cord ends → cauda equina) → LMN lesion (flaccid) + autonomic dysfunction.

• Causes: Massive central disc herniation (L4/L5 or L5/S1); intraspinal tumour; trauma; epidural abscess/haematoma
• Clinical:

• Bilateral leg weakness (LMN) — flaccid; ↓ reflexes; absent ankle jerk
• Saddle anaesthesia (perianal/perineal/inner thigh sensory loss — the saddle area touched by riding horse)
• Bladder/bowel dysfunction — urinary retention (painless overflow incontinence) + faecal incontinence; autonomic denervation; paralytic bladder
• Sexual dysfunction; bilateral sciatica

• MRI (emergency; do NOT delay); surgical decompression within 48 hours (best outcome if within 24 hrs of onset)
• Investigations: urgent MRI of the whole spine is the key investigation; add inflammatory and infective screens for non-traumatic cord lesions (MS, transverse myelitis, abscess).
• Management of Brown-Sequard: treat the underlying cause - surgical decompression/stabilisation for trauma or compression, steroids for inflammatory myelitis, antibiotics and drainage for epidural abscess; rehabilitation.
• Cauda equina red flags: bilateral sciatica, saddle anaesthesia, urinary retention or incontinence and reduced anal tone mandate emergency MRI and decompression within 24-48 h to preserve function.

TRIGEMINAL NEURALGIA (TN)

TN (Tic douloureux) = recurrent paroxysmal unilateral facial pain in the distribution of the trigeminal nerve (V2 maxillary division most common; V3 mandibular; V1 ophthalmic rare), lasting 1 second to 2 minutes, severe, electric shock-like/stabbing.

• Trigger zones — touching upper lip, eating, talking, brushing teeth, cold wind; allodynia (light touch causes severe pain); strictly unilateral; no sensory deficit (distinguishes from multiple sclerosis TN which may have sensory loss)
• Cause: Idiopathic (95%) — often vascular loop compression (SCA compressing V root at pons); secondary: MS (suspect if < 50 yrs, bilateral, or sensory deficit)

▶ Carbamazepine 200–1200 mg/day — DOC ; 70–80% initial response; monitor CBC (agranulocytosis ) + Na (hyponatraemia ); check HLA-B*1502 (Asian patients — SJS risk )

▶ Oxcarbazepine — better tolerated than carbamazepine; fewer drug interactions

• Surgical: Microvascular decompression (MVD — gold standard; Jannetta procedure; Teflon pad between vessel and nerve at REZ); excellent long-term results; Stereotactic radiosurgery (Gamma Knife ) for poor surgical candidates

ALZHEIMER'S DISEASE

Alzheimer's disease (AD) = most common cause of dementia (70%); characterised by amyloid plaques (Aβ) + neurofibrillary tangles (tau) + neuronal loss. Early: episodic memory loss; visuospatial problems. Late: aphasia; apraxia; agnosia; behavioural changes; total dependence.

• Pathology: Aβ42 plaques (amyloid precursor protein APP processing); hyperphosphorylated tau tangles; loss of basal forebrain cholinergic neurons → ↓ acetylcholine → memory loss
• Risk factors: APOE-ε4 allele (strongest genetic risk); Down syndrome (trisomy 21 → extra APP gene ); advanced age; family history; head injury; vascular risk factors

▶ AChEIs (Donepezil 5–10 mg OD; Rivastigmine; Galantamine) — modest symptomatic benefit; slow decline; not disease-modifying; side effects: nausea, bradycardia, nightmares

▶ Memantine — NMDA receptor antagonist; moderate-severe AD; additive to AChEI

▶ Lecanemab (Leqembi) — anti-Aβ monoclonal antibody; FDA approved 2023; reduces amyloid + slows decline in early AD; ARIA (amyloid-related imaging abnormalities — haemorrhage risk on MRI) monitoring required

VIRAL ENCEPHALITIS

Viral encephalitis = viral infection of brain parenchyma → inflammatory oedema → altered consciousness + seizures ± fever. MOST IMPORTANT: Herpes Simplex Encephalitis (HSE) — most common sporadic viral encephalitis; fatal without treatment; treatable.

• HSE: HSV-1 (adults); HSV-2 (neonates); temporal lobe predilection → acute behavioural change (personality change, hallucinations — especially olfactory/gustatory ) + seizures (temporal focus) + fever + headache + focal deficits
• MRI: T2/FLAIR hyperintensity in medial temporal lobe + insular cortex (limbic encephalitis pattern); unilateral or bilateral; petechial haemorrhage
• EEG: Periodic lateralised epileptiform discharges (PLEDs ) from temporal lobe; pathognomonic of HSE
• CSF: Lymphocytic pleocytosis + ↑ protein + RBCs (haemorrhagic) + normal glucose; PCR for HSV DNA — gold standard (sensitivity > 95%)

▶ Aciclovir IV 10 mg/kg q8h × 14–21 days — start IMMEDIATELY on clinical suspicion (do NOT wait for PCR result ); dramatically reduces mortality from 70% to < 20%

MENINGOCOCCAL DISEASE

*Neisseria meningitidis* — gram-negative diplococcus; serogroups B, C, W, Y most important. Most common cause of bacterial meningitis in children + young adults and most common cause of bacterial meningitis epidemic. Incubation 2–10 days. Transmitted respiratory droplets.

• Meningococcaemia — bacteraemia without meningitis; non-blanching petechial/purpuric rash (haemorrhage from endothelial damage — endotoxin); Waterhouse-Friderichsen syndrome (bilateral adrenal haemorrhage → adrenal failure → refractory shock)
• Meningococcal meningitis — most rapid bacterial meningitis; can be fatal in 24 hours; classical bacterial CSF

▶ Benzylpenicillin 2.4 g IV IMMEDIATELY (in community — even before hospital transfer); Ceftriaxone 2 g IV BD in hospital × 7 days + Dexamethasone

• Prophylaxis: All close contacts within 24 hrs — Ciprofloxacin 500 mg single dose (preferred; rifampicin alternative)

• Malignant (accelerated) hypertension: severe BP (often > 180/120) with grade III/IV retinopathy (haemorrhages, exudates, papilloedema) +/- encephalopathy, AKI or heart failure; lower BP gradually (about 25% in the first hours) with IV labetalol, nicardipine or sodium nitroprusside to avoid watershed ischaemia.
• Resistant hypertension: BP above target despite three drugs (including a diuretic) at optimal doses; check adherence, white-coat effect and secondary causes; spironolactone is the preferred fourth agent.
• Work-up for secondary HTN: U&E, renin:aldosterone ratio (Conn syndrome), plasma/urine metanephrines (phaeochromocytoma), overnight dexamethasone suppression (Cushing syndrome), renal Doppler/imaging (renal artery stenosis) and TFTs.

TETANY

• Tetany = spontaneous electrical activity in peripheral nerves from hypocalcaemia , hypomagnesaemia, or alkalosis (respiratory or metabolic)
• Signs: Trousseau's sign (inflate BP cuff > SBP for 3 min → carpal spasm — 'obstetric hand' = carpopedal spasm); Chvostek's sign (tap facial nerve anterior to ear → ipsilateral facial muscle twitch); perioral tingling; muscle cramps
• Causes: Hypoparathyroidism (post-thyroid surgery ); hypomagnesaemia; vitamin D deficiency; renal failure; hungry bone syndrome; hyperventilation (respiratory alkalosis)

▶ Acute tetany: IV Calcium gluconate 10% 10 mL over 10 min (cardiac monitoring); repeat as needed; follow with oral calcium + Vitamin D

ESSENTIAL TREMOR

• Most common movement disorder (30% prevalence); autosomal dominant (familial tremor); bilateral action/postural tremor (worsens with outstretched hands; worse during intentional movement); hands > head (titubation) > voice; improves with alcohol (pathognomonic)

▶ Propranolol 40–160 mg BD (first-line); Primidone 50–250 mg OD (second-line); DBS of VIM for refractory

BABINSKI SIGN

• Babinski (extensor plantar) = slow stroking of lateral sole with blunt object → dorsiflexion (extension) of great toe + fanning of other toes = POSITIVE (= UMN lesion or normal in infants < 18 months ); flexion = NORMAL in adults
• Spasticity: a velocity-dependent increase in tone from UMN lesions (stroke, cord injury, MS, cerebral palsy); managed with physiotherapy, baclofen or tizanidine, and botulinum toxin for focal spasticity.
• Investigations for tetany: serum calcium (corrected), magnesium, phosphate, PTH, vitamin D, U&E and ABG (alkalosis); ECG may show a prolonged QT in hypocalcaemia.
• Trousseau and Chvostek signs: Trousseau - inflate BP cuff above SBP for 3 minutes causes carpal spasm (main en accoucheur/obstetric hand) - most sensitive sign of hypocalcaemia; Chvostek - tapping the facial nerve 2 cm anterior to the ear lobe causes ipsilateral facial muscle twitching - less specific (positive in 25% of normal people).
• Spasticity management: physiotherapy and regular stretching are the cornerstone; baclofen 5-80 mg/day (GABA-B agonist); tizanidine (alpha-2 agonist); botulinum toxin type A injections for focal spasticity (most effective for upper limb in post-stroke patients); intrathecal baclofen pump for severe generalised spasticity.

• GBS (Guillain-Barre syndrome): acute inflammatory demyelinating polyradiculoneuropathy, usually post-infective (Campylobacter jejuni, CMV, EBV, Zika); ascending symmetrical flaccid paralysis with areflexia, +/- autonomic instability; CSF shows albuminocytological dissociation (high protein, normal cells); treat with IVIG or plasmapheresis + monitor respiratory function (FVC); steroids are NOT effective.
• AFP (Acute Flaccid Paralysis): sudden-onset flaccid weakness in a child < 15 years; a WHO surveillance category for poliomyelitis; causes include poliomyelitis, GBS, traumatic neuritis and transverse myelitis; investigate with two stool samples for poliovirus 24-48 h apart.
• Peripheral neuropathy causes: see table below.
• GBS - prognostic factors: poor outcome predicted by rapid progression, need for ventilation, preceding Campylobacter jejuni diarrhoea, axonal subtype (AMAN/AMSAN), older age, and low compound muscle action potential amplitude on NCS; the MRC disability scale is used for follow-up.
• Peripheral neuropathy - axonal vs demyelinating: axonal (length-dependent, most common - DM, alcohol, uraemia, drugs, deficiencies) shows reduced amplitudes with relatively preserved conduction velocity; demyelinating (GBS, CIDP, hereditary) shows slowed conduction velocity, prolonged distal latencies, and conduction block.

PHENYTOIN

• Indications: Focal seizures; GTC seizures; Status epilepticus (IV load ); trigeminal neuralgia (2nd line); cardiac arrhythmias (class IB)
• Toxicity signs: Nystagmus (first sign); ataxia; diplopia; sedation; gingival hyperplasia (>50% on long-term); hirsutism (females — distressing); coarse facies; megaloblastic anaemia (folate antagonism); osteomalacia (↑ vitamin D metabolism); SJS/TEN (HLA-B*1502 in Asians)
• Zero-order kinetics — at therapeutic levels, phenytoin saturates metabolism → small dose increase → disproportionate rise in plasma level → toxicity; narrow therapeutic window (10–20 μg/mL)
• Interactions: Strong CYP450 INDUCER (↓ warfarin, OCP, cyclosporine, carbamazepine, steroids levels); many drugs alter phenytoin levels

DIGOXIN

• Uses: Rate control in AF/flutter + heart failure (HFrEF); paroxysmal SVT
• Mechanism: Inhibits Na/K-ATPase → ↑ intracellular Na → ↑ Ca via Na/Ca exchange → ↑ contractility (positive inotrope ); also increases vagal tone → AV node slowing (rate control)
• Toxicity: Therapeutic range: 0.5–0.9 ng/mL; narrow therapeutic window
• GI: Nausea + vomiting + anorexia (EARLIEST signs ); abdominal pain
• Cardiac: AV block (most common arrhythmia — all degrees); Ventricular bigeminy (PVC every other beat); ventricular tachycardia; atrial tachycardia with AV block (pathognomonic ); bradycardia
• Neurological: Visual disturbance — xanthopsia (yellow-green vision) ; confusion; headache
• Precipitating factors: Hypokalaemia (K⁺ competes with digoxin at ATPase); hypomagnesaemia; hypercalcaemia; renal failure (↓ excretion); amiodarone, quinidine, CCB (↑ digoxin levels)
• Treatment of toxicity: Stop digoxin; correct hypokalaemia; Digoxin-Fab (Digibind) — specific antibody fragments; bind digoxin → inactive complex → excreted; lidocaine for VT; temporary pacing for AV block

• After benzodiazepines: if seizures continue, give a second-line IV agent - levetiracetam, sodium valproate or phenytoin/fosphenytoin (loading dose) - while correcting glucose, electrolytes and giving thiamine in alcoholics.
• Refractory and super-refractory status: seizures continuing despite first- and second-line therapy require general anaesthesia (midazolam, propofol or thiopentone) with intubation and continuous EEG; super-refractory status is anaesthesia-resistant or recurs on weaning.
• General measures and monitoring: secure the airway, give oxygen and IV access, monitor ECG/BP/oxygenation, identify and treat the cause (imaging, lumbar puncture), and watch for rhabdomyolysis, aspiration and arrhythmia.
• Termination goals: goal is to terminate seizure activity within 60 minutes; clinical seizures may terminate before electrographic activity; continuous EEG is essential in refractory and super-refractory status to detect non-convulsive status and monitor treatment response.
• Identify the cause: urgent blood glucose, electrolytes, calcium, magnesium, toxicology screen, AED levels (in known epilepsy), ABG; neuroimaging (CT first if unknown cause) and lumbar puncture if CNS infection suspected after excluding raised ICP.