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// ─── SLIDE 1: TITLE ──────────────────────────────────────────────────────────
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// ─── SLIDE 2: DEFINITION & OVERVIEW ─────────────────────────────────────────
contentSlide(
  "Definition & Overview",
  [
    "Bibrachial MND (Flail Arm Syndrome / Brachial Amyotrophic Diplegia) is a regional variant of ALS",
    "Selective degeneration of LOWER MOTOR NEURONS supplying both upper extremities",
    "Also called 'Hanging Man Syndrome' or 'Man-in-a-Barrel Syndrome'",
    "Accounts for ~10% of all ALS cases",
    "Predominantly affects men (male:female ratio ~5–9:1)",
    "Mean age at onset: 55–65 years",
    "Longer median survival vs typical ALS (median >4 years)",
    "##Key distinction",
    "Proximal shoulder-girdle muscles affected early → distal spread",
    "Legs and bulbar muscles relatively SPARED until late",
    "UMN signs in arms may be mild or absent initially; LMN signs dominate",
  ],
  [
    "##ALS Variant Spectrum",
    "Classical ALS — UMN + LMN, limbs + bulbar",
    "Progressive Muscular Atrophy (PMA) — LMN only",
    "Progressive Bulbar Palsy (PBP) — bulbar only",
    "Primary Lateral Sclerosis (PLS) — UMN only",
    "Flail Arm Syndrome (FAS) — proximal UE predominant",
    "Flail Leg Syndrome (FLS) — LE predominant",
    "##Eponym",
    "Originally described as 'Brachial Amyotrophic Diplegia' by Vulpian (1886)",
    "Re-described as 'Man-in-a-Barrel Syndrome' — bilateral arm weakness with intact legs",
  ],
  "Variant Spectrum"
);

// ─── SLIDE 3: PATHOPHYSIOLOGY OVERVIEW ───────────────────────────────────────
sectionSlide("PATHOPHYSIOLOGY", "How does Bibrachial MND occur? — Proximal & Distal mechanisms");

// ─── SLIDE 4: PATHOPHYSIOLOGY — PROXIMAL ─────────────────────────────────────
contentSlide(
  "Pathophysiology — Proximal Pattern (Shoulder-Girdle Onset)",
  [
    "##Site of primary LMN degeneration",
    "Anterior horn cells at C5–C6 spinal segments (shoulder/arm)",
    "Motor cortex neurons projecting via corticospinal tract",
    "##Mechanism",
    "TDP-43 / FUS protein aggregation in motor neurons → toxic gain-of-function",
    "Glutamate excitotoxicity → calcium influx → mitochondrial dysfunction",
    "SOD1 mutations (20% familial) → oxidative stress → cell death",
    "C9ORF72 GGGGCC repeat expansion → most common genetic cause",
    "##Why shoulder-girdle first?",
    "Proximal C5–C6 neurons may be selectively vulnerable due to:",
    "Higher metabolic demand (large motor units innervating deltoid, biceps)",
    "Neurofilament accumulation → impaired axonal transport in long neurons",
    "Local astrocyte dysfunction: SOD1-mutant astrocytes toxic to motor neurons",
  ],
  [
    "##Gross pathology",
    "Atrophy of precentral gyrus (motor cortex)",
    "Sclerosis and pallor of corticospinal tracts",
    "Thinning of ventral nerve roots C5–C6",
    "Atrophy of deltoid, infraspinatus, biceps, supraspinatus",
    "##Microscopy",
    "50% loss of spinal motor neurons at cervical levels",
    "Diffuse astrocytic gliosis in spinal gray matter",
    "TDP-43 immunoreactive inclusions in surviving neurons",
    "Ubiquitin-positive cytoplasmic inclusions",
    "##Spared structures",
    "Onuf nucleus (sacral — pelvic floor) → bladder control intact",
    "CN III, IV, VI nuclei → eye movements intact",
    "Sensory neurons (posterior horn) → no sensory loss",
  ],
  "Pathology"
);

// ─── SLIDE 5: PATHOPHYSIOLOGY — DISTAL SPREAD ────────────────────────────────
contentSlide(
  "Pathophysiology — Distal Spread & Rostro-Caudal Pattern",
  [
    "##Distal arm involvement (C7–T1 segment)",
    "After shoulder-girdle atrophy: spread to forearm flexors/extensors, intrinsics",
    "Wrist drop, finger weakness, thenar/hypothenar wasting follow",
    "Fasciculations appear distally as motor units become unstable",
    "##Why 'flail arm'?",
    "Combined proximal (C5-C6) + distal (C7-T1) LMN loss",
    "Arms hang limp, adducted, internally rotated — 'dangling arms'",
    "Patient cannot lift, abduct, or flex elbow against gravity",
    "##Temporal sequence",
    "1. Proximal weakness (shoulder abduction, elbow flexion) → months",
    "2. Distal weakness (wrist/fingers) → months to 1–2 years later",
    "3. Contralateral arm involved (hence 'bilateral')",
    "4. Legs involved much later (>18–24 months after onset)",
    "5. Bulbar involvement last (dysphagia, dysarthria)",
  ],
  [
    "##UMN component in distal pattern",
    "Corticospinal neurons to cervical cord degenerate in parallel",
    "Initially: LMN signs dominate (atrophy + hyporeflexia)",
    "Later: UMN signs may emerge (brisk knee jerks, Babinski)",
    "Reflex dissociation: absent biceps jerk (C5/C6 LMN) but preserved knee jerk",
    "##Molecular basis of spread",
    "Prion-like propagation of misfolded TDP-43 / SOD1 aggregates",
    "Anterograde/retrograde axonal spread via neuromuscular synapses",
    "Corticomotoneuronal hyperexcitability drives LMN degeneration",
    "##Why legs spared longer?",
    "Lumbar anterior horn cells less vulnerable initially",
    "Possible 'dying-back' upper motor neuron pattern from cervical to lumbar",
    "FAS shows preferential cervical neuronal vulnerability vs. typical ALS",
  ],
  "UMN Component & Spread"
);

// ─── SLIDE 6: CLINICAL FEATURES ──────────────────────────────────────────────
sectionSlide("CLINICAL FEATURES", "Signs, Symptoms & Disease Course");

// ─── SLIDE 7: CLINICAL FEATURES — SYMPTOMS ───────────────────────────────────
contentSlide(
  "Clinical Features — Presenting Symptoms",
  [
    "##Cardinal Presenting Complaint",
    "Bilateral proximal arm weakness — cannot raise arms above head",
    "Initially UNILATERAL, then spreads to contralateral arm (weeks–months)",
    "Difficulty combing hair, reaching shelves, lifting objects",
    "Shoulder-girdle wasting noticed in mirror",
    "##Early phase (months 1–12)",
    "Arm hangs limply at side — adducted, internally rotated",
    "Progressive weight loss in arm musculature",
    "Coarse fasciculations visible in deltoid, biceps, triceps, forearm",
    "Cramps common especially at night",
    "NO sensory symptoms (paraesthesia, numbness) — key negative",
    "NO sphincter disturbance",
  ],
  [
    "##Late phase",
    "Bilateral flail arms — completely dependent arms",
    "Distal weakness: wrist drop, grip weakness, claw hand",
    "Respiratory embarrassment: paradoxical breathing if diaphragm involved",
    "Mild dysarthria / dysphagia may appear late",
    "##Negative features (help confirm diagnosis)",
    "No bladder/bowel dysfunction",
    "No sensory loss",
    "No eye movement disorder (CN III/IV/VI spared)",
    "Cognitive function usually intact (rare FTD-ALS overlap)",
    "No pain in early stages",
    "##Progression",
    "Median survival: 4–5 years (better than classic ALS 2–3 years)",
    "Death usually from respiratory failure or aspiration pneumonia",
  ],
  "Late & Negative Features"
);

// ─── SLIDE 8: CLINICAL FEATURES — SIGNS ──────────────────────────────────────
contentSlide(
  "Clinical Features — Neurological Signs",
  [
    "##LMN signs (dominant, bilateral arms)",
    "Wasting and atrophy — deltoid, biceps, brachioradialis, intrinsics",
    "Fasciculations — coarse, visible; deltoid, biceps, forearm",
    "Hypotonia of upper limbs",
    "Absent / diminished biceps (C5/C6) and brachioradialis (C5/C6) reflexes",
    "Absent triceps jerk (C7) as disease progresses distally",
    "##Reflex dissociation (pathognomonic clue)",
    "Absent biceps + brachioradialis jerk (LMN arm)",
    "PRESERVED / brisk knee jerk (UMN leg)",
    "Absent jaw jerk or brisk jaw jerk depending on bulbar involvement",
    "Extensor plantar response (Babinski) may appear with leg UMN involvement",
  ],
  [
    "##UMN signs",
    "Spasticity in legs (if involved late)",
    "Brisk knee and ankle jerks",
    "Bilateral Babinski signs",
    "Hoffman's sign may be present or absent in arms",
    "##Bulbar signs (late)",
    "Tongue fasciculations and wasting",
    "Dysarthria (spastic + flaccid — 'hot potato' voice)",
    "Dysphagia (solids first, then liquids)",
    "Drooling / excessive salivation",
    "Emotional lability (pseudobulbar affect)",
    "##Respiratory signs",
    "Paradoxical diaphragmatic movement",
    "Orthopnoea / exertional dyspnoea",
    "Use of accessory muscles of respiration",
  ],
  "UMN / Bulbar / Respiratory"
);

// ─── SLIDE 9: DIFFERENTIAL DIAGNOSIS ─────────────────────────────────────────
sectionSlide("DIFFERENTIAL DIAGNOSIS", "Conditions that mimic Bibrachial MND");

// ─── SLIDE 10: DD TABLE ───────────────────────────────────────────────────────
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    [{ text:"Kennedy Disease (SBMA)", options:{bold:true,color:TEXT,fontSize:11} }, { text:"X-linked; gynecomastia; perioral fasciculations; sensory features; androgen receptor CAG repeat expansion", options:{color:TEXT,fontSize:11} }, { text:"AR gene testing; slow progression; sensory NCS abnormal", options:{color:TEXT,fontSize:11} }],
    [{ text:"Cervical Myelopathy + Radiculopathy", options:{bold:true,color:TEXT,fontSize:11} }, { text:"Pain; sensory symptoms; UMN signs caudal to LMN; bladder symptoms; precipitated by neck movement", options:{color:TEXT,fontSize:11} }, { text:"MRI cervical spine; nerve conduction studies", options:{color:TEXT,fontSize:11} }],
    [{ text:"Brachial Neuritis (Parsonage-Turner)", options:{bold:true,color:TEXT,fontSize:11} }, { text:"Acute onset severe shoulder pain followed by weakness; patchy unilateral; usually monophasic", options:{color:TEXT,fontSize:11} }, { text:"Spontaneous partial recovery; EMG/NCS; MRI brachial plexus", options:{color:TEXT,fontSize:11} }],
    [{ text:"Multifocal Motor Neuropathy (MMN)", options:{bold:true,color:TEXT,fontSize:11} }, { text:"Pure LMN; asymmetric; conduction block on NCS; anti-GM1 antibodies raised; responds to IVIG", options:{color:TEXT,fontSize:11} }, { text:"NCS: conduction block; anti-GM1 Ab; IVIG response", options:{color:TEXT,fontSize:11} }],
    [{ text:"Inclusion Body Myositis (IBM)", options:{bold:true,color:TEXT,fontSize:11} }, { text:"Finger flexor + quadriceps weakness pattern; CK moderately raised; muscle biopsy diagnostic", options:{color:TEXT,fontSize:11} }, { text:"EMG: myopathic; biopsy: rimmed vacuoles, IBM deposits", options:{color:TEXT,fontSize:11} }],
    [{ text:"Hirayama Disease (Monomelic Amyotrophy)", options:{bold:true,color:TEXT,fontSize:11} }, { text:"Young males; unilateral or asymmetric distal upper limb; self-limiting; cervical flexion MRI shows dural shift", options:{color:TEXT,fontSize:11} }, { text:"Flexion MRI cervical; arrested progression", options:{color:TEXT,fontSize:11} }],
    [{ text:"Progressive Muscular Atrophy (PMA)", options:{bold:true,color:TEXT,fontSize:11} }, { text:"Pure LMN variant of ALS; symmetric; generalized; no regional predilection; no UMN signs", options:{color:TEXT,fontSize:11} }, { text:"Generalized vs. arm-predominant distribution; EMG", options:{color:TEXT,fontSize:11} }],
    [{ text:"Syringomyelia", options:{bold:true,color:TEXT,fontSize:11} }, { text:"Cape-like dissociated sensory loss; pain; scoliosis; Chiari association; MRI diagnostic", options:{color:TEXT,fontSize:11} }, { text:"MRI spine: syrinx cavity; sensory dissociation present", options:{color:TEXT,fontSize:11} }],
    [{ text:"Radiation Myelopathy", options:{bold:true,color:TEXT,fontSize:11} }, { text:"History of prior neck/thorax radiotherapy (e.g., Hodgkin lymphoma); onset years after treatment", options:{color:TEXT,fontSize:11} }, { text:"Radiation history; MRI cord changes in radiation field", options:{color:TEXT,fontSize:11} }],
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// ─── SLIDE 11: MORE DD ────────────────────────────────────────────────────────
contentSlide(
  "Differential Diagnosis — Additional Conditions",
  [
    "##Neuromuscular Junction disorders",
    "Myasthenia Gravis — fatigable weakness; ptosis; diplopia; positive Tensilon test; AChR antibodies",
    "Lambert-Eaton Syndrome — proximal LL > UL; autonomic features; anti-VGCC Ab; incremental NCS",
    "##Hereditary Motor Neuropathies (CMT)",
    "Family history; distal wasting; foot deformity; slow progressive; abnormal NCS",
    "##Spinal Muscular Atrophy (Adult SMA type 3/4)",
    "Symmetric proximal weakness; SMN1 gene deletion; purely LMN; slow progression",
    "##Post-Polio Syndrome",
    "History of acute poliomyelitis decades earlier; fatigue + new weakness; no active denervation on EMG",
    "##Lead / Heavy Metal Neuropathy",
    "Exposure history; wrist drop; pure motor; blood lead level elevated; basophilic stippling on smear",
  ],
  [
    "##Paraneoplastic Motor Neuron Syndrome",
    "Underlying malignancy (lymphoma, lung, breast); anti-amphiphysin / anti-Hu antibodies",
    "##Bilateral Brachial Plexopathy",
    "Trauma / infiltration / radiation; imaging shows plexus lesion; sensory abnormalities usually present",
    "##Cervical Cord Infarction (Bibrachial Pattern)",
    "Acute onset; bilateral arm weakness + sensory level; anterior spinal artery territory",
    "MRI spine: diffuse cord T2 signal; 'owl-eye' or 'snake-eye' sign",
    "##Sjogren Syndrome Motor Neuropathy",
    "Non-motor features (dry eyes, dry mouth, parotid enlargement); anti-Ro/La antibodies",
    "##Thyrotoxicosis with Myopathy",
    "Systemic features of hyperthyroidism; proximal weakness; TFTs abnormal; CK mild rise",
  ],
  "NMJ & Hereditary"
);

// ─── SLIDE 12: INVESTIGATIONS ────────────────────────────────────────────────
sectionSlide("INVESTIGATIONS", "Diagnosis & Work-up of Flail Arm Syndrome");

// ─── SLIDE 13: INVESTIGATIONS ────────────────────────────────────────────────
contentSlide(
  "Investigations — Electrophysiology & Blood Tests",
  [
    "##EMG (most important test)",
    "Active denervation: fibrillations + positive sharp waves in multiple cervical myotomes",
    "Fasciculation potentials in affected muscles (deltoid, biceps, first dorsal interosseous)",
    "Large-amplitude, long-duration, polyphasic motor unit potentials (chronic denervation)",
    "Reduced recruitment pattern bilaterally in upper limb muscles",
    "EMG must show changes in ≥2 of 4 body regions (Awaji-Shima / El Escorial criteria)",
    "##Nerve Conduction Studies (NCS)",
    "Motor NCS: normal conduction velocity (axonal loss only, no demyelination)",
    "CMAP amplitude reduced in median, ulnar, radial nerves (axonal loss)",
    "Sensory NCS: NORMAL — distinguishes from sensory neuropathies",
    "NO conduction block — distinguishes from Multifocal Motor Neuropathy (MMN)",
  ],
  [
    "##Blood Tests",
    "FBC, ESR, CRP — usually normal; rule out inflammatory/infective causes",
    "Serum CK — mildly elevated (2–4× normal) due to denervation atrophy",
    "TFTs — exclude thyrotoxic myopathy",
    "Serum electrolytes — hypokalaemia (periodic paralysis)",
    "Vitamin B12, folate — exclude deficiency neuropathy",
    "Anti-GM1 antibodies — if raised, suggests MMN (treatable!)",
    "Anti-Hu, Anti-amphiphysin — paraneoplastic screen",
    "Androgen receptor (AR) CAG repeat — if Kennedy disease suspected",
    "Heavy metal screen (lead, mercury) — if exposure history",
    "HIV serology — HIV-associated brachial amyotrophic diplegia described",
    "SMN1 gene analysis — rule out adult SMA",
  ],
  "Blood Tests"
);

// ─── SLIDE 14: IMAGING & CRITERIA ────────────────────────────────────────────
contentSlide(
  "Investigations — Neuroimaging & Diagnostic Criteria",
  [
    "##MRI Brain",
    "Bilateral T2 hypointensity along corticospinal tracts (iron deposition)",
    "Atrophy of precentral gyrus bilaterally in established disease",
    "T1 cortical thinning in motor strip",
    "Important to EXCLUDE mimics: brainstem tumours, cortical lesions",
    "##MRI Cervical Spine",
    "Essential to exclude structural causes (disc herniation, osteophytes, tumour)",
    "May show mild cord atrophy at C5–C6 in FAS",
    "Cervical flexion MRI: anterior dural shift in Hirayama — differentiates",
    "##MRI Brachial Plexus",
    "When unilateral, asymmetric, or pain is present — exclude plexopathy",
    "T2 STIR: increased signal in affected roots in CIDP or Parsonage-Turner",
  ],
  [
    "##Diagnostic Criteria (El Escorial / Awaji-Shima)",
    "Definite ALS: UMN + LMN signs in 3 regions",
    "Probable ALS: UMN + LMN in 2 regions; UMN signs rostral to LMN",
    "Possible ALS: UMN + LMN in 1 region",
    "FAS often enters as 'possible' or 'probable' ALS early on",
    "##Pulmonary Function Tests",
    "Forced Vital Capacity (FVC) <50% predicted — trigger for NIV",
    "Sniff Nasal Inspiratory Pressure (SNIP) — diaphragm assessment",
    "Nocturnal oximetry — detect nocturnal hypoventilation",
    "##CSF Analysis",
    "Usually NORMAL — helps exclude inflammatory/infective causes",
    "May show mildly elevated protein (non-specific)",
    "##Muscle Biopsy",
    "If IBM or inflammatory myopathy suspected — shows denervation features in MND",
    "Grouped atrophy, type I and II fibre grouping, angular fibres",
  ],
  "Criteria & PFTs"
);

// ─── SLIDE 15: MANAGEMENT OVERVIEW ───────────────────────────────────────────
contentSlide(
  "Management Overview",
  [
    "##Disease-Modifying",
    "Riluzole 50 mg BD — anti-glutamatergic; modest survival benefit (+3–6 months)",
    "Edaravone (IV) — anti-oxidant; slows functional decline in selected patients",
    "##Respiratory Support",
    "Non-invasive ventilation (NIV/BiPAP) when FVC <50%",
    "Tracheostomy ventilation in selected patients for prolonged survival",
    "Cough assist devices / manually assisted cough",
    "##Nutritional Support",
    "PEG insertion early (when FVC >50%) — prophylactic feeding",
    "High-calorie diet — weight maintenance improves prognosis",
    "##Communication",
    "AAC devices — speech generating devices as dysarthria worsens",
    "Eye-tracking technology for late-stage communication",
  ],
  [
    "##Physiotherapy & OT",
    "Upper limb orthoses — arm slings, balanced forearm orthosis",
    "Shoulder subluxation prevention strapping",
    "Passive ROM exercises to prevent contractures",
    "Wrist/finger splints for functional positioning",
    "##Symptom Management",
    "Sialorrhoea: Glycopyrronium, hyoscine, amitriptyline, Botulinum toxin",
    "Muscle cramps: Quinine, magnesium, mexiletine",
    "Spasticity: Baclofen, tizanidine, botulinum toxin",
    "Pain: Regular paracetamol, NSAIDs, opioids in late stage",
    "Emotional lability: Dextromethorphan/quinidine (Nuedexta), SSRIs",
    "##Prognosis",
    "Median survival FAS: 4–5 years (vs 2–3 years classic ALS)",
    "Better prognosis: younger age, limb onset, longer diagnostic delay",
    "Death from respiratory failure / aspiration pneumonia",
  ],
  "Physiotherapy & Prognosis"
);

// ─── SLIDE 16: SUMMARY ───────────────────────────────────────────────────────
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    { text:"Bibrachial MND = Flail Arm Syndrome = Brachial Amyotrophic Diplegia — a regional ALS variant", options:{ bullet:true, color:WHITE, fontSize:14, fontFace:"Calibri", breakLine:true } },
    { text:"LMN degeneration at C5–T1 anterior horn cells → proximal (C5–C6) followed by distal (C7–T1) arm weakness", options:{ bullet:true, color:WHITE, fontSize:14, fontFace:"Calibri", breakLine:true } },
    { text:"Prion-like TDP-43 / SOD1 spread, excitotoxicity, and oxidative stress underlie pathogenesis", options:{ bullet:true, color:WHITE, fontSize:14, fontFace:"Calibri", breakLine:true } },
    { text:"Bilateral flail arms, fasciculations, wasting — NO sensory loss, NO bladder symptoms", options:{ bullet:true, color:ACCENT, fontSize:14, fontFace:"Calibri", breakLine:true, bold:true } },
    { text:"Reflex dissociation: absent biceps jerk (LMN) + brisk knee jerk (UMN) is a diagnostic clue", options:{ bullet:true, color:WHITE, fontSize:14, fontFace:"Calibri", breakLine:true } },
    { text:"DD: Kennedy disease, MMN, IBM, Hirayama, brachial plexopathy, cervical myelopathy", options:{ bullet:true, color:WHITE, fontSize:14, fontFace:"Calibri", breakLine:true } },
    { text:"Investigations: EMG (active denervation, no conduction block), normal sensory NCS, MRI brain + cervical spine", options:{ bullet:true, color:WHITE, fontSize:14, fontFace:"Calibri", breakLine:true } },
    { text:"Median survival 4–5 years; better than classic ALS; death from respiratory failure", options:{ bullet:true, color:ACCENT, fontSize:14, fontFace:"Calibri", breakLine:true, bold:true } },
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// ═══════════════════════════════════════════════════════════════════════════
// SLIDE 1: MASTER TITLE
// ═══════════════════════════════════════════════════════════════════════════
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// ═══════════════════════════════════════════════════════════════════════════
// PART 1 — MYASTHENIA GRAVIS
// ═══════════════════════════════════════════════════════════════════════════
sectionCard("PART 1: MYASTHENIA GRAVIS", "Treatment — Symptomatic, Immunotherapy, Thymectomy, Crisis Management", ACCENT);

// SLIDE 3: Overview of MG treatment
contentSlide(
  "Treatment Overview — Goals & Framework",
  [
    "##Goal of treatment (MGFA 2016 Task Force)",
    "No symptoms or functional limitations from MG",
    "No more than mild side effects requiring no intervention",
    "Treatment must be individualised: ocular vs. generalized, mild vs. severe",
    "##3 Pillars of MG Treatment",
    "1. Symptomatic — Cholinesterase Inhibitors (ChEIs)",
    "2. Immunotherapy — Corticosteroids + Steroid-sparing agents",
    "3. Surgical — Thymectomy",
    "##Rapid therapy for crisis / acute worsening",
    "Plasmapheresis (plasma exchange) — fastest acting",
    "Intravenous Immunoglobulin (IVIG)",
    "Intubation + mechanical ventilation if respiratory failure",
  ],
  [
    "##Clinical stratification guides therapy",
    "Ocular MG (ptosis, diplopia only) → ChEI ± low-dose steroids",
    "Mild generalised → ChEI + immunosuppression",
    "Moderate–severe generalised → aggressive immunotherapy",
    "Myasthenic crisis → ICU + plasmapheresis/IVIG",
    "##Predictors of response",
    "AChR antibody positive: responds well to thymectomy + steroids",
    "MuSK antibody positive: may worsen with ChEIs; use rituximab",
    "LRP4 antibody positive: rare; treatment similar to AChR+",
    "Seronegative MG: treat empirically as AChR+",
    "##Goal remission rates",
    "85% ocular MG achieve remission/minimal manifestations",
    "47% thymoma-associated MG achieve remission",
  ],
  "Stratification"
);

// SLIDE 4: ChEIs
contentSlide(
  "Symptomatic Treatment — Cholinesterase Inhibitors (ChEIs)",
  [
    "##Pyridostigmine (Mestinon) — First-line symptomatic",
    "Mechanism: inhibits acetylcholinesterase → ↑ ACh at NMJ",
    "Dose: 30–60 mg PO every 4–8 hours (adults)",
    "Paediatric dose: 1 mg/kg PO",
    "Syrup formulation (60 mg/5 mL) for children or NG tube",
    "Timed-release tablet 180 mg at bedtime (erratic absorption)",
    "Adjust dose for best effect in most disabled muscle group",
    "Patients with oropharyngeal weakness: time dose to meals",
    "##Side effects (muscarinic excess)",
    "GI: nausea, vomiting, abdominal cramps, diarrhoea",
    "Increased bronchial/oral secretions (dangerous if bulbar weakness)",
    "Bradycardia, miosis, urinary urgency",
    "##Management of GI side effects",
    "Glycopyrrolate, hyoscyamine sulfate, propantheline bromide",
    "Diphenoxylate + atropine, loperamide",
    "⚠ MuSK MG may WORSEN with ChEIs — avoid or use cautiously",
  ],
  [
    "##Amifampridine (3,4-DAP)",
    "Voltage-gated K+ channel blocker → ↑ ACh release",
    "Small studies show improvement in acquired MG",
    "Adjunct to pyridostigmine in selected patients",
    "##Tensilon (Edrophonium) Test",
    "Short-acting ChEI — used diagnostically",
    "2 mg IV test dose; if no reaction → 8 mg IV",
    "Positive: transient improvement in weakness within 60 sec",
    "Also distinguishes myasthenic from cholinergic crisis",
    "Have atropine ready (1 mg IV) for cholinergic overshoot",
    "##When ChEIs are insufficient",
    "Pyridostigmine dose reduction/discontinuation signals remission",
    "Addition of immunotherapy required for generalized disease",
    "If symptoms persist after optimal ChEI dose → escalate to IS therapy",
    "##Key monitoring",
    "Target: definite improvement within 30–45 minutes of dose",
    "Medication wearing off before next dose = under-dosing",
    "Increasing weakness after dose increase = over-dosing (cholinergic crisis)",
  ],
  "Amifampridine & Tensilon"
);

// SLIDE 5: Corticosteroids + IS
contentSlide(
  "Immunotherapy — Corticosteroids & Steroid-Sparing Agents",
  [
    "##Corticosteroids — First-line immunotherapy",
    "Prednisone: most widely used; 85% response rate",
    "Start LOW, titrate UP to avoid initial steroid exacerbation",
    "Low-start: 15–20 mg/day, increase by 5 mg every 1–2 weeks",
    "Target: 1 mg/kg/day (max 60–80 mg/day) until remission",
    "Then taper slowly over months to minimum effective dose",
    "⚠ Rapid high-dose initiation → paradoxical worsening in 1st week",
    "##Azathioprine (AZA) — First-choice steroid-sparing agent",
    "Dose: 2–3 mg/kg/day PO; onset of effect 6–18 months",
    "Check TPMT enzyme activity before starting",
    "Monitor CBC + LFTs regularly",
    "Allows prednisone dose reduction over time",
    "##Mycophenolate Mofetil (MMF)",
    "Dose: 1000–1500 mg BD; alternative to AZA",
    "Better tolerated GI side effect profile",
    "Second-choice steroid-sparing agent if AZA fails/intolerant",
  ],
  [
    "##Ciclosporin A (CYA)",
    "Dose: 2–2.5 mg/kg BD; onset 1–2 months (faster than AZA)",
    "Monitor renal function, BP, drug levels",
    "Second-choice if AZA/MMF inadequate",
    "##Tacrolimus",
    "Calcineurin inhibitor; used in refractory MG",
    "May be particularly effective in MuSK+ MG",
    "##Rituximab",
    "Anti-CD20 monoclonal antibody; depletes B cells",
    "Especially effective in MuSK antibody-positive MG",
    "Used in refractory or corticosteroid-dependent MG",
    "##Eculizumab (Soliris) — FDA approved 2017",
    "Anti-C5 complement inhibitor — blocks MAC formation",
    "For generalised AChR antibody-positive MG",
    "##Efgartigimod (Vyvgart) — anti-FcRn",
    "Reduces IgG (including AChR Ab) levels",
    "IV formulation; approved for generalised AChR+ MG",
    "##Key principle",
    "Avoid abrupt IS withdrawal → risk of crisis",
    "Maintain minimum effective dose indefinitely",
  ],
  "Novel Biologics"
);

// SLIDE 6: Thymectomy
contentSlide(
  "Thymectomy — Surgical Immunotherapy",
  [
    "##Indication",
    "Thymoma present: ALWAYS thymectomy (mandatory)",
    "Non-thymomatous generalised AChR+ MG: strongly recommended",
    "Age <65 years, early in disease course: best outcomes",
    "##Evidence base",
    "MGTX RCT (Wolfe et al 2016/2019): thymectomy + prednisone",
    "→ Lower QMG scores at 3 and 5 years vs prednisone alone",
    "→ Less prednisone required long-term",
    "Response gradual — continues months to years post-surgery",
    "##Timing",
    "Always elective — operate when patient is stable",
    "Ensure respiratory function optimised pre-op",
    "May need pre-op plasmapheresis/IVIG if poorly controlled",
    "##Not recommended for",
    "Ocular MG (generally) — unless refractory to drugs",
    "MuSK antibody-positive MG — less clear benefit",
    "Age >65 years or significant comorbidities (relative)",
  ],
  [
    "##Surgical approaches",
    "Trans-sternal (classic): widest mediastinal exploration",
    "Transcervical: less morbidity, good for small thymus",
    "VATS (Video-Assisted Thoracoscopic): minimally invasive",
    "Robot-assisted VATS: best cosmesis, similar outcomes to open",
    "##Pre-operative preparation",
    "Optimise MG control (ChEIs + immunotherapy)",
    "Pre-op plasmapheresis/IVIG if generalized, severe or unstable",
    "Monitor FVC and NIF — target FVC >1.5 L before elective surgery",
    "##Post-operative",
    "May require ICU monitoring for respiratory decompensation",
    "Continue ChEIs post-operatively",
    "Gradual tapering of immunosuppression months after surgery",
    "##Outcome",
    "Remission rates highest in young women, AChR+, early disease",
    "Improvement can occur even after many years of symptoms",
    "Thymoma MG: more difficult; 5-year survival depends on stage",
  ],
  "Approaches & Outcomes"
);

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// SLIDE 8: Crisis Management
contentSlide(
  "Management of Myasthenic Crisis",
  [
    "##Triggers of myasthenic crisis",
    "Infections (esp. respiratory): most common trigger",
    "Rapid tapering of immunosuppression",
    "Medications (aminoglycosides, fluoroquinolones, β-blockers, Mg²⁺, neuromuscular blockers)",
    "Surgery, trauma, emotional stress",
    "Aspiration pneumonia",
    "##Immediate management",
    "ADMIT to ICU if FVC <1 L or NIF < −20 cmH₂O",
    "Monitor FVC/NIF every 4–6 hours (20-30-40 rule)",
    "FVC <20 mL/kg OR NIF < −30 cmH₂O OR PaO₂ <70 → intubate",
    "Intubate EARLY — do NOT wait for respiratory arrest",
    "##Rapid therapy",
    "PLASMAPHERESIS: 5 exchanges over 1–2 weeks; fastest response",
    "IVIG: 2 g/kg over 2–5 days; equivalent efficacy to PE",
    "Start/continue corticosteroids (carefully to avoid initial exacerbation)",
  ],
  [
    "##Plasmapheresis",
    "Removes circulating AChR antibodies from plasma",
    "Response in 3–5 days; duration 4–6 weeks",
    "Indicated: crisis, pre-thymectomy, refractory MG",
    "Complications: hypotension, citrate toxicity, infection",
    "##IVIG",
    "Mechanism: blocks Fc receptors, reduces Ab production",
    "Dose: 2 g/kg over 2–5 days",
    "Response: similar to PE, onset in 3–5 days",
    "Safer than PE for cardiovascular instability",
    "Complications: headache, fluid overload, IgA anaphylaxis",
    "##20-30-40 Intubation rule",
    "FVC <20 mL/kg → intubate",
    "NIF < −30 cmH₂O → intubate",
    "PaO₂ <40 mmHg → intubate",
    "##Post-crisis",
    "Identify and treat precipitating cause",
    "Optimise long-term immunosuppression",
    "Early pulmonary rehabilitation",
  ],
  "Plasmapheresis & IVIG"
);

// ═══════════════════════════════════════════════════════════════════════════
// PART 2 — SAH
// ═══════════════════════════════════════════════════════════════════════════
sectionCard("PART 2: SUBARACHNOID HEMORRHAGE", "Grading Criteria — Management — Triple-H Therapy", ACCENT2);

// SLIDE 10: SAH Overview
contentSlide(
  "Subarachnoid Hemorrhage — Overview",
  [
    "##Definition",
    "Bleeding into the subarachnoid space between arachnoid and pia mater",
    "Most common cause: rupture of intracranial saccular (berry) aneurysm (80%)",
    "Other causes: AVM, trauma, cocaine use, idiopathic",
    "##Epidemiology",
    "Incidence: 6–8 per 100,000 per year",
    "Peak age: 40–60 years; female > male (3:2)",
    "Overall mortality: 40–50%",
    "~10% die before reaching hospital; another 10% before evaluation",
    "##Classic presentation",
    "'Thunderclap headache' — worst headache of life (sentinel headache)",
    "Sudden onset at peak intensity; may occur during exertion",
    "Nausea, vomiting, neck stiffness (meningism), photophobia",
    "Loss of consciousness (brief or prolonged)",
    "Focal neurological deficit, cranial nerve palsy (CN III)",
  ],
  [
    "##Aneurysm size classification",
    "Small: <10 mm diameter",
    "Large: 10–24 mm",
    "Giant: >24 mm",
    "Rupture risk: significantly increases for >6 mm → requires treatment",
    "##Key complications to anticipate",
    "Rebleeding — highest risk in first 2–12 hours",
    "Vasospasm / Delayed Cerebral Ischemia (DCI) — days 4–14",
    "Hydrocephalus — 25% of survivors",
    "Seizures — 13% of cases",
    "Hyponatremia — 10–34% (SIADH or cerebral salt wasting)",
    "Neurogenic pulmonary edema",
    "Cardiac dysfunction, arrhythmias (massive sympathetic discharge)",
    "##Initial investigation",
    "Non-contrast CT brain (97% sensitive within 6 hours)",
    "LP if CT negative but high clinical suspicion (xanthochromia)",
    "CT angiography for aneurysm localisation",
    "DSA (Digital Subtraction Angiography) — gold standard",
  ],
  "Complications & Investigations", ACCENT2
);

// SLIDE 11: Grading criteria — Hunt & Hess + WFNS
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    [{ text:"0", options:{color:TEXT,fontSize:11,fontFace:"Calibri"} }, { text:"Unruptured aneurysm — asymptomatic", options:{color:TEXT,fontSize:11,fontFace:"Calibri"} }, { text:"—", options:{color:TEXT,fontSize:11,fontFace:"Calibri"} }],
    [{ text:"1", options:{color:TEXT,fontSize:11,fontFace:"Calibri"} }, { text:"Minimal headache, slight nuchal rigidity", options:{color:TEXT,fontSize:11,fontFace:"Calibri"} }, { text:"~5%", options:{color:TEXT,fontSize:11,fontFace:"Calibri"} }],
    [{ text:"2", options:{color:TEXT,fontSize:11,fontFace:"Calibri"} }, { text:"Moderate–severe headache, nuchal rigidity ± CN palsy", options:{color:TEXT,fontSize:11,fontFace:"Calibri"} }, { text:"~10%", options:{color:TEXT,fontSize:11,fontFace:"Calibri"} }],
    [{ text:"3", options:{color:TEXT,fontSize:11,fontFace:"Calibri"} }, { text:"Mildly obtunded, confused, mild focal deficit", options:{color:TEXT,fontSize:11,fontFace:"Calibri"} }, { text:"~37%", options:{color:TEXT,fontSize:11,fontFace:"Calibri"} }],
    [{ text:"4", options:{color:TEXT,fontSize:11,fontFace:"Calibri"} }, { text:"Stuporous, hemiparesis, early decerebrate posturing", options:{color:TEXT,fontSize:11,fontFace:"Calibri"} }, { text:"~71%", options:{color:TEXT,fontSize:11,fontFace:"Calibri"} }],
    [{ text:"5", options:{color:TEXT,fontSize:11,fontFace:"Calibri"} }, { text:"Deep coma, decerebrate posturing, moribund", options:{color:TEXT,fontSize:11,fontFace:"Calibri"} }, { text:"~100%", options:{color:TEXT,fontSize:11,fontFace:"Calibri"} }],
  ];
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  // WFNS
  s.addText("WFNS GRADING SCALE (Based on GCS + Motor Deficit)", { x:6.65, y:0.82, w:6.0, h:0.38, fontSize:12.5, bold:true, color:ACCENT2, fontFace:"Calibri", margin:0 });
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    [{ text:"Grade", options:{bold:true,color:WHITE,fill:{color:MID},fontSize:11,fontFace:"Calibri"} }, { text:"GCS Score", options:{bold:true,color:WHITE,fill:{color:MID},fontSize:11,fontFace:"Calibri"} }, { text:"Motor Deficit", options:{bold:true,color:WHITE,fill:{color:MID},fontSize:11,fontFace:"Calibri"} }],
    [{ text:"I", options:{color:TEXT,fontSize:11,fontFace:"Calibri"} }, { text:"15", options:{color:TEXT,fontSize:11,fontFace:"Calibri"} }, { text:"Absent", options:{color:TEXT,fontSize:11,fontFace:"Calibri"} }],
    [{ text:"II", options:{color:TEXT,fontSize:11,fontFace:"Calibri"} }, { text:"13–14", options:{color:TEXT,fontSize:11,fontFace:"Calibri"} }, { text:"Absent", options:{color:TEXT,fontSize:11,fontFace:"Calibri"} }],
    [{ text:"III", options:{color:TEXT,fontSize:11,fontFace:"Calibri"} }, { text:"13–14", options:{color:TEXT,fontSize:11,fontFace:"Calibri"} }, { text:"Present", options:{color:TEXT,fontSize:11,fontFace:"Calibri"} }],
    [{ text:"IV", options:{color:TEXT,fontSize:11,fontFace:"Calibri"} }, { text:"7–12", options:{color:TEXT,fontSize:11,fontFace:"Calibri"} }, { text:"Present or absent", options:{color:TEXT,fontSize:11,fontFace:"Calibri"} }],
    [{ text:"V", options:{color:TEXT,fontSize:11,fontFace:"Calibri"} }, { text:"3–6", options:{color:TEXT,fontSize:11,fontFace:"Calibri"} }, { text:"Present or absent", options:{color:TEXT,fontSize:11,fontFace:"Calibri"} }],
  ];
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  s.addText("Higher grade = higher likelihood of poor outcome. Two-thirds of hospital-admitted patients present WFNS Grade III or better.", {
    x:6.65, y:4.15, w:6.0, h:0.6, fontSize:11, color:SUB, fontFace:"Calibri", italic:true
  });
}

// SLIDE 12: Fisher Grade
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  s.addShape(pres.ShapeType.rect, { x:0, y:0, w:0.12, h:0.7, fill:{ color: ACCENT2 } });
  s.addText("Modified Fisher CT Rating Scale — Prediction of Vasospasm", { x:0.28, y:0, w:13.0, h:0.7, fontSize:19, bold:true, color:WHITE, fontFace:"Calibri", valign:"middle", margin:0 });
  s.addShape(pres.ShapeType.rect, { x:0, y:0.7, w:"100%", h:"100%", fill:{ color: LIGHT } });

  s.addText("Based on CT brain findings — predicts risk of delayed cerebral ischemia (DCI) from vasospasm", {
    x:0.3, y:0.82, w:12.7, h:0.4, fontSize:12, color:SUB, fontFace:"Calibri", italic:true
  });

  const fisher = [
    [
      { text:"Grade", options:{bold:true,color:WHITE,fill:{color:MID},fontSize:12,fontFace:"Calibri"} },
      { text:"CT Criteria", options:{bold:true,color:WHITE,fill:{color:MID},fontSize:12,fontFace:"Calibri"} },
      { text:"Frequency", options:{bold:true,color:WHITE,fill:{color:MID},fontSize:12,fontFace:"Calibri"} },
      { text:"Delayed Cerebral Ischemia", options:{bold:true,color:WHITE,fill:{color:MID},fontSize:12,fontFace:"Calibri"} },
      { text:"Infarction", options:{bold:true,color:WHITE,fill:{color:MID},fontSize:12,fontFace:"Calibri"} },
    ],
    [{ text:"0", options:{color:TEXT,fontSize:12,fontFace:"Calibri"} }, { text:"No SAH, no IVH", options:{color:TEXT,fontSize:12,fontFace:"Calibri"} }, { text:"5%", options:{color:TEXT,fontSize:12,fontFace:"Calibri"} }, { text:"0%", options:{bold:true,color:"1E6B52",fontSize:12,fontFace:"Calibri"} }, { text:"0%", options:{color:TEXT,fontSize:12,fontFace:"Calibri"} }],
    [{ text:"1", options:{color:TEXT,fontSize:12,fontFace:"Calibri"} }, { text:"Minimal/thin SAH, NO biventricular IVH", options:{color:TEXT,fontSize:12,fontFace:"Calibri"} }, { text:"30%", options:{color:TEXT,fontSize:12,fontFace:"Calibri"} }, { text:"12%", options:{color:TEXT,fontSize:12,fontFace:"Calibri"} }, { text:"6%", options:{color:TEXT,fontSize:12,fontFace:"Calibri"} }],
    [{ text:"2", options:{color:TEXT,fontSize:12,fontFace:"Calibri"} }, { text:"Minimal/thin SAH, WITH biventricular IVH", options:{color:TEXT,fontSize:12,fontFace:"Calibri"} }, { text:"5%", options:{color:TEXT,fontSize:12,fontFace:"Calibri"} }, { text:"21%", options:{color:TEXT,fontSize:12,fontFace:"Calibri"} }, { text:"14%", options:{color:TEXT,fontSize:12,fontFace:"Calibri"} }],
    [{ text:"3", options:{color:TEXT,fontSize:12,fontFace:"Calibri"} }, { text:"Thick SAH (filling ≥1 cistern/fissure), NO biventricular IVH", options:{color:TEXT,fontSize:12,fontFace:"Calibri"} }, { text:"43%", options:{color:TEXT,fontSize:12,fontFace:"Calibri"} }, { text:"19%", options:{color:TEXT,fontSize:12,fontFace:"Calibri"} }, { text:"12%", options:{color:TEXT,fontSize:12,fontFace:"Calibri"} }],
    [{ text:"4", options:{bold:true,color:ACCENT,fontSize:12,fontFace:"Calibri"} }, { text:"Thick SAH, WITH biventricular IVH", options:{bold:true,color:ACCENT,fontSize:12,fontFace:"Calibri"} }, { text:"17%", options:{color:TEXT,fontSize:12,fontFace:"Calibri"} }, { text:"40%", options:{bold:true,color:ACCENT,fontSize:12,fontFace:"Calibri"} }, { text:"28%", options:{bold:true,color:ACCENT,fontSize:12,fontFace:"Calibri"} }],
  ];

  s.addTable(fisher, {
    x:0.3, y:1.28, w:12.7, h:3.2,
    colW:[0.8, 4.3, 1.5, 3.2, 1.4],
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    fontFace:"Calibri", align:"left",
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  s.addText("IVH = Intraventricular Hemorrhage  |  Thick SAH = completely filling at least one cistern or fissure  |  Grade 4 has highest risk of DCI (40%) and infarction (28%)", {
    x:0.3, y:4.6, w:12.7, h:0.55, fontSize:11, color:SUB, fontFace:"Calibri", italic:true
  });
}

// SLIDE 13: SAH Management
contentSlide(
  "SAH Management — Acute Phase",
  [
    "##Immediate stabilisation",
    "Monitored critical care / ICU admission",
    "Reassess GCS and pupils regularly (GCS drop of 1 = complication)",
    "##Blood pressure control (to prevent rebleeding)",
    "Target SBP 120–160 mmHg (before aneurysm secured)",
    "Titratable IV antihypertensive: labetalol or nicardipine preferred",
    "AVOID: nitroprusside, nitroglycerin (↑ ICP)",
    "##Aneurysm occlusion — WITHIN 48 hours",
    "Endovascular coiling: first-line for most aneurysms (less invasive)",
    "Surgical clipping: best for wide-neck, MCA aneurysms",
    "Goal: secure aneurysm before vasospasm onset (day 4–14)",
    "##Rebleeding prevention",
    "Early aneurysm occlusion is primary prevention",
    "Short-term antifibrinolytics (tranexamic acid / aminocaproic acid):",
    "Only if unavoidable delay in treatment (consult neurosurgery)",
    "Risk of increased cerebral ischemia with prolonged use",
  ],
  [
    "##Vasospasm prevention — Nimodipine",
    "Oral nimodipine 60 mg every 4 hours × 21 days: STANDARD OF CARE",
    "Mechanism: cytoprotective (↓ intracellular Ca²⁺); improves microvascular flow",
    "Reduces cerebral infarction and poor outcome; does NOT reduce angiographic vasospasm",
    "⚠ Stop if causes hypotension",
    "##Hydrocephalus (25% of survivors)",
    "Blood in ventricles obstructs CSF drainage",
    "External ventricular drain (EVD) if symptomatic",
    "Minority require permanent VP shunt",
    "##Seizure prophylaxis",
    "Prophylactic anticonvulsants: short-term in immediate post-haemorrhage period",
    "Long-term use NOT supported by evidence",
    "##Hyponatremia management",
    "SIADH (euvolemia/hypervolemia) vs Cerebral Salt Wasting (hypovolemia)",
    "Fluid restriction CONTRAINDICATED in SAH (risk of vasospasm)",
    "Fludrocortisone 0.05 mg/day to prevent natriuresis",
    "Hypertonic saline (250–500 mL) if needed; correct slowly",
  ],
  "Nimodipine & Complications", ACCENT2
);

// SLIDE 14: TRIPLE-H THERAPY
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  s.addText("Triple-H Therapy — Hypervolemia, Hypertension, Hemodilution", { x:0.28, y:0, w:13.0, h:0.7, fontSize:18, bold:true, color:WHITE, fontFace:"Calibri", valign:"middle", margin:0 });
  s.addShape(pres.ShapeType.rect, { x:0, y:0.7, w:"100%", h:"100%", fill:{ color: LIGHT } });

  // 3 boxes
  const boxes = [
    { label:"HYPER-\nVOLEMIA", desc:"Volume expansion\nto ↑ cerebral blood flow\nIV crystalloids / colloids\nTarget CVP 8–12 mmHg", x:0.3, col:ACCENT2 },
    { label:"HYPER-\nTENSION", desc:"Induced hypertension\nto overcome vasospasm\nNoradrenaline / phenylephrine\nTarget SBP 160–200 mmHg\n(post-occlusion)", x:4.85, col:ACCENT },
    { label:"HEMO-\nDILUTION", desc:"Reduce blood viscosity\nto ↑ microvascular flow\nTarget Hct 30–35%\n⚠ Hct <30% — NOT beneficial\n(O₂ delivery impaired)", x:9.4, col:"7B3FA0" },
  ];
  boxes.forEach(b => {
    s.addShape(pres.ShapeType.rect, { x:b.x, y:0.85, w:4.15, h:1.3, fill:{color:b.col}, line:{color:b.col} });
    s.addText(b.label, { x:b.x, y:0.85, w:4.15, h:1.3, fontSize:22, bold:true, color:WHITE, fontFace:"Calibri", align:"center", valign:"middle" });
    s.addShape(pres.ShapeType.rect, { x:b.x, y:2.2, w:4.15, h:2.1, fill:{color:WHITE}, line:{color:b.col, pt:1.5} });
    s.addText(b.desc, { x:b.x, y:2.2, w:4.15, h:2.1, fontSize:12, color:TEXT, fontFace:"Calibri", align:"center", valign:"middle" });
  });

  s.addText("CURRENT EVIDENCE & UPDATED RECOMMENDATIONS (Barash Clinical Anesthesia, 9e)", {
    x:0.3, y:4.4, w:12.7, h:0.3, fontSize:12, bold:true, color:ACCENT, fontFace:"Calibri"
  });
  const bullets = [
    { text:"Historical use: Triple-H was a mainstay for prevention & treatment of DCI from SAH vasospasm", options:{bullet:true,color:TEXT,fontSize:12,fontFace:"Calibri",breakLine:true} },
    { text:"Rationale: hypovolemia associated with poor outcome; anemia improves CBF rheology; hypertension overcomes vasospastic resistance", options:{bullet:true,color:TEXT,fontSize:12,fontFace:"Calibri",breakLine:true} },
    { text:"Current guidelines (Neurocritical Care Society): Triple-H in its classic form is NO LONGER recommended for prophylaxis", options:{bullet:true,bold:true,color:ACCENT,fontSize:12,fontFace:"Calibri",breakLine:true} },
    { text:"UPDATED approach: Maintain EUVOLEMIA + controlled stepwise blood pressure augmentation only in CONFIRMED DCI", options:{bullet:true,bold:true,color:ACCENT2,fontSize:12,fontFace:"Calibri",breakLine:true} },
    { text:"Intentional hemodilution AVOIDED — hematocrit <30% reduces O₂ delivery and is harmful", options:{bullet:true,color:TEXT,fontSize:12,fontFace:"Calibri"} },
  ];
  s.addText(bullets, { x:0.3, y:4.72, w:12.7, h:0.9, fontFace:"Calibri" });
}

// SLIDE 15: Triple-H — Mechanism and Practice
contentSlide(
  "Triple-H Therapy — Mechanism, Protocol & Complications",
  [
    "##Pathophysiology of vasospasm",
    "Onset: day 4–14 post-SAH (peak day 7–10)",
    "Blood products (oxyhemoglobin) → endothelium → ↓ NO, ↑ ET-1",
    "Smooth muscle contraction → arterial narrowing → DCI",
    "Symptoms: new neurological deficit, confusion, drowsiness",
    "Diagnosis: TCD monitoring (MCA velocity >120 cm/s = suspicious)",
    "Confirm: CT perfusion or DSA",
    "##When to initiate vasospasm therapy",
    "New focal deficit OR TCD showing elevated velocities",
    "Maintain euvolemia with IV isotonic saline",
    "Step 1: Ensure euvolemia → check volume status",
    "Step 2: BP augmentation → vasopressors if needed",
    "Target MAP: augment by 20–40 mmHg above baseline",
    "Balloon angioplasty: if medical therapy fails; done early",
  ],
  [
    "##Blood pressure augmentation protocol",
    "Only after aneurysm has been secured (clipped/coiled)",
    "Pre-occlusion: hypertension CONTRAINDICATED (↑ rebleeding risk)",
    "Post-occlusion: SBP target 160–200 mmHg for DCI",
    "Agents: noradrenaline, phenylephrine, dopamine (vasopressors)",
    "Discontinue nimodipine if it causes significant hypotension",
    "##Complications of Triple-H (reason guideline changed)",
    "Hyponatremia: dilutional (from aggressive hypervolemia)",
    "Pulmonary oedema: fluid overload (neurogenic + iatrogenic)",
    "Cerebral oedema: fluid overload",
    "Myocardial infarction: aggressive hypertension",
    "Cardiogenic shock (rare) — intra-aortic balloon pump needed",
    "Catheter-related infections (CVP lines for monitoring)",
    "##Interventional rescue",
    "Balloon angioplasty: reverses vasospasm mechanically (observational benefit)",
    "Intra-arterial vasodilators: papaverine, verapamil, nicardipine",
    "Used if stepwise medical augmentation fails",
  ],
  "BP Augmentation & Complications", ACCENT2
);

// SLIDE 16: Summary
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  s.addText("KEY TAKEAWAYS", { x:0.8, y:0.0, w:11.7, h:0.62, fontSize:26, bold:true, color:WHITE, fontFace:"Calibri", valign:"middle", charSpacing:3, margin:0 });

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    { text:"MYASTHENIA GRAVIS", options:{bold:true,color:ACCENT,fontSize:14,fontFace:"Calibri",breakLine:true,bullet:false} },
    { text:"ChEI (pyridostigmine): first-line symptomatic; dose to effect", options:{bullet:true,color:WHITE,fontSize:12,fontFace:"Calibri",breakLine:true} },
    { text:"Immunotherapy: prednisone + AZA/MMF; rituximab for MuSK+; eculizumab/efgartigimod for refractory", options:{bullet:true,color:WHITE,fontSize:12,fontFace:"Calibri",breakLine:true} },
    { text:"Thymectomy: mandatory for thymoma; beneficial for generalised AChR+ MG", options:{bullet:true,color:WHITE,fontSize:12,fontFace:"Calibri",breakLine:true} },
    { text:"Myasthenic crisis: intubate early (20-30-40 rule); plasmapheresis / IVIG are fastest acting", options:{bullet:true,color:ACCENT,fontSize:12,fontFace:"Calibri",bold:true,breakLine:true} },
    { text:"Cholinergic crisis: STOP ChEIs; give atropine — key distinction via Tensilon test", options:{bullet:true,color:WHITE,fontSize:12,fontFace:"Calibri",breakLine:true} },
  ];
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  const right = [
    { text:"SAH — GRADING & MANAGEMENT", options:{bold:true,color:ACCENT2,fontSize:14,fontFace:"Calibri",breakLine:true,bullet:false} },
    { text:"Hunt & Hess: clinical grading 1–5; higher grade = worse prognosis", options:{bullet:true,color:WHITE,fontSize:12,fontFace:"Calibri",breakLine:true} },
    { text:"WFNS: GCS-based grading; Fisher scale: CT-based vasospasm risk (Grade 4 = 40% DCI)", options:{bullet:true,color:WHITE,fontSize:12,fontFace:"Calibri",breakLine:true} },
    { text:"Nimodipine 60 mg q4h × 21 days: ONLY drug proven to improve outcome", options:{bullet:true,color:ACCENT2,fontSize:12,fontFace:"Calibri",bold:true,breakLine:true} },
    { text:"Aneurysm occlusion within 48 hours (coiling or clipping) — prevents rebleeding", options:{bullet:true,color:WHITE,fontSize:12,fontFace:"Calibri",breakLine:true} },
    { text:"Triple-H: now replaced by euvolemia + stepwise BP augmentation only for confirmed DCI", options:{bullet:true,color:ACCENT,fontSize:12,fontFace:"Calibri",bold:true,breakLine:true} },
    { text:"Hemodilution + prophylactic hypervolemia NO LONGER recommended", options:{bullet:true,color:WHITE,fontSize:12,fontFace:"Calibri"} },
  ];
  s.addText(right, { x:6.75, y:0.78, w:6.0, h:4.4, fontFace:"Calibri" });
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// ─── WRITE ────────────────────────────────────────────────────────────────────
pres.writeFile({ fileName: "/home/daytona/workspace/bibrachial-mnd/MG_SAH_Treatment.pptx" })
  .then(() => console.log("DONE"))
  .catch(e => { console.error(e); process.exit(1); });