Epilepsy seizures
"epilepsy" AND "seizure classification"
| Old Term | New Term |
|---|---|
| Simple partial seizure | Focal aware seizure |
| Complex partial seizure | Focal impaired awareness seizure |
| Partial seizure with secondary generalization | Focal-to-bilateral tonic-clonic seizure |
| Type | Notes |
|---|---|
| Generalized tonic-clonic (grand mal) | Most dramatic; loss of consciousness + convulsions |
| Absence seizure (petit mal) | Brief staring spells; typical in childhood absence epilepsy |
| Myoclonic seizure | Sudden brief muscle jerks; seen in juvenile myoclonic epilepsy, Dravet syndrome |
| Atonic seizure (drop seizure) | Sudden loss of muscle tone; seen in Lennox-Gastaut syndrome |
| Epileptic spasms | Infantile spasms (West syndrome) |

| Syndrome | Age Onset | Key Features |
|---|---|---|
| West syndrome | Infancy (3-12 mo) | Infantile spasms, hypsarrhythmia on EEG, developmental regression |
| Dravet syndrome | Infancy | Febrile + afebrile seizures, SCN1A mutation, drug-resistant |
| Childhood absence epilepsy | 4-12 years | Typical absence seizures, 3 Hz spike-wave |
| Benign epilepsy with centrotemporal spikes (BECTS) | 3-13 years | Nocturnal focal motor seizures, self-limiting |
| Juvenile myoclonic epilepsy (JME) | Adolescence | Morning myoclonus, GTC seizures, absence; lifelong but responsive to valproate |
| Lennox-Gastaut syndrome | Childhood | Multiple seizure types, drug-resistant, intellectual disability |
| Temporal lobe epilepsy (mesial) | Any age | Focal impaired awareness seizures; hippocampal sclerosis on MRI; surgically remediable |
| Seizure Type | First-Line Drugs |
|---|---|
| Generalized tonic-clonic | Valproate, levetiracetam, lamotrigine |
| Absence | Ethosuximide, valproate, lamotrigine |
| Focal (any) | Carbamazepine, oxcarbazepine, levetiracetam, lamotrigine, lacosamide |
| Juvenile myoclonic epilepsy | Valproate, levetiracetam |
| Lennox-Gastaut | Valproate, clobazam, lamotrigine, rufinamide |
| Stage | Intervention |
|---|---|
| First-line | IV lorazepam or IM midazolam (benzodiazepine) |
| Second-line | IV levetiracetam, valproate, fosphenytoin, or phenytoin (equally effective after benzo failure; ~50% response each) |
| Refractory SE (seizure continues ≥30 min after 1st + 2nd line) | Anesthetic doses of pentobarbital, propofol, or midazolam infusion |
Epilepsy seizures
Epilepsy seizures definition epidemiology pathophysiology investigation treatment prevention give me all details and search in all medical book and give me 50 slide power point
mkdir -p /home/daytona/workspace/epilepsy-pptx && ls /home/daytona/workspace/epilepsy-pptx
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{ text: "Epilepsy = ≥2 unprovoked seizures; seizure = paroxysmal abnormal cerebral discharge", options: { bullet: true, breakLine: true } },
{ text: "ILAE 2017: Focal onset | Generalized onset | Unknown onset", options: { bullet: true, breakLine: true } },
{ text: "EEG + MRI are the cornerstones of investigation", options: { bullet: true, breakLine: true } },
{ text: "~2/3 of patients achieve seizure control with appropriate ASM monotherapy", options: { bullet: true, breakLine: true } },
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// ════════════════════════════════════════════════════════════════
// SLIDE CONTENT
// ════════════════════════════════════════════════════════════════
// SLIDE 1 – Title
titleSlide("Epilepsy & Seizures", "A Comprehensive Medical Review\nDefinition · Epidemiology · Pathophysiology · Classification\nInvestigation · Treatment · Prevention");
// SLIDE 2 – Overview / Agenda
bodySlide("Presentation Outline", [
"1. Definition & Historical Background",
"2. Epidemiology",
"3. Aetiology & Risk Factors",
"4. Pathophysiology",
"5. ILAE 2017 Classification of Seizures",
"6. Epilepsy Syndromes",
"7. Clinical Features of Seizure Types",
"8. Differential Diagnosis",
"9. Investigations",
"10. Treatment – Antiseizure Medications (ASMs)",
"11. Treatment – Non-pharmacological",
"12. Status Epilepticus – Emergency Management",
"13. Special Populations",
"14. Prevention & Seizure Triggers",
"15. Prognosis & SUDEP",
], { fs: 13 });
// ── SECTION 1: DEFINITION ───────────────────────────────────────
sectionSlide(1, "Definition & Historical Background");
// SLIDE 4
bodySlide("Definitions", [
"SEIZURE – a paroxysmal, abnormal electrical discharge from cerebral neurons producing loss of consciousness, altered perception, convulsive movements, sensory disturbance, or autonomic features.",
"EPILEPSY – a disorder characterised by ≥2 unprovoked seizures occurring >24 h apart; OR 1 unprovoked seizure with ≥60% risk of recurrence over the next 10 years.",
"CONVULSION – subset of seizure involving involuntary repetitive muscular contractions; does NOT capture the full spectrum.",
"STATUS EPILEPTICUS – seizure lasting ≥5 min (GTC) or ≥10 min (focal/absence), or repeated seizures without full recovery.",
"PROVOKED (ACUTE SYMPTOMATIC) SEIZURE – occurs in direct relation to acute CNS insult (metabolic, toxic, structural); NOT classified as epilepsy.",
], { fs: 13 });
// SLIDE 5
bodySlide("Historical Milestones", [
"Ancient times – epilepsy called the 'Sacred Disease' (Hippocrates, ~400 BC); he attributed it to brain disorder, not divine intervention.",
"Medieval era – known as the 'Falling Sickness' or 'Falling Evil.'",
"1870 – Hughlings Jackson: seizures are 'an excessive and disorderly discharge of cerebral nervous tissue on muscles.'",
"1929 – Hans Berger invents the EEG, revolutionising seizure diagnosis.",
"1938 – First clinical use of phenytoin (Merritt & Putnam) — first non-sedating ASM.",
"1989 – ILAE first formal classification of epilepsies and epileptic syndromes.",
"2017 – ILAE revised Operational Classification of Seizure Types adopted worldwide.",
]);
// ── SECTION 2: EPIDEMIOLOGY ─────────────────────────────────────
sectionSlide(2, "Epidemiology");
// SLIDE 7
bodySlide("Global Burden", [
"~50 million people worldwide have epilepsy – one of the most common neurological disorders.",
"~2 million individuals with epilepsy in the United States alone.",
"Incidence: ~44 new cases per 100,000 persons/year (USA).",
"Lifetime prevalence: ~1 in 26 people in the US will develop epilepsy.",
"Nearly 1% of persons in the US will have epilepsy by age 20.",
"Over two-thirds of all epileptic seizures begin in childhood (peak: first year of life).",
"Second incidence peak occurs after age 60 – due to stroke, neurodegeneration, tumours.",
"80% of people with epilepsy live in low- and middle-income countries; many never receive treatment.",
]);
// SLIDE 8
twoColSlide("Epidemiology – Age & Sex Distribution",
"Age Distribution",
[
"Bimodal incidence: childhood & elderly",
"Neonates: metabolic, hypoxic-ischaemic causes",
"Infancy–childhood: genetic/structural syndromes",
"Adolescence: JME, absence epilepsy",
"Adults 15-64: trauma, CNS infections, tumours",
"Elderly >65: cerebrovascular disease #1 cause",
"Absence & myoclonic seizures peak in childhood",
"Complex partial (focal impaired awareness) predominate in adults",
],
"Sex & Socioeconomic",
[
"Slight male predominance overall",
"Some syndromes female-predominant (Rett syndrome, PCDH19 epilepsy)",
"Mortality 2–3× higher than general population",
"SUDEP (Sudden Unexpected Death in Epilepsy) ~1/1000 patient-years",
"Significant psychosocial burden: depression, anxiety, stigma",
"Employment and driving restrictions common",
"Annual economic cost in USA: >$15 billion",
]
);
// ── SECTION 3: AETIOLOGY ────────────────────────────────────────
sectionSlide(3, "Aetiology & Risk Factors");
// SLIDE 10
twoColSlide("Aetiology – ILAE Framework (2017)",
"Structural",
[
"Post-stroke or post-traumatic gliosis (50% of new adult focal)",
"Hippocampal sclerosis (mesial temporal lobe epilepsy)",
"Cortical dysplasia / malformations of cortical development",
"Brain tumours (primary & metastatic) – 15%",
"Vascular malformations (cavernomas, AVMs) – 15%",
"Traumatic brain injury",
"Post-infectious encephalitis/abscess",
"Perinatal hypoxic-ischaemic injury",
],
"Genetic / Metabolic / Immune / Unknown",
[
"Genetic: ion channel mutations (SCN1A, KCNQ2, GABRG2); copy-number variants",
"Metabolic: pyridoxine deficiency, mitochondrial disease, GLUT1 deficiency",
"Immune: autoimmune encephalitis (anti-NMDAR, LGI1, CASPR2)",
"Infectious: neurocysticercosis (most common cause worldwide), HSV encephalitis, HIV",
"Unknown – no cause found in ~40%",
"Risk factors: family history, febrile seizures, head trauma, CNS infections, prematurity",
]
);
// ── SECTION 4: PATHOPHYSIOLOGY ──────────────────────────────────
sectionSlide(4, "Pathophysiology");
// SLIDE 12
bodySlide("Cellular & Molecular Mechanisms", [
"Core principle: imbalance between EXCITATION and INHIBITION in neuronal networks.",
"Seizure initiation – 'paroxysmal depolarisation shift' (PDS): prolonged abnormal depolarisation of a neuron (epileptic focus) → burst of action potentials.",
"Excessive glutamate (AMPA & NMDA receptor) activation drives depolarisation.",
"Impaired GABA-mediated inhibition allows synchronous firing to spread.",
"Ion channel dysfunction is central: Na⁺ channel gain-of-function (e.g. SCN1A in Dravet), K⁺ channel loss-of-function (KCNQ2 in BFNC), GABA_A receptor mutations.",
"Focal seizures: abnormal discharge confined to one cortical network.",
"Generalised seizures: thalamocortical circuits involved from the outset; corticothalamic loop drives synchrony.",
"Epileptogenesis: process by which a normal brain becomes chronically epileptic — involves structural/synaptic remodelling, mossy fibre sprouting in hippocampus.",
]);
// SLIDE 13
bodySlide("Neuropathology of Common Epileptic Substrates", [
"HIPPOCAMPAL SCLEROSIS – neuronal loss in CA1, CA3, CA4 (Sommer's sector); gliosis; mossy fibre sprouting into molecular layer. Hallmark of mesial temporal lobe epilepsy.",
"FOCAL CORTICAL DYSPLASIA (FCD) – abnormal cortical lamination and neuronal morphology; highly epileptogenic; identified on high-resolution MRI (FLAIR sequences).",
"TUMOUR-RELATED EPILEPSY – low-grade tumours (DNET, ganglioglioma) near cortex are particularly epileptogenic; mechanisms include K⁺/glutamate dysregulation by tumour cells.",
"CORTICAL SCARS – post-traumatic or post-infarct gliosis creates irritative zone that generates ictal discharges.",
"STATUS EPILEPTICUS INJURY – prolonged seizure activity causes glutamate excitotoxicity → hippocampal neuronal death → worsening epileptogenesis (secondary hippocampal sclerosis).",
]);
// ── SECTION 5: CLASSIFICATION ───────────────────────────────────
sectionSlide(5, "ILAE 2017 Classification of Seizures");
// SLIDE 15
tableSlide("ILAE 2017 Seizure Classification", ["Category", "Type", "Former Name", "Key Feature"],
[
["Focal Onset", "Focal Aware", "Simple Partial", "Consciousness preserved"],
["Focal Onset", "Focal Impaired Awareness", "Complex Partial", "Consciousness impaired; automatisms"],
["Focal Onset", "Focal-to-Bilateral Tonic-Clonic", "Secondarily Generalised", "Focal onset → bilateral spread"],
["Generalised Onset", "Tonic-Clonic (GTC)", "Grand Mal", "LOC + tonic → clonic phases"],
["Generalised Onset", "Absence (typical)", "Petit Mal", "Brief stare; 3 Hz spike-wave"],
["Generalised Onset", "Absence (atypical)", "—", "Slower spike-wave; Lennox-Gastaut"],
["Generalised Onset", "Myoclonic", "—", "Sudden brief muscle jerks"],
["Generalised Onset", "Atonic (drop)", "Astatic", "Sudden loss of muscle tone"],
["Generalised Onset", "Epileptic Spasms", "Infantile Spasms", "West syndrome"],
["Unknown Onset", "Unknown", "—", "Insufficient data to classify"],
],
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);
// ── SECTION 6: SYNDROMES ────────────────────────────────────────
sectionSlide(6, "Epilepsy Syndromes");
// SLIDE 17
tableSlide("Major Epilepsy Syndromes – Childhood Onset",
["Syndrome", "Age Onset", "Seizure Types", "EEG / Key Feature", "Prognosis"],
[
["West Syndrome", "3–12 mo", "Infantile spasms", "Hypsarrhythmia", "Poor if untreated; developmental regression"],
["Dravet Syndrome", "6–12 mo", "Febrile + afebrile; multiple types", "Non-specific; SCN1A mutation", "Drug-resistant; intellectual disability"],
["Childhood Absence Epilepsy", "4–12 yr", "Typical absence", "3 Hz generalised spike-wave", "Often resolves in adolescence"],
["Lennox-Gastaut Syndrome", "1–7 yr", "Tonic, atonic, atypical absence", "Slow spike-wave <2.5 Hz", "Drug-resistant; lifelong disability"],
["BECTS (Rolandic)", "3–13 yr", "Focal motor; nocturnal GTC", "Centrotemporal spikes", "Self-limiting; resolves by 16 yr"],
["Panayiotopoulos Syndrome", "3–6 yr", "Autonomic focal seizures", "Occipital spikes", "Benign; spontaneous remission"],
],
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// SLIDE 18
tableSlide("Major Epilepsy Syndromes – Adolescent & Adult Onset",
["Syndrome", "Age Onset", "Seizure Types", "Key Feature", "Treatment"],
[
["Juvenile Myoclonic Epilepsy (JME)", "12–20 yr", "Morning myoclonus + GTC ± absence", "4–6 Hz poly-spike-wave; photosensitive", "Valproate / levetiracetam; lifelong"],
["Juvenile Absence Epilepsy", "10–17 yr", "Absence + GTC", "3.5–4 Hz spike-wave", "Valproate / ethosuximide"],
["Mesial Temporal Lobe Epilepsy", "Any; peak 20s", "Focal impaired awareness; aura", "Hippocampal sclerosis on MRI", "Surgically remediable"],
["Autosomal Dom. Nocturnal Frontal Lobe", "Childhood–adult", "Nocturnal hypermotor seizures", "CHRNA4/CHRNB2 mutations", "Carbamazepine"],
["Progressive Myoclonic Epilepsies", "Variable", "Myoclonus + GTC + cerebellar signs", "Multiple causes (Unverricht, Lafora)", "Symptomatic; poor prognosis"],
],
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// ── SECTION 7: CLINICAL FEATURES ────────────────────────────────
sectionSlide(7, "Clinical Features of Seizure Types");
// SLIDE 20
bodySlide("Generalised Tonic-Clonic Seizure – Phase by Phase", [
"PRODROME (hours before): mood change, irritability, myoclonic jerks on awakening — not universal.",
"AURA: epigastric rising sensation, déjà vu, fear (if focal onset preceding GTC).",
"TONIC PHASE (10–20 sec): sudden LOC + fall; brief flexion → sustained rigid extension of neck, back, limbs; piercing cry (air through closed cords); apnea → cyanosis; pupils dilated & unreactive.",
"CLONIC PHASE (~30 sec): rhythmic flexor spasms at 8/sec → 4/sec; tongue bite (lateral margin); hypersalivation, sweating, tachycardia, elevated BP, urinary incontinence.",
"TERMINAL PHASE: movements cease; deep coma; stertorous breathing; pupils return to light.",
"POSTICTAL PHASE (min–hours): gradual awakening; confusion, agitation, amnesia for event; headache; muscle soreness.",
]);
// SLIDE 21
twoColSlide("Clinical Features – Focal & Absence Seizures",
"Focal Aware (Simple Partial)",
[
"Consciousness PRESERVED",
"Symptoms reflect cortical origin:",
"• Motor: Jacksonian march (hand → arm → face)",
"• Somatosensory: tingling, numbness",
"• Visual: lights, spots, formed images",
"• Auditory: buzzing, voices",
"• Autonomic: flushing, epigastric sensation",
"• Psychic: déjà vu, jamais vu, fear",
"Todd's paralysis: post-ictal focal weakness",
],
"Absence (Typical) Seizure",
[
"Sudden onset & offset (5–20 sec)",
"Blank staring, unresponsive",
"Subtle automatisms (eye blinking, lip smacking)",
"NO fall, NO postictal confusion",
"Easily induced by hyperventilation",
"EEG: classic 3 Hz generalised spike-wave",
"Multiple episodes per day possible",
"May be mistaken for daydreaming",
]
);
// SLIDE 22
twoColSlide("Clinical Features – Focal Impaired Awareness & Myoclonic",
"Focal Impaired Awareness (Complex Partial)",
[
"Consciousness IMPAIRED (not fully lost)",
"Most often temporal lobe origin",
"Typical aura: rising epigastric sensation",
"Automatisms: lip smacking, hand fumbling, chewing, ambulation",
"Duration: 1–3 minutes",
"Post-ictal confusion & amnesia",
"Can spread to bilateral tonic-clonic",
"Hippocampal sclerosis on MRI common",
],
"Myoclonic & Atonic Seizures",
[
"MYOCLONIC: sudden brief bilateral jerks, typically proximal limbs",
"• Morning predominance in JME",
"• Preserved consciousness",
"• Can cause drop or fall",
"ATONIC (Drop Attacks):",
"• Sudden loss of muscle tone → fall",
"• Risk of head injury → helmet use",
"• Common in Lennox-Gastaut syndrome",
"• Very brief; rapid recovery",
]
);
// ── SECTION 8: DIFFERENTIAL DIAGNOSIS ───────────────────────────
sectionSlide(8, "Differential Diagnosis");
// SLIDE 24
bodySlide("Differential Diagnosis of Seizures", [
"SYNCOPE – most common mimic; prodrome of lightheadedness, dimming vision; brief convulsive movements possible (anoxic convulsions); rapid full recovery; triggered by standing/pain/emotion.",
"TRANSIENT ISCHAEMIC ATTACK (TIA) – usually negative symptoms (weakness, numbness) vs positive motor symptoms of seizure; no postictal phase.",
"MIGRAINE with aura – slow spreading aura (minutes); headache follows; no LOC.",
"PSYCHOGENIC NON-EPILEPTIC SEIZURES (PNES) – resemble seizures; variable across episodes; prominent pelvic thrusting, eye closure during 'convulsions'; no EEG correlate; often history of trauma/abuse.",
"PANIC ATTACKS – prolonged duration (>5 min); linked to specific triggers; no tonic-clonic activity; no postictal state.",
"HYPOGLYCAEMIA / HYPONATRAEMIA – acute symptomatic seizures; blood tests reveal cause; correct metabolic abnormality.",
"PAROXYSMAL MOVEMENT DISORDERS – dyskinesias, chorea; maintain consciousness; no EEG correlate.",
"NARCOLEPSY / CATAPLEXY – sudden muscle atonia triggered by emotion; mimics atonic seizures.",
]);
// ── SECTION 9: INVESTIGATIONS ────────────────────────────────────
sectionSlide(9, "Investigations");
// SLIDE 26
bodySlide("Investigation Overview", [
"History & Eyewitness Account – cornerstone; detailed description of events before, during, and after episode.",
"ELECTROENCEPHALOGRAM (EEG) – keystone investigation in all patients with seizures and epilepsy.",
"BRAIN MRI – should be performed in essentially ALL patients with new-onset seizures.",
"BLOOD TESTS – electrolytes, glucose, calcium, magnesium, liver/renal function, FBC, toxicology screen.",
"LUMBAR PUNCTURE – indicated if CNS infection suspected or in HIV-positive patients.",
"GENETIC TESTING – guided by syndrome; highest yield with intellectual disability + autism + dysmorphic features.",
"Functional imaging (PET, SPECT), magnetoencephalography (MEG) – used in pre-surgical evaluation.",
"Neuropsychological assessment – pre-surgical mapping of cognitive function.",
]);
// SLIDE 27
bodySlide("EEG – The Keystone Investigation", [
"EEG diagnoses epilepsy definitively ONLY if electrical seizure is recorded simultaneously with clinical event.",
"Interictal initial EEG is NORMAL in up to 60% of known epilepsy patients — normal EEG does NOT exclude epilepsy.",
"Epileptiform abnormalities present in >80% of focal epilepsy patients if 3 or more EEGs are performed.",
"Syndrome-specific patterns:",
" • Generalised absence epilepsy: 3 Hz spike-and-wave",
" • West syndrome: hypsarrhythmia (chaotic high-amplitude pattern)",
" • Rolandic epilepsy: centrotemporal spikes",
" • Juvenile myoclonic epilepsy: 4–6 Hz poly-spike-and-wave",
" • Lennox-Gastaut: slow spike-and-wave (<2.5 Hz)",
"Video-EEG monitoring – mandatory for pre-surgical evaluation and when diagnosis is uncertain.",
"Continuous EEG – used in ICU for suspected nonconvulsive status epilepticus in comatose patients.",
]);
// SLIDE 28
bodySlide("Neuroimaging in Epilepsy", [
"BRAIN MRI (preferred over CT) – performed in essentially all patients with new-onset seizures.",
"Most common findings in adults with new-onset focal seizures:",
" • Post-stroke/post-traumatic gliosis: ~50%",
" • Tumours (primary/metastatic): ~15%",
" • Vascular malformations: ~15%",
" • Developmental abnormalities (FCD, cortical dysplasia): ~15%",
" • Mesial temporal sclerosis: ~9%",
"FLAIR sequences – increased sensitivity for hippocampal sclerosis and focal cortical dysplasia.",
"PET (FDG-PET) – identifies hypometabolic seizure focus; used in pre-surgical workup.",
"SPECT (ictal > interictal) – blood flow imaging; ictal SPECT identifies hyperperfused seizure onset zone.",
"MEG (magnetoencephalography) – maps interictal discharges + eloquent cortex for surgical planning.",
]);
// ── SECTION 10: ASM TREATMENT ────────────────────────────────────
sectionSlide(10, "Treatment – Antiseizure Medications (ASMs)");
// SLIDE 30
bodySlide("General Principles of ASM Therapy", [
"Goal: complete seizure freedom with minimal adverse effects.",
"Monotherapy preferred — reduces adverse effects; adequate in ~2/3 of patients.",
"Choice depends on seizure type / epilepsy syndrome and patient factors.",
"Start low, titrate slowly to effective dose.",
"Pharmacoresistance: failure of ≥2 appropriate ASMs at adequate doses = drug-refractory epilepsy (affects ~30–40%).",
"Women of childbearing age: avoid valproate if possible due to teratogenicity (neural tube defects, cognitive effects on offspring).",
"Monitor for idiosyncratic reactions: rash (carbamazepine, lamotrigine — SJS), hepatotoxicity (valproate), aplastic anaemia (felbamate).",
"Drug interactions: enzyme-inducers (carbamazepine, phenytoin, phenobarb) reduce efficacy of OCP, anticoagulants, immunosuppressants.",
]);
// SLIDE 31
tableSlide("ASM Selection by Seizure Type",
["Seizure Type", "First-Line ASMs", "Alternative ASMs", "Avoid"],
[
["Generalised Tonic-Clonic", "Valproate, Levetiracetam, Lamotrigine", "Topiramate, Zonisamide", "Carbamazepine (worsens absence/myoclonus)"],
["Typical Absence", "Ethosuximide, Valproate, Lamotrigine", "Zonisamide, Clobazam", "Carbamazepine, Phenytoin, Gabapentin"],
["Myoclonic", "Valproate, Levetiracetam, Clonazepam", "Zonisamide, Topiramate", "Carbamazepine, Gabapentin, Pregabalin"],
["Focal (Aware/Impaired)", "Carbamazepine, Oxcarbazepine, Levetiracetam, Lamotrigine", "Lacosamide, Brivaracetam", "—"],
["Focal-to-Bilateral TC", "Carbamazepine, Levetiracetam, Lamotrigine", "Lacosamide, Eslicarbazepine", "—"],
["Lennox-Gastaut", "Valproate, Lamotrigine, Clobazam, Rufinamide", "Fenfluramine, Cannabidiol (CBD)", "Vigabatrin (worsens absence)"],
["Infantile Spasms (West)", "ACTH, Vigabatrin, Prednisolone", "Pyridoxine (if B6-dep.)", "—"],
],
{ colW: [2.0, 2.5, 2.5, 2.5], rowH: 0.44 }
);
// SLIDE 32
bodySlide("Mechanisms of Major ASMs", [
"SODIUM CHANNEL BLOCKERS (most common mechanism) – phenytoin, carbamazepine, oxcarbazepine, lamotrigine, lacosamide, eslicarbazepine → reduce sustained repetitive firing by prolonging Na⁺ channel inactivation.",
"CALCIUM CHANNEL MODIFIERS – ethosuximide, valproate → block T-type Ca²⁺ channels in thalamic neurons → suppress absence seizures.",
"GABA ENHANCEMENT – benzodiazepines (GABA_A Cl⁻ channel opening), phenobarbitone (GABA_A duration), vigabatrin (inhibits GABA transaminase → ↑ GABA), tiagabine (blocks GABA reuptake).",
"GLUTAMATE ANTAGONISM – perampanel (AMPA receptor antagonist) — first in class.",
"SV2A (Synaptic Vesicle Protein 2A) modulation – levetiracetam, brivaracetam → reduce presynaptic neurotransmitter release.",
"MULTIPLE MECHANISMS – valproate (Na⁺ block + T-Ca²⁺ block + ↑GABA), topiramate (Na⁺ + GABA + AMPA block + CA inhibition), zonisamide (Na⁺ + T-Ca²⁺).",
]);
// ── SECTION 11: NON-PHARM TREATMENT ─────────────────────────────
sectionSlide(11, "Treatment – Non-Pharmacological");
// SLIDE 34
bodySlide("Epilepsy Surgery", [
"Indicated in pharmacoresistant epilepsy (failed ≥2 ASMs) with identifiable seizure focus.",
"Pre-surgical evaluation: video-EEG, high-resolution MRI, neuropsychological testing, PET, MEG, Wada test (language/memory lateralisation).",
"TEMPORAL LOBE RESECTION – most commonly performed; ~60–70% seizure-free rate at 2 years; most effective for mesial temporal lobe epilepsy with hippocampal sclerosis.",
"EXTRATEMPORAL CORTICAL RESECTION – lower success rates; requires precise localisation.",
"LESIONECTOMY – resection of discrete lesion (tumour, cavernoma, FCD); potentially curative.",
"HEMISPHERECTOMY / HEMISPHEROTOMY – for severe unilateral hemisphere disease (Rasmussen's encephalitis, large perinatal stroke); best outcomes when done early.",
"CORPUS CALLOSOTOMY – palliative for drop attacks (atonic seizures); reduces spread between hemispheres.",
]);
// SLIDE 35
bodySlide("Neurostimulation & Dietary Therapies", [
"VAGUS NERVE STIMULATOR (VNS) – implanted pulse generator; helical electrode on left vagus nerve; open-loop stimulation; approved for drug-refractory focal seizures; ~50% achieve ≥50% seizure reduction.",
"RESPONSIVE NEUROSTIMULATOR (RNS) – closed-loop system; detects abnormal EEG pattern in seizure focus → delivers stimulation to prevent seizure.",
"DEEP BRAIN STIMULATION (DBS) – bilateral open-loop stimulation of anterior nuclei of thalamus; indicated as adjunctive therapy for focal seizures ± secondary generalisation.",
"KETOGENIC DIET – high fat, low carbohydrate, controlled protein; produces ketosis → anticonvulsant effects; particularly effective in children with refractory epilepsy; beneficial in specific metabolic epilepsies (GLUT1 deficiency, pyruvate dehydrogenase deficiency).",
"MODIFIED ATKINS DIET / LOW GLYCAEMIC INDEX DIET – less restrictive alternatives to classic ketogenic diet; comparable efficacy in some studies.",
"TRANSCRANIAL MAGNETIC STIMULATION (TMS) – investigational; may reduce cortical excitability at seizure focus.",
]);
// ── SECTION 12: STATUS EPILEPTICUS ───────────────────────────────
sectionSlide(12, "Status Epilepticus – Emergency Management");
// SLIDE 37 – emergency style
emergencySlide("Status Epilepticus – Recognition", [
"DEFINITION: GTC seizure ≥5 minutes OR focal/absence seizure ≥10 minutes OR repeated seizures without full recovery between.",
"TYPES:",
" 1. Generalised Convulsive SE – bilateral limb jerking + impaired consciousness; LIFE-THREATENING",
" 2. Nonconvulsive SE (NCSE) – behaviour change + continuous EEG epileptiform activity WITHOUT major motor signs",
" • Absence SE, Focal SE with/without impaired awareness",
" • NCSE in coma – often follows undertreated convulsive SE; requires EEG for diagnosis",
"RISKS OF DELAY: neuronal injury (glutamate excitotoxicity → hippocampal cell death), systemic complications (hyperthermia, acidosis, rhabdomyolysis), death",
"ECG and O₂ monitoring mandatory; establish IV access; check glucose",
]);
// SLIDE 38 – emergency style
emergencySlide("Status Epilepticus – Treatment Algorithm", [
"T = 0: Assess ABCs; O₂; IV access; bloods (glucose, electrolytes, drug levels, toxicology); ECG monitoring",
"T = 5 min — FIRST LINE (Benzodiazepines):",
" • IV Lorazepam 0.1 mg/kg (max 4 mg) — preferred",
" • IV Diazepam 0.15–0.2 mg/kg (max 10 mg) — alternative",
" • IM Midazolam 10 mg (>40 kg) or 5 mg (13–40 kg) — prehospital / no IV access",
" • Rectal diazepam / intranasal midazolam — if above unavailable",
"T = 20 min — SECOND LINE (if seizure continues): IV Levetiracetam 60 mg/kg (max 4500 mg) OR IV Valproate 40 mg/kg (max 3000 mg) OR IV Fosphenytoin 20 PE/kg (max 1500 PE) — equally effective",
"T = 40 min — REFRACTORY SE: ICU admission; anaesthetic infusions — Propofol OR Midazolam infusion OR Thiopental/Pentobarbital; continuous EEG monitoring required",
"SUPER-REFRACTORY SE (≥24h): consider ketamine, lacosamide, ketogenic diet, immunotherapy",
]);
// ── SECTION 13: SPECIAL POPULATIONS ─────────────────────────────
sectionSlide(13, "Special Populations");
// SLIDE 40
twoColSlide("Special Populations",
"Women with Epilepsy",
[
"Catamenial epilepsy: seizures cluster around menstruation (progesterone withdrawal)",
"Contraception: enzyme-inducing ASMs reduce OCP efficacy; use ≥50 µg EE pill or non-hormonal method",
"Pregnancy counselling BEFORE conception:",
"• Lowest effective ASM dose",
"• Avoid valproate (teratogen; 4–10× risk NTD; cognitive effects in child)",
"• Folic acid 5 mg/day pre-conception",
"• Lamotrigine / levetiracetam safest",
"• Seizure monitoring frequency ↑",
"Breastfeeding: generally permitted; most ASMs low excretion",
],
"Elderly & Paediatric",
[
"ELDERLY:",
"• Most common new epilepsy after stroke",
"• Drug interactions with polypharmacy",
"• Prefer levetiracetam, lamotrigine, gabapentin (better tolerated)",
"• Fall risk with sedating ASMs",
"PAEDIATRIC:",
"• Fever can lower seizure threshold",
"• Febrile seizures (6 mo – 6 yr): usually benign; prophylactic ASMs rarely needed",
"• Neonatal seizures: treat underlying cause (hypoglycaemia, hypocalcaemia) first",
"• Infantile spasms: ACTH or vigabatrin — early treatment critical",
]
);
// SLIDE 41
twoColSlide("Epilepsy & Driving / Psychosocial Issues",
"Driving",
[
"Most countries: seizure-free period required (6–12 months) before driving",
"Physician must counsel patients and document",
"Reporting obligations vary by jurisdiction",
"Commercial vehicle licensing has stricter rules",
"Breakthrough seizures while driving = significant mortality risk",
],
"Psychiatric & Social Comorbidities",
[
"Depression: 2–3× more prevalent in epilepsy than general population",
"Anxiety disorders: highly prevalent",
"Cognitive impairment: memory deficits common in TLE",
"Stigma: major barrier to treatment adherence globally",
"Employment: epilepsy affects career choices and job security",
"SUDEP risk: highest in nocturnal uncontrolled GTC; sleeping alone increases risk",
"Comprehensive epilepsy care includes neurologist + neuropsychologist + social worker",
]
);
// ── SECTION 14: PREVENTION ───────────────────────────────────────
sectionSlide(14, "Prevention & Seizure Triggers");
// SLIDE 43
twoColSlide("Seizure Triggers (Common)",
"Lifestyle Triggers",
[
"Sleep deprivation – most potent trigger; adequate sleep critical",
"Alcohol consumption / alcohol withdrawal",
"Recreational drug use (cocaine, amphetamines)",
"Missed ASM doses – most common preventable cause of breakthrough seizure",
"Physical or emotional stress",
"Fever / systemic illness",
"Menstrual cycle (catamenial epilepsy)",
"Flashing lights / visual patterns (photosensitive epilepsy – ~3% of epilepsy)",
"Overhydration / electrolyte disturbance",
],
"Medical / Pharmacological Triggers",
[
"Withdrawal of ASMs (abrupt)",
"Medications lowering seizure threshold:",
"• Antibiotics: fluoroquinolones, imipenem",
"• Antidepressants: bupropion, clomipramine",
"• Antipsychotics: clozapine, chlorpromazine",
"• Theophylline, tramadol, lithium toxicity",
"Drug–drug interactions reducing ASM levels",
"Hypoglycaemia, hyponatraemia, hypocalcaemia",
"Contrast agents (intrathecal – rare)",
]
);
// SLIDE 44
bodySlide("Primary & Secondary Prevention", [
"PRIMARY PREVENTION (preventing epilepsy from developing):",
" • Reduce head trauma: helmet laws, seatbelts, fall prevention in elderly",
" • Reduce CNS infections: vaccination (measles, H. influenzae, Neisseria meningitidis), anthelmintic campaigns (neurocysticercosis)",
" • Perinatal care: prevent hypoxic-ischaemic birth injury with skilled obstetric care",
" • Stroke prevention (hypertension, AF management, lipid control) — critical in elderly",
" • Avoid teratogenic exposure in utero (valproate in pregnancy)",
"SECONDARY PREVENTION (preventing seizure recurrence once epilepsy diagnosed):",
" • Adherence to ASMs — missed doses are #1 cause of breakthrough seizures",
" • Avoid known personal triggers (maintain diary)",
" • Regular adequate sleep; avoid sleep deprivation",
" • Abstain from alcohol / recreational drugs",
" • Wear medical alert bracelet; ensure caregivers know rescue medication protocol",
"TERTIARY PREVENTION (minimising disability):",
" • Access to epilepsy specialist care; surgical evaluation when pharmacoresistant",
" • Psychosocial support; driving safety counselling; vocational rehabilitation",
]);
// SLIDE 45
bodySlide("Patient & Caregiver Education – First Aid for Seizures", [
"STAY calm and stay with the person.",
"TIME the seizure — call emergency services if >5 minutes.",
"PROTECT from injury: clear area, cushion head, loosen tight clothing.",
"POSITION: place in recovery (lateral) position when convulsions stop — prevents aspiration.",
"DO NOT restrain movements or put anything in the mouth.",
"DO NOT give food or water until fully conscious.",
"RESCUE MEDICATION: administer prescribed rescue benzodiazepine (rectal diazepam, intranasal midazolam, buccal midazolam) if seizure ≥5 minutes.",
"AFTER seizure: stay until fully conscious; explain what happened; be supportive.",
"DOCUMENT: date, time, duration, nature of seizure; report to physician.",
]);
// ── SECTION 15: PROGNOSIS & SUDEP ───────────────────────────────
sectionSlide(15, "Prognosis & SUDEP");
// SLIDE 47
bodySlide("Prognosis of Epilepsy", [
"Overall: ~60–70% of patients achieve long-term seizure remission with appropriate treatment.",
"~2/3 of patients achieve seizure control with first or second appropriate ASM.",
"~30–40% are pharmacoresistant; surgical evaluation should be pursued early.",
"Favourable prognosis: idiopathic/genetic epilepsy (especially childhood onset), normal neurological exam, normal MRI, single seizure type.",
"Unfavourable prognosis: structural aetiology, abnormal MRI, early onset, multiple seizure types, intellectual disability.",
"Seizure remission after ASM withdrawal: ~60% remain seizure-free after slow taper if seizure-free ≥2 years and normal EEG/MRI.",
"Temporal lobe epilepsy surgery: ~60–70% seizure-free at 2 years vs <10% with continued medical management.",
]);
// SLIDE 48
bodySlide("SUDEP – Sudden Unexpected Death in Epilepsy", [
"DEFINITION: sudden, unexpected, witnessed or unwitnessed, non-traumatic and non-drowning death in epilepsy, with or without evidence of seizure.",
"INCIDENCE: ~1 per 1000 patient-years in adults; up to 1 per 150 in high-risk groups.",
"RISK FACTORS:",
" • Nocturnal generalised tonic-clonic seizures – strongest risk factor",
" • High seizure frequency (≥3 GTC/year)",
" • Sleeping alone (unable to intervene)",
" • Uncontrolled epilepsy; non-adherence to ASMs",
" • Male sex; early onset; duration of epilepsy >15 years",
"MECHANISM (incompletely understood): post-ictal autonomic dysfunction → cardiac arrhythmia (prolonged QT, bradycardia), central respiratory depression → asphyxia.",
"PREVENTION: optimise seizure control; nocturnal monitoring devices / mattress sensors; supervised sleeping; avoid prone sleeping position.",
]);
// SLIDE 49
bodySlide("Antiseizure Drug Reference Summary", [
"VALPROATE – broad spectrum; Na⁺ + T-Ca²⁺ + ↑GABA; avoid in women of childbearing age; monitor LFTs, platelets; pancreatitis, weight gain, tremor.",
"LAMOTRIGINE – broad spectrum; Na⁺ blocker; slow titration required (SJS risk); interacts with valproate; safe in pregnancy (relatively).",
"LEVETIRACETAM – broad spectrum; SV2A; well tolerated; IV form available; behavioural side effects (irritability, depression) notable.",
"CARBAMAZEPINE / OXCARBAZEPINE – focal epilepsy; Na⁺ blocker; enzyme inducer (carbamazepine); hyponatraemia with oxcarbazepine; avoid in generalised epilepsy.",
"ETHOSUXIMIDE – absence only; T-Ca²⁺ blocker; nausea; not effective for GTC.",
"PHENYTOIN / FOSPHENYTOIN – Na⁺ blocker; narrow therapeutic window; gingival hyperplasia, hirsutism, ataxia; zero-order kinetics (non-linear).",
"TOPIRAMATE – Na⁺ + AMPA + CA; cognitive side effects ('Dopamax'); kidney stones; weight loss; teratogenic.",
"LACOSAMIDE – Na⁺ (slow inactivation); focal seizures; PR prolongation; IV form.",
"PHENOBARBITONE – GABA_A; sedation; cognitive impairment; enzyme inducer; widely used in low-income settings.",
]);
// SLIDE 50 – Closing
closingSlide();
// ── WRITE FILE ───────────────────────────────────────────────────
pres.writeFile({ fileName: "/home/daytona/workspace/epilepsy-pptx/Epilepsy_Seizures_Comprehensive.pptx" })
.then(() => console.log("✅ PPTX saved successfully"))
.catch(e => { console.error("❌ Error:", e); process.exit(1); });
cd /home/daytona/workspace/epilepsy-pptx && node build.js 2>&1
ls -lh /home/daytona/workspace/epilepsy-pptx/Epilepsy_Seizures_Comprehensive.pptx
Epilepsy Seizures Comprehensive
Presentation · PPTX
| # | Section | Slides |
|---|---|---|
| 1 | Title & Outline | 1–2 |
| 2 | Definition & History | 3–5 (Hughlings Jackson, EEG history, terminology) |
| 3 | Epidemiology | 6–8 (global burden, age/sex distribution, bimodal incidence) |
| 4 | Aetiology & Risk Factors | 9–10 (structural, genetic, metabolic, immune, infectious) |
| 5 | Pathophysiology | 11–13 (PDS, ion channels, GABA/glutamate imbalance, hippocampal sclerosis, FCD) |
| 6 | ILAE 2017 Classification | 14–15 (full table: focal / generalised / unknown onset with old vs new terms) |
| 7 | Epilepsy Syndromes | 16–18 (West, Dravet, Childhood Absence, LGS, BECTS, JME, MTLE — with tables) |
| 8 | Clinical Features | 19–22 (GTC phase-by-phase, focal aware, absence, focal impaired awareness, myoclonic/atonic) |
| 9 | Differential Diagnosis | 23–24 (syncope, TIA, PNES, panic, migraine, metabolic) |
| 10 | Investigations | 25–28 (EEG patterns, MRI findings, genetic testing, MEG, PET/SPECT) |
| 11 | ASM Treatment | 29–32 (principles, selection by seizure type table, mechanisms) |
| 12 | Non-pharmacological Tx | 33–35 (surgery, VNS, RNS, DBS, ketogenic diet) |
| 13 | Status Epilepticus | 36–38 (recognition + emergency algorithm — red slide design) |
| 14 | Special Populations | 39–41 (women, elderly, paediatric, driving, psychosocial) |
| 15 | Prevention & Triggers | 42–45 (triggers, primary/secondary/tertiary prevention, first aid) |
| 16 | Prognosis & SUDEP | 46–48 (remission rates, surgery outcomes, SUDEP risk factors) |
| 17 | Drug Reference | 49 (valproate, lamotrigine, levetiracetam, carbamazepine, phenytoin, etc.) |
| 18 | Key Takeaways | 50 |