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Week 24 – Tony Bates

Epilepsy. Week 24 – Tony Bates. Defined . Seizure: a paroxysmal event due to abnormal, excessive, hypersynchronous discharges from an aggregate of CNS neurons Epilepsy: A condition involving recurrent seizures due to a chronic, underlying process Prevalence: 5-10/1000.

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Week 24 – Tony Bates

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  1. Epilepsy Week 24 – Tony Bates

  2. Defined Seizure: a paroxysmal event due to abnormal, excessive, hypersynchronous discharges from an aggregate of CNS neurons Epilepsy: A condition involving recurrent seizures due to a chronic, underlying process Prevalence: 5-10/1000

  3. Classification

  4. Partial Seizures • Restricted to discrete areas of cerebral cortex Simple Partial Seizure: Consciousness: fully preserved Duration: usually <1min, can last hours or days - epilepsiapartialiscontinua Clinical Features: motor, sensory, autonomic or psychic sxs Jacksonian March: spread of seizure activity over a progressively larger area of cerebral cortex

  5. Partial Seizures Complex Partial Seizure: Consciousness: Unable to respond to commands, impaired recollection of ictal phase Duration: 30s-3min Clinical Features: Often begin with aura, then behavioural arrest/motionless stare, automatisms. Post-ictal: confusion, anterograde amnesia, aphasia EEG: May be normal or brief epileptiform spikes

  6. Partial Seizures Partial Seizure with Secondary Generalisation: • Usually of the tonic-clonic type • Frequently follows simple partial seizures, especially those originating in frontal lobe • May be difficult to differentiate from primary generalised seizure

  7. Generalised Seizures • Arise from both hemispheres simultaneously Absence Seizures: • Main type in 15-20% of children with epilepsy • May be provoked by hyperventilation Consciousness: Sudden, brief lapse Duration: a few seconds Clinical Features: none or rapid eye blinking, chewing, small frequency clonic hand movements EEG: sudden, generalised, symmetric, 3Hz spike

  8. Generalised Seizures Tonic-Clonic Seizures: • Main seizure in 10% of epileptic patients • Most common seizure due to metabolic derangements Tonic Phase: 10-20sec, tonic contraction of muscles, expiration -> loud moan, respiration impaired -> cyanosis, ↑ sympathetic tone Clonic Phase: 30-60sec, periods of muscle relaxation on muscle contraction Postictal Phase: Mins-hours, unresponsive, flaccid, ↑ salivation, bladder or bowel incontinence Once conscious: Headache, Fatigue, Muscle ache

  9. Generalised Seizures Atonic Seizures: Consciousness: Briefly impaired, no post-ictal confusion Duration: 1-2sec Clinical Features: sudden loss of postural muscle tone EEG: brief, generalized spike-and-wave discharges followed immediately by diffuse slow waves that correlate with the loss of muscle tone

  10. Generalised Seizures MyoclonicSeizures: • Most commonly seen due to metabolic disorders, degenerative CNS diseases, or anoxic brain injury • Usually coexist with other generalised seizure disorders Consciousness: Fully preserved Duration: 1-2sec Clinical Features: Sudden, brief muscle contraction EEG: bilaterally synchronous spike-and-wave discharges synchronized with the myoclonus

  11. Unclassified Seizures • Don’t fit partial or generalised classification • Usually occur in neonates or infants • Unclassified likely due to differences in neuronal function and connectivity in the immature CNS

  12. Epilepsy Syndromes Juvenile Myoclonic Epilepsy: • Single or repetitive, bilateral, myoclonic jerks • Most frequent in morning or sleep deprivation • Polygenic inheritance Lennox-GastautSyndrome: • Multiple seizure types • EEG shows slow spike and wave discharges • Usually impaired cognitive function Mesial Temporal Lobe Epilepsy Syndrome: • Most common syndrome associated with complex partial seizures • Responds well to surgical Tx but not anticonvulsants

  13. Mechanisms • Remodeling/loss of neurons, CNS development, genetic mutations in ion channel function, metabolic disturbance Initiation Phase: • High frequency bursts of APs – due to long depolarisation • Hypersynchronisation Propagation Phase: • Recruitment of surrounding neurons and/or loss of inhibitory neurons

  14. Etiology and Ix Epileptogenic Factors: Trauma, surgery, stroke, infection/inflammation, neural degenerative disorders, intracranial mass, abnormal CNS development Precipitating Factors: Psychological/physical stress, sleep deprivation, hormonal changes, drugs/alcohol, photosensitivity, metabolic abnormalities hypocalcaemia, hypoglycaemia, hyponatraemia, uraemia, acute hypoxia Investigations: FBC, U & E, LFT, BSL, Ca²⁺, Magnesium, INR, PTT, toxicology screens, CT/MRI, EEG

  15. Medications Na⁺ Channel Inhibitors: use-dependent VG Na⁺ channel inhibition Phenytoin, Carbamazepine, Valproate, Lamotrigine Ca²⁺ Channel Inhibitors: Gabapentin, Phenytoin, Ethosuximide ↑ GABA Action: Barbituates, Benzos, Valproate, Gabapentin, Vigabatrin Phenytoin:SEs = vertigo, ataxia, headache, nystagmus, hirsutism, gum hyperplasia Carbamazepine:SEs = drowsiness, dizziness, ataxia, blurred vision, water retention, neutropenia (rare) Valproate:SEs = thinning/curling of hair, transient GI effects, hepatotoxicity, teratogenic (spina bifida) Benzodiazepines:used for status epilepticus, too sedative for maintenance use

  16. Medications First Line Treatment:

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