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Epilepsy
This document provides an overview of epilepsy, including its pathogenesis, clinical features, diagnostic approach, and management. It discusses how epilepsy results from an imbalance between excitation and inhibition in the central nervous system. Seizures occur due to factors that lower the seizure threshold or precipitate an attack. Diagnosis involves obtaining a medical history, clinical examination, and tests like EEG and imaging. Treatment primarily involves antiepileptic drugs to control seizures, though surgery may be an option for refractory cases. Proper management of epilepsy requires long-term medical treatment as well as attention to any psychiatric comorbidities.
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Epilepsy
- 1. EPILEPSY Presented by: Post graduatestudents Course: MD Phase A (Psychiatry) BSMMU, Dhaka 18/8/2013 1
- 2. Contents • Introduction • Pathogenesis •Clinical features & Diagnostic approach • Management • Interphase & Summary 2
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- 4. Past • Oldest recordSakikKu -babilonian medcal text 1067 B.C • Aurvedic description as “Apasmara” 400 B.C • “epilambanein” to be overwhelmed by surprise • Falling sickness • Demonic possession 4
- 5. Past • “its causelies in the brain” • 1920- Human EEG (Hans Berger) 5
- 6. Basics Seizure: • Any clinicalevent • Abnormal brain discharge 6
- 7. Basics Epilepsy : • Recurrence •Seizure attack Pseudo seizure/PNES: • Resemblance • Psychology • No abnormal brain discharge 7
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- 9. Basics SEIZURE PSEUDO SEIZURE SYNCOPE • Sudden •Unconscious • Cyanosis • Injury • Sec to mints • Hand on face • Post ictal confusion • EEG,CPK, Prolactin • Gradual • Conscious • Thrusting • Mins to hr • Eye opening • Pupil- Normal • Psycho social • Suggestive • Light headedness • Standing • Preventive- lying • Brief- lost consciousness 9
- 10. Current scenario • 60million people worldwide • 85% people-inadequate/not at all • Specialist care: LIC- 56%, HIC-89% • AEDs: Govt priority, high cost , PB 10
- 11. Current scenario • Age:any age (childhood, old age) • Prevalence: Single episode - 5% Repeated- 0.5 to 2.5% Our country- 2% Developing country- 5 times higher 11
- 12. Classification FOCAL (Partial) GENERALIZED Unclassified-MAY BE Focal/Generalized/ Unclear (Complex) With Dyscognitive features (Simple) Without Dyscognitive features Absence Tonic Clonic Atonic Myoclonic Epilepticspasms Febrile convulsion Infeantile spasm Lennox-Gastaut Sydrome • Motor • Sensory • Versive • Visual 12
- 13. Cause • Family history 5to 10% of all epilepsies Usually- 10 GTCS, Febrile convulsion, Absence, Juvenile myoclonic epilepsy • Primary generalized- 75% idiopathic • Partial & 20 generalized- definite cause 75% adult 13
- 14. Cause Neonates <1 month Infants < 12years Adolescents 12-18 years Young adult 18-35 years Older >35 years Perinatal hypoxia and ischemia ICH Ca++ , Glucose Bilirubin Water intoxication Inborn error of metabolism Trauma Febrile seizures CNS infection Trauma Developmental disorder Inborn error of metabolism Trauma CNS infection AVM Infection Congenital defect Tumors Trauma CNS infection Brain tumor AVM Drugs and alcohol Drugs and alcohol Trauma Tumor CVD Degenerative CNS infection 14
- 15. Cause GROUP Names ALKYLATING AGENTSBusulfan, Chlorambucil ANTIMALARIALS Chloroquine, mefloquine ANTIMICROBIAL Beta lactam , Quinolones, Acyclovir, Isoniazid, Ganciclovir ANESTHETICS, ANALGESICS Meperidine, Tramadol, Local anaesthetics DIETARY SUPPLEMENTS Gingko, Ephedra IMMUNOMODULATORY DRUGS Cyclosporine, Tacrolimus, Interferron PSYCHOTROPICS Antidepressants, Antipsychotics, Lithium CONTRAST AGENTS Theophylline SEDATIVE , HYPNOTIC (WITHDRAWL) BZD, Barbiturates, Alcohol 15
- 16. What happens inside? DrMd Saleh Uddin 16
- 17. Why & How? •Shift of balance: Excitation & Inhibition(CNS) 17
- 18. Why & How? •Endogenous factor Neuronal propensity to burst Intrinsic : conductance to ion channel, receptor response, second messenger, translation etc. Extrinsic : neuro transmitter, receptor, temporal /spatial property 18
- 19. Why & How? •Epileptogenesis Transformation - normal to hyper excitable(structural change) Lowered seizure threshold Lost inhibition Sprouting of surviving neurons 19
- 20. Why & How? •Precipitating factor Sleep deprivation Alcohol Recreational drug misuse Physical and mental exhaustion Flickering lights Intercurrent infections and metabolic disturbance 20
- 21. What & How? Seizureinitiation and propagation • Initiation: Bursts of action potential Hyper synchronization • Propagation: Extracellular K+ Presynaptic Ca2+ Cortical connections & Commissural fibers 21
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- 25. Clinical features & Diagnosticapproach Dr Hosnea Ara 25
- 26. GTCS/Grand mal • Prodrome •Aura • Tonic phase • Clonic phase • Relaxation • Post ictal phase 26
- 27. Absence Seizure • Petitmal • Childhood • Frequency • Stops doing, vacant stares • Hyperventilation • No post ictal symptoms • EEG diagnostic 27
- 28. Complex partial seizure •Temporal lobe/psychomotor epilepsy • Never fall • Mood ,memory, perception • Features : 28
- 29. Atonic seizure • Briefloss of muscle tone • Heavy fall • Consciousness 29
- 30. Simple partial • Motor •Sensory • Versive • Visual 30
- 31. Diagnostic approach • History •Clinical exam • Lab enquiry • Differentials 31
- 32. Diagnostic approach • HISTORY Agegroup Past history of illness Personal history Triggering factors Eye witness description 32
- 33. Diagnostic approach • CLINICALEXAM General survey Vital signs Cyanosis, Jaundice Tongue bite mark Systemic exam Neurological, CVS, HBS, Resp System 33
- 34. Diagnostic approach • LABINQUIRY Hematology Biochemistry Serology CSF, Hormone, ECG Imaging • Late in onset • Partial / 2o generalized • Refractory to drug • Focal neuro deficit • Status epilepticus • Suspected ICSOL • EEG shows focal seizure MRI/CT brain Indication 34
- 35. Diagnostic approach • LABENQUIRY EEG Type of epilepsy Drug choice Advanced lab test Sphenoidal intra operative oval and telemetric EEG Ambulatory EEG, Videotelemetry PET, SPET 35
- 36. Diagnostic approach • DIFFERENTIALS Syncope TIA Migraine Dropattack Panic attack Hypoglycemia Cataplexy/Narcolepsy Pseudoseizure Cardiac arrhythmia Episodic confusion 36
- 37. Management Dr Mahjabeen AftabSolaiman 37
- 38. Management • Immediate care •Medical treatment • Pregnancy • Status epilepticus • Surgical treatment 38
- 39. Management • Immediate Care: FirstAid Move Semi prone Airway Don’t insert Immediately Patency of airway O2, IV diazepam, blood 39
- 40. Management • Medical treatment AEDs: Carbamazepine Na valproate Phenytoin Phenobarbitone 40
- 41. Management • Indication AEDs: Singleseizure( lesion , EEG, family history) Unprovoked seizure Adult- > 1 Child- > 2 41
- 42. Management • AEDs- Single drug, Low dose, Compliance Switching 3rd drug prior combination Two drugs at a time Resistant to drug- metabolic/structural 42
- 43. Type First lineSecond line Third line Partial / Secondary GTCS Carbamazepine Lamotrigine Na Valproate Topiramaate Tigabine Gabapentin Clobazam Phenytoin Primidone Phenobarbital Oxcarbazepine Levetiracetam Vigabatrin Acetazoalmide Primary GTCS Na Valproate Lamotrigine Topiramate Carbamazepine Phenytoin Gabapentin Primidone Phenobarbital Tigabine Acetazolamide Absence Ethosuximide Na Valproate Lamotirizine Clonazepam Acetazolamide Myoclonic Na Valproate Clonazepam Piracetam Lamotrizine Phenobarbital 43
- 44. Management AEDs withdrawal : Control2 to 4 years Gradually, 6-12 months Prognosis: Primary generalized Absence-Best Others- Recurrence 44
- 45. Management Pregnancy • AEDs: Enzyme inducer Congenitalabnormalities(First trimester) Number & risk % • Folic acid supplement • Partial seizure-little risk • Vit K supplement 45
- 46. Management • Status epilepticus Seriesof seizures Without regaining awareness 30 minutes Management: General Pharmacological 46
- 47. Surgical treatment: • 20-30%patients • Localization (video EEG, MRI, SPET,PET, Cortical mapping at surgery) • Temporal lobectomy • Hemispherectomy • Corpus callosotomy • VNS 47
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- 50. Interphase • Psychiatric disordersin epilepsy 50% patient with epilepsy. Ictal, peri-ictal , inter ictal (depression) • Treatment related psychiatric problem Depression, psychosis etc AEDs (PB, Vigabatrin etc) “Forced normalization” 50
- 51. Summary 51 History, Exam, Exclusion D/D Historyof Epilepsy Adequacy Sub therapeutic Level Increase the dose Therapeutic Level Max dose, Alternative drug Lab features (biochemistry hematology) Positive Treat the cause No History of epilepsy Lab features (Biochemistry, Hematology) Positive Further work up Drug Normal Imaging Treat cause Drug Idiopathic Drug
- 52. References • Davidson’s principal& practice of Medicine, 21st edition, elsevier publisher, 2012 • Harrison’s Principales of internal medicine, 18th edition. • Lecture Notes-Prof AKM Anwarullah • Epilepsia, 44(suppl 6): 12-143. 2003, Blackwell publishing Inc, ILAE • History of epilepsy 1909-2009: The ILAE century • Recognition of psychogenic non epileptic seizure: acurable neurophobia, S S O Sallivan et al, Journal of Neurosurg Psychiatry, 2013, 84: 228-231 • Why do some brain seize? Molecular ,cellular and network mechanism, Andrew Trevelyan, Jphysiol(editorial)591.4(2013) 751-752 • The treatment gap in epilepsy, A Neliga, J W Sander, Epileptology 1 (2013) 28-30 52
- 53. “The sadness willlast forever” (Vincent van Gogh) 53 Wheat field with crows (1890)
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