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epilepsy-131129104031-phpapp01 (1).pptx
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- 3. Seizure A suddenwave of synchronous electrical activity in brain that usually affects how a person feels or acts for a short time Some seizures can hardly be noticed, while others are totally disabling
- 4. Epilepsy A conditionthat affects central nervous system (CNS) had at least 2 seizures not caused by some known medical condition like alcohol withdrawal or extremely low blood sugar not indicate anything about the cause of the seizures, what type they are, or how severe they are
- 5. Momentary loss of consciousness Fit Faint Fake(False)
- 6. Transient loss ofconsciousness Déjà vu Jamais vu Aphasia Olfactory aura Epigastric sensation Tongue biting Post event delirium Focal neurodeficit Light-headedness Sweating Prolonged standing Precipitants eg.micturition Chest pain Palpitation Slow heart rate Low blood pressure History and Physical Witness account Aphasia Delirium Head turn Automatism Posturing Convulsion Postictal delirium Myoclonus or convulsion after pallor, sweating and collapse Pallor Sweating Slow pulse Low BP Syncope Seizure Convulsive syncope Syncope Seizure
- 7. Character Syncope Epilepticseizure Position usually upright any Time daytime day or nighttime Color pallor normal or cyanotic Aura dizziness, visual blurring possible specific aura Autonomic common uncommon Duration brief brief or prolonged Incontinence rare more common
- 8. Character Syncope Epilepticseizure Motor activity occasionally brief tonic seizure or clonic jerks variable Automatism none absence,CPS Disorientation, posictal rare can occur with GTC,CPS
- 9. Nonepileptic causes forspells Physiologic Tremor Vasovagal syncope Cardiac arrhythmias Migraine Medication adverse effects Transient ischemic attacks Autonomic dysfunction
- 10. Nonepileptic causes forspells Psychologic Anxiety Panic attacks Mood disorder Personality disorder Psychosis Somatiform illness Psychogenic seizures
- 11. Phase of seizures Preictal phase or aura or warning Ictal phase : simple or complex partial or generalized tonic-clonic seizure Postictal phase or recovery period : last from seconds to minutes to hours
- 12. Precipitants of seizure Sleep and lack of sleep Drugs and alcohol Intercurrent illness : infection, fever electrolyte imbalance Menstruation Stress and worry Other precipitants-reflex epilepsy
- 13. Classification of seizure Partial (focal, localized) seizures Generalized seizures (convulsive or non- convulsive) Unclassified epileptic seizures
- 14. Partial (focal, localized)seizures 1.Simple partial seizures (preserved consciousness) 2. Complex partial seizures (impaired consciousness) 3. Partial seizures evolving to secondarily generalized seizures
- 15. 1. Simple partialseizures (preserved consciousness) With - motor signs -somatosensory or special sensory systems - autonomic symptoms or signs - psychic symptoms
- 16. 2. Complex partialseizures (impaired consciousness) -Simple partial onset followed by impairment of conscious -With impairment of consciousness at onset
- 17. 3. Partial seizuresevolving to secondarily generalized seizures -Simple partial seizures evolving to generalized seizures -Complex partial seizures evolving to generalized seizures -Simple partial seizures evolving to complex partial seizures evolving to generalized seizures
- 18. Generalized seizures (convulsive ornonconvulsive) - Absence seizures Typical absences Atypical absences - Myoclonic seizures - Clonic seizures - Tonic seizures - Tonic-clonic seizures - Atonic seizures (astatic seizures)
- 19. Unclassified epileptic seizures -Neonatal seizures - Recurrent status epilepticus - Rare or ‘isolated’ seizures
- 20. Epileptic seizure Seizure type (s) Etiology Allclinical a laboratory neuroimagi Seizure description and EEG
- 21. Seizure Idiopathic Generalized epilepsy likely Features of focal epilepsy Epilepsy orPNES Provoked seizures EEG EEG MRI/CT brain Video EEG Treat cause +/-AED PNES=psychogenic non-epileptic seizures AED=antiepileptic drug
- 22. Laboratory investigation Mg+2 CBC FBS, BUN,Creatinine Electrolyte , Liver function test , Ca+2 Electro-encephalography (EEG) Video EEG Neuroimaging : CT Scan, MRI, MR Spect, PET Special investigation : ammonia, lactate, pyruvate etc.
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- 24. What value isthe EEG? Add weight to the clinical diagnosis Aid classification of epilepsy Detection of the structural brain lesion.
- 25. EEG 30 minuteinterictal EEG –useful when clinical suspicion of epilepsy Timing is important Within 24 hr of generalized convulsion: 50% have abnormal EEG First 48 hr: 21-34% have epileptiform activity Sleep EEG or sleep-deprived EEG might increase diagnostic yield
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- 29. Burst of generalizedspike and wave discharges—typical absence seizure
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- 31. Video Monitoring Helpfulin determining nature of seizure disorder (epilepsy, convulsive syncope, or psychogenic seizures)
- 32. Indication for neuroimagingin patients with seizures Partial seizure Late onset unprovoked seizure (age > 25) Unexplained neurological signs Focal slow waves EEG poor control or new symptoms / signs
- 33. Neuroimaging In theabsence of trauma: CT and MRI brain for patients presenting with suspected first unprovoked seizure or with a focal neurological deficit. MRI is preferable for looking for neuronal migrational disorders, major malformations, vascular anomalies, tumors
- 34. The causes ofepilepsy Genetic factor Congenital abnormalities Trauma and the effect of craniotomy CNS infection Cerebrovascular disease Cerebral tumors Alzheimer’s disease and other degenerative disease Others
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- 38. Brain tumor ormetastasis
- 39. Lt mesial temporalsclerosis
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- 41. 52 year oldwoman with intractable seizure PET scan
- 42. PET using F-18FDG-- Decreased FDG uptake in both temporal lobes, right worse then left but otherwise relatively symmetric
- 43. What to do? Generalized seizure Loosening the patient’s clothing Lower the patient gently to the floor, turn them onto their side and cushion head Nothing is put into the mouth Remove any items that could cause injury
- 44. What to do?---Generalized seizure When the seizure is over, allow the patient to rest or sleep If they are able to return to their feet, help them home Obtain medical help if they continue to experience breathing problems once the seizure is over, or if the seizure lasts a long time(over 10 mins), or when another attack quickly follows the first
- 45. What to do? Partial seizures Stay with the patients throughout the seizure Protect them from any dangerous object Taking care not to restrain them in anyway
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- 49. Choose a drug: considering the following factors The seizure type and prognosis Age The possibility of pregnancy Toxicity Drug interaction
- 50. The recurrencerisk follow a first unprovoked seizure 50 recurrence occur within 3 months Over 10 within 2 years of initial seizures twice as likely to have another seizure if you have a known brain injury or brain abnormality RISK OF RECURRENT SEIZURE
- 51. RISK OF RECURRENTSEIZURE (cont) If you do have two seizures, there's about 80% chance that you'll have more
- 52. Factors predictive ofa high rate of seizure recurrence after the first unprovoked seizure Abnormal neurologic status by NE or imaging EEG abnormalities (especially epileptiform) Partial seizures
- 53. Counseling before treatment 1.Aims of treatment 2. Prognosis and duration of the expected treatment 3. Importance of compliance 4. Side effects
- 54. Starting antiepileptic treatment Prospective risksUsual clinical Factors that may modify of epilepsy practice usual practice Single seizure No treatment Progressive cerebral disorder Clearly epileptic EEG 2 or more seizure widely separated precipitating, Monotherapy Seizures in time (> 1 year) Identified factors eg, drugs, alcohol,reflex stimuli)
- 55. Antiepileptic Drug Development 18401860 1880 1900 1960 1980 2000 5 10 15 20 Bromide 0 Phenobarbital Phenytoin Primidone Ethosuximide Zonisamide SodiumV alproate Lamotrigine Vigabatrin Carbamazepine Benzodiazepines Tiagabine T opiramate Felbamate Levetiracetam More 1920 1940 Calendar year Antiepileptic drugs Pregabalin Oxcarbazepine Fosphenytoin Gabapentin
- 56. First-line choice ofAEDs according to seizure type Seizure type First line Absence (typical and VPA, LTG atypical) Myoclonic VPA Tonic-clonic VPA, CBZ, PHT, PB Atonic VPA Simple and complex partial, with or without secondary generalization CBZ, PHT, PB,OXC,LTG,TPM, GBP Unclassifiable VPA
- 57. Advantages of Monotherapy Better seizure control Reduced side effects Absence of drug interactions Reduced teratogenic effects Better compliance Reduced cost of medication Improved quality of life
- 58. Expected outcomes ofAED therapy Well controlled 65% Unsatisfactorily controlled 35% Well controlled 10% Unsatisfactorily controlled 25% Well controlled 5% Unsatisfactorily controlled 20% Monotherapy Add-on therapy Multiple drug therapy
- 59. Managing newly diagnosed epilepsy Newlydiagnosed epilepsy Seizure free First drug Second drug Refractory Surgical assessment Rational duotherapy Seizure free 47% 13%
- 60. Adverse effect ofAED Dose related Idiosyncratic / allergic Chronic toxicity Teratogenicity
- 61. Older AEDs Drugs Sideeffects CBZ Tegretol Diplopia, headache, dizziness, N/V, rash, mild leukopenia, mild hyponatremia PHT Ataxia,nystagmus, dysarthria, somnolence,gingival hyperplasia, hirsutism, acne, facial coarsening, folate, deficiency, osteopenia, peripheral neuropathy, cerebellar atropy VPA Dose-related tremor, weight gain,loss of hair, menstrual irregularities, PCOS, stupor and encephalopathy(rare), hepatotoxicity PB Somnilleta Sedation and behavioral problem(depression, agitation, hyperactivity) CZP clonezipzm revotril Sedation, ataxia, behavioral changes(depression)
- 62. AED interactions CBZ: autoinduction, VPA, PHT, -PB PHT : PB : VPA : CBZ, VPA, PB CBZ, VPA, PHT CBZ, PB, PHT
- 63. AEDs Drug interactionwith AED and other drugs: via effect on hepatic CYP450 enzyme system PB, primidone, PHT, CBZ induce CYP enz. : Accelerate breakdown of many prescribed lipid-soluble drugs metabolized by the same system: OCP, cytotoxic, antiarrythmic, warfarin VPA is a weak CYP enz. Inhibitor: Slow clearance of other AEDs such as PHT, LTG. Newer AEDs : less likely to interfere with hepatic metabolism. GBP, LEV,PGB,VGB do not undergo hepatic metabolism
- 64. Newer AEDs Adjunctivetreatment of refractory epilepsy Some of these AEDs: LTG, GBP, OXC, TPM have also demonstrated efficacy as monotherapy
- 65. Effects of phenytoinlevels Level (mg/ml) Effect 0-10 10-20 20-30 30-40 > 40 Subtherapeutic Therapeutic Mild toxicity; nystagmus, mild ataxia Moderate toxicity ; ataxia prominent Severe toxicity; ataxia, conscious - ness, encephalopathy
- 66. Potential Causes ofTreatment Resistant Epilepsy Diagnostic errors: Non-epileptic events Wrong diagnosis of seizure types epileptic syndrome Missing of underlying causes lesions Patient’s errors: Non-compliance Inappropriate life style, inappropriate metabolism
- 67. Potential Causes ofTreatment Resistant Epilepsy Treatment errors: Wrong choice of drugs Less optimal doses of drugs Inadequate dosing schedules Antiepileptic drug toxicity Disease itself: Treatment resistant epilepsy metabolic disorder
- 68. Absolute requirement - years freeof all seizures Stopping antiepileptic treatment
- 69. Factors in favour Childhood epilepsy Primary generalized epilepsy Absence of cerebral disorder Short duration of epilepsy Normal EEG
- 70. Adverse prognostic factors Symptomaticetiology, identifiable brain pathology Partial-onset seizures or Atonic seizures Late-onset or first-year epilepsy Specific epilepsy syndrome (particularly JME) Abnormal EEGs Multiple seizure types in the same patient Additional mental or motor handicap Long duration or severe epilepsy prior to treatment Poor initial response to treatment
- 71. Features common tothe surgically privileged seizure disorders Presence of a well-circumscribed structural lesion on the MRI (lesional epilepsy) Presence of well-localized interictal epileptiform discharged on the EEG Clinical features of habitual seizures indicating focal onset Absence of discordance between above feature Focus localized by above features is surgically accessible and involves little or no eloquent cortex Absence of other potentially epileptogenic abnormalities
- 72. Status epilepticus A conditionin which epileptic activity persists for 30 minutes or more
- 73. Common etiologies forstatus epilepticus in children and adolescents Idiopathic Acute symptomatic Electrolyte disturbance Encephalitis Head trauma Remote symptomatic Past stroke CNS infection Cerebral palsy Progressive encephalopathy Tuberous sclerosis Other neurodegeneration Febrile
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- 77. Epilepsy and pregnancy Seizurecontrol Obstetric complication Neonatal outcome
- 78. Neonatal outcome Riskof seizure (3 times > normal population) developmental outcome congenital anomalies 4-8% (2-3 times > normal population)
- 79. The most commonmalformation Congenital heart disease orofacial cleft neural tube defect intestinal atresia urogenital defects Neural tube defect
- 80. Fetal antiepileptic drug syndrome(minor anomalies) Facial dysmorphism Distal digital hypoplasia Developmental delay Mental deficiency
- 81. Factors affecting neonataloutcome AED genetics folic acid socioeconomic maternal health
- 82. Recommendations for managingWomen With Epilepsy Before Conception Educate the family regarding risks Review classification of epilepsy Determine most appropriate medicine for seizure control
- 83. Determine needfor continued medication -may discontinue if seizure-free for 2 or more years -do not discontinue medication if epilepsy syndrome suggests continued need for treatment Reduce medicines to monotherapy, lowest dose possible Start folic acid 1 mg/day Eliminate other risk factors – smoking, drugs, alcohol
- 84. After conception Donot change antiepileptic medication Refer for prenatal care Prescribe vitamins, including folic acid Check ‘free’ drug levels every trimester and change doses as needed Evaluate for neural tube defects at 12 to 16 weeks (ultrasound, alpha-fetoprotein, amniocentesis)
- 85. Consider vitaminK predelivery Check antiepileptic drug levels prior to delivery and increase doses if needed
- 86. After Delivery Checklevels Examine infant
- 87.