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Childhood seizure and its management

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Childhood seizure and its management

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Childhood seizure and its management

  1. 1. CHILDHOOD SEIZURE AND ITS MANAGEMENT Dr. TAUHID IQBALI MBBS (JIPMER) MD PEAD Jr.II ( PMCH Patna )
  2. 2. Learning Objectives Define what we mean by seizures and related terminology Understand the different types of seizures Understand the pathophysiology of seizures Understand AED mechanism of actions and common side effects Approach to the child with a suspected seizure disorder Know the emergency and long term management of seizure
  3. 3. SEIZURE WHAT IS IT? A Seizure is a transient occurrence of signs and/or symptoms resulting from abnormal excessive or synchronous neuronal activity in the brain.
  4. 4. RELATED TERMINOLOGIES Symptomatic epilepsy Epilepsy is called ‘symptomatic’ when it has a known cause • Acute symptomatic seizure • Remote symptomatic seizure Idiopathic epilepsy Epilepsy is called ‘idiopathic’ when it is thought to be due to a genetic tendency (which could have been inherited from one or both parents) or due to a change that happens in the person's genes before they are born. Cryptogenic epilepsy( presumed symptomatic epilepsy) This is when the cause for a person's epilepsy has not yet been found, despite investigations but there is presumed underlying brain disorder. Epilepsy ≥ 2 unprovoked seizures occur in a time frame of > 24 hr secondary to a distant brain injury such as a old stroke. secondary to an acute problem affecting brain excitability such as electrolyte imbalance or meningitis etc. Brain disorder with an enduring predisposition to generate epileptic seizure
  5. 5. RELATED TERMINOLOGIES Epileptic encephalopathy Epilepsy syndrome in which the severe EEG abnormality is thought to result in cognitive and other impairments in the patient. Febrile seizure • Seizures that occur between the age of 6 and 60 months • With a temperature of 38 ° C or higher • That are not the result of central nervous system infection or any metabolic imbalance • And that occur in the absence of a history of prior afebrile seizures Status Epilepticus Two or more seizures without recovery of consciousness in between Single seizure >30 min (operationally >5 min) Epileptic syndrome Seizure disorder that manifests one or more specific seizure types and has a specific age of onset and a specific prognosis
  6. 6. SEIZURE- PATHOPHYSIOLOGY PATHOPHYSIOLOGY OF GENESIS OF SEIZURES CONSIST OF CONSIST OF: - 4 DISTINCT - OFTEN SEQUENTIAL( But not always) AND THESE ARE: 1. UNDERLYING ETIOLOGY 2. EPILEPTOGENESIS 3. PDS AFTERHYPERPOLARIZATION DISRUPTION 4. SEIZURE RELATED NEURONAL INJURY MECHANISTIC PROCESS
  7. 7. SEIZURE- PATHOPHYSIOLOGY UNDERLYING ETIOLOGY (ANY PROCESS THAT CAN DISRUPT NEURONAL FUNCTION AND CONNECTIVITY) LEADS TO PROCESS OF MAKING THE BRAIN EPILEPTIC EPILEPTOGENESIS (MECHANISM DURING WHICH BRAIN TURNS EPILEPTIC) PDS AFTERHYPERPOLARIZATION DISRUPTION LEADS TO SEIZURE FOCUS SEIZURE SEIZURE RELATED NEURONAL INJURY APOPTOSIS AND NECROSIS OF NEURONS FURTHER SEIZURE
  8. 8. SEIZURE- PATHOPHYSIOLOGY MECHANISM OF EPILEPTOGENESIS REPETATIVE STIMULATION ACTIVATES METABOTROPIC AND IONOTROPIC GLUTAMATE RECEPTORS AS WELL TrKB AND NT-4 RECEPTORS INCREASES INTRANEURAL CALCIUM ACTIVATES CaMKII AND CALCINEURIN Ca DEPENDENT EPILEPTOGENIC GENE EXPRESSION (eg c-fos) PROMOTE MOSSY FIBRE SPROUTING INCREASED EXCITABILITY EXCITATORY INTERNEURON INHIBITORY INTERNEURON NO SEIZURE
  9. 9. SEIZURE- PATHOPHYSIOLOGY PDS (PAROXYSMAL DEPOLARIZATION SHIFT) STEREOTYPIC SYNCHRONIZED RESPONSE OF EACH NEURON IN A SEIZURE FOCUS IT CONSIST OF : • DEPOLARIZATION PHASE • AFTERHYPERPOLARIZATION PHASE DEPOLARIZATION PHASE IT OCCUR DUE TO GLUTAMATE AND CALCIUM CHANNEL ACTIVATION RESULTING IN SERIES OF ACTION POTENTIALS AFTERHYPERPOLARIZATION PHASE IT OCCUR DUE TO ACTIVATION OF POTASSIUM CHANNELS AND GABA RECEPTORS RESULTING IN INHIBITION OF ACTION POTENTIALS SO WHEN PDS AFTERHYPERPOLARIZATION IS DISRUPTED, THE INHIBITORY SURROUND IS LOST AND THE NEURONS FIRES CONTINIOUSLY RESULTING IN SEIZURE FOCUS
  10. 10. Types of seizures Absence Myoclonic Tonic-Clonic Tonic Atonic Partial Generalised Seizures Simple Complex specific area in one cerebral hemisphere both cerebral hemispheres no loss of conciousness conciousness impaired Secondary generalized seizure
  11. 11. GENERALIZED SEIZURE
  12. 12. GENERALIZED SEIZURE TONIC-CLONIC SEIZURE
  13. 13. GENERALIZED SEIZURE CLONIC SEIZURE Repetitive jerking movements
  14. 14. GENERALIZED SEIZURE TONIC SEIZURE Muscle stiffness Rigidity
  15. 15. GENERALIZED SEIZURE ATONIC SEIZURE The ictal phenomenon in these seizures is a sudden generalized loss of tone. This may manifest as a head drop or if the patient is standing as a forward fall
  16. 16. GENERALIZED SEIZURE MYOCLONIC SEIZURE These are brief jerks of the extremities and/or axial trunk muscles
  17. 17. GENERALIZED SEIZURE ABSENCE SEIZURE Typical • Behavioral and mental arrest for a few seconds • The patient typically resumes their activity as if nothing had happened Atypical • Behavioral arrest may be longer • More difficult to ascertain the arrest as such, compared to the patient’s behavior at baseline
  18. 18. PARTIAL SEIZURE
  19. 19. ANTIEPILEPTIC DRUGS
  20. 20. Old drugs (Before 1993) Carbamazepine Clonazepam Ethosuximide Phenobarbital Phenytoin Primidone Valproic acid New drugs (Since 1993) Felbamate Gabapentin Lamotrigine Levetiracetam Lacosamide Oxcarbazepine Pregabalin Tiagabine Topiramate Vigabatrine Zonisamide Ezogabine Rufinamide Eslicarbazepine
  21. 21. Mechanism of Action of AED Seizure!!! Control EPSPs Na+ Influx Ca++ Currents Paroxysmal Depolarization IPSPs K+ Efflux(GABA mediated) Cl- Influx(GABA mediated) Channel(Glutamate mediated) Low pH
  22. 22. Enhanced Sodium channel inactivation Na + Na + Valproate Carbamazepine Phenytoin Lamotrigine Topiramate Zonisamide Activation gate Inactivation gate Felbamate Rufinamide Lacosamide Resting state Active state Inactive state
  23. 23. • P-Phenytoin • V-Valproate • R-Rufinamide • T-Topiramate • F-Felbamate • C-Carbamazepine • Zinger chicken -zonisamide • Le-Lamotrigine • Lo-Lacosamide
  24. 24. Ca++ Ca++ Ethosuximide Valproate Reduced current through T type Calcium channels Zonisamide
  25. 25. GABA Enhancers TiagabineGabapentin Valproate BarbiturateBZD Vigabatrine
  26. 26. Glutamate blockers Metabotrophic Under research AMPA Blocker Topiramate NMDA Blockers Felbamate Levetiracetam
  27. 27. Carbonic anhydrase inhibitors Inhibition of the enzyme carbonic anhydrase Concentration of hydrogen ions intra cellularly and decreases the pH Potassium ions shift (efflux) to the extracellular compartment to buffer the acid-base status Hyperpolarization Increase seizure threshold
  28. 28. AED Adverse effects
  29. 29. Cerebellar Phenytoin Carbamazepine Valproic acid Lamotrigine Ethosuximide Gabapentin Lacosamide Rufinamide Psychomotor slowing Language problems Topiramate Tiagabine Mood changes Felbamate Levetiracetam Zonisamide
  30. 30. Cardiac conduction Lacosamide Rufinamide Hepatotoxicity Valproate Benzodiapine Felbamate BM Suppression Carbamazepine Ethosuximide Levetiracitam Valproate Felbamate Skin rash Lamotrigine Phenytoin Carbamazepine Phenobarbitone
  31. 31. Phenytoin Gum hyperplasia Hirsutism Osteomalacia CBZ Hyponatremia VPA Increase NH3 Weight gain Topiramate Renal stones Weight loss Glaucoma
  32. 32. AED-DRUG INTERACTIONS ENZYME INDUCERS Phenobarbital Carbamazepine Phenytoin Primidone ENZYME INHIBITOR Valporate Reduces levels of: Valporate Lamotrigine Topiramate Zosnisamide Inhibits metabolism and increases levels of: Phenobarbital Lamotrigine Felbamate
  33. 33. AED- INTERACTIONS VALPORATE DISPLACES PROTEIN BOUND PHENYTOIN FROM PROTEIN BINDING SITE THUS INCREASING FREE FRACTION OF PHENYTOIN - SO WHEN BOTH ARE BEING USED FREE FRACTION OF PHENYTOIN SHOULD BE CHECKED. MEDICATION EXCLUSIVELY EXCREATED BY KIDNEY LEVETIRACETAM GABAPENTIN LESS INTERACTION WITH OTHER DRUGS
  34. 34. AED AND ATT INTERACTIONS INH increase PHT and CBZ level INH and Rifampicin increase Carbamazepine level Rifampicin reduces Phenytoin and valproate level
  35. 35. AED AND ART INTERACTIONS With Phenytoin -- ↑Dose of Ritonavir & Lopinavir With Valproate -- ↓ Dose of Zidovudine With Ritonavir / Atazanavir --↑Dose of Lamotrigine Avoid enzyme inducing AED with PI/NNRTI
  36. 36. APPROACH TO THE CHILD WITH A SUSPECTED SEIZURE DISORDER
  37. 37. APPROACH TO THE CHILD WITH A SUSPECTED SEIZURE DISORDER DID THE CHILD HAVE A SEIZURE? NO YES BENIGN PAROXYSMAL VERTIGO SYNCOPE FAMILIAL CHOREOATHETOSIS HEREDITARY CHIN TREMBLING SHUDDERING ATTACKS NARCOLEPSY NIGHT TERROR PSEUDOSEIZURES NIGHT TERROR RAGE ATTACK BENIGN MYOCLONUS OF INFANCY TICS INITIAL SEIZURE RBS SERUM CALCIUM MAGNESIUM POTASSIUM SODIUM EEG? CT BRAIN? MRI BRAIN? CSF EXAMINATION? RECURRENT SEIZURES DRUG COMPLIANCE? IMPROPER DOSE? INCORRECT DRUG? METABOLIC DISORDER? UNDERLYING STRUCTURAL LESION? DRUG INTERACTION? CNS DEGENERATIVE DISEASE? INTRACTABLE SEIZURE? STUDIES AND EXAMINATION ABNORMAL SYMPTOMATIC SEIZURE TREAT UNDERLYING CAUSE AED IF NECESSARY NORMAL ISOLATED FIRST SEIZURE WITH NORMAL EEG NEGATIVE FAMILY HISTORY NO CONTINUOUS DRUG RX CLOSE OBSERVATION PRESCRIBE RESCUE MEDICATIONS FOR SEIZURE NORMAL( EXCEPT EEG) CONSIDER DRUG THERAPY FOLLOW UP
  38. 38. APPROACH TO THE CHILD WITH A SUSPECTED SEIZURE DISORDER FOLLOW UP GOOD CONROL REGULAR FOLLOW –UP AED DRUG LEVELS MONITOR TOXICITY(CBC,LFT, BEHAVIOUR, LEARNING) EEG AS INDICATED POOR CONTROL CONSIDER HOSPITALIZATION PROLONGED EEG RECORDING AND VIDEO MONITORING FOR POSSIBLE EPILEPSY READJUST MEDICATION CONSIDER UNDERLYING PATHOLOGY AND REINVETIGATE WITH CT OR MRI FREQUENT FOLLOW UP
  39. 39. Febrile Seizures-Criteria Seizures that occur between the age of 6 and 60 months With a temperature of 38 ° C or higher That are not the result of central nervous system infection or any metabolic imbalance And that occur in the absence of a history of prior afebrile seizures
  40. 40. Febrile Seizures-Types Simple febrile seizure (all of the following) 70-75% Duration of less than 15 minutes Generalized No previous neurologic problems Occur once in 24 hours Complex febrile seizure (any of the following) 20-25% More prolonged ( > 15 min) Focal And/or recurs within 24 hr. Febrile status epilepticus Febrile seizure lasting > 30 min. Symptomatic febrile seizure 5% Age and fever are the same as for simple febrile seizure The child has a preexisting neurologic abnormality or acute illness
  41. 41. • The underlying pathophysiology is unknown. • But genetic predisposition clearly contributes to the occurrence of this disorder. • Although clear evidence exists for a genetic basis of febrile seizures, the mode of inheritance is unclear. • While polygenic inheritance is likely, a small number of families are identified with an autosomal dominant pattern of inheritance of febrile seizures, leading to the description of a "febrile seizure susceptibility trait" with an autosomal dominant pattern of inheritance with reduced penetrance. Mutations have been found in genes encoding the sodium channel and the gamma amino-butyric acid A receptor. Febrile Seizures-Pathophysiology
  42. 42. Febrile Seizures-Epidemiology Frequency: United States Between 2% and 5% of children have febrile seizures by their fifth birthday India between 5% and 10% Mortality: simple febrile seizures- No risk of mortality Complex febrile seizure- 2-fold increased risk of mortality Morbidity: 2-7% of children who experience febrile seizures proceed to develop epilepsy later in life Race: Febrile seizures occur in all races. Sex: Some studies demonstrate a slight male predominance. Age: By definition, febrile seizures occur in children aged 6months to 5 years.
  43. 43. Febrile Seizures-Risk factor Risk factors for developing febrile seizures are as follows: • Family history of febrile seizures • High temperature • Parental report of developmental delay • Neonatal discharge at an age greater than 28 days (suggesting perinatal illness requiring hospitalization) • Daycare attendance Maternal alcohol intake and smoking during pregnancy - Two-fold increased risk Presence of 2 of these risk factors - Increases the probability of a first febrile seizure to about 30%
  44. 44. Febrile Seizures- Trigger Febrile seizures often occur in the context of: Otitis media Roseola Human herpesvirus 6 (HHV6) Shigella Infection
  45. 45. Febrile Seizures- Recurrence risk factors (Low fever)
  46. 46. Febrile Seizures- Predictors of epilepsy
  47. 47. 10 first aid steps (when someone has a convulsive seizure) • Stay calm • Look around • Note the time • Stay with them • Cushion their head • Don't hold them down • Don't put anything in their mouth • Check the time again. If a convulsive seizure doesn't stop after 5 minutes or they have another seizure without recovering fully from the first seizure (status epilepticus) • After the seizure has stopped, put them into the recovery position • Stay with them until they are fully recovered. Emergency management of seizure
  48. 48. MANAGEMENT OF STATUS EPILEPTICUS
  49. 49. Approach to a child with suspected febrile seizures
  50. 50. Work-up • No specific studies are indicated for a simple febrile seizure • Focus should be on diagnosing the cause of fever Blood Studies recommendations: • Blood studies (serum electrolytes, calcium, phosphorus, magnesium, and complete blood count [CBC]) are not routinely recommended in the work-up of a child with a first simple febrile seizure • Blood glucose should be determined only in children with prolonged postictal obtundation or those with poor oral intake
  51. 51. Lumbar Puncture-Indication in FS RECOMMENDATIONS: • Strongly consider Lumbar puncture in children younger than 12 months, because the signs and symptoms of bacterial meningitis may be minimal or absent in this age group. • Lumbar puncture should be considered in children aged 12-18 months, because clinical signs and symptoms of bacterial meningitis may be subtle in this age group. • In children older than 18 months, the decision to perform lumbar puncture rests on the clinical suspicion of meningitis.
  52. 52. Neuroimaging in FS RECOMMENDATIONS: According to the AAP practice parameter, a CT or MRI is not recommended in evaluating the child after a first simple febrile seizure INDICATION: Complex febrile seizure (4%) Febrile status epilepticus Intermediate or high risk of recurrence of FS
  53. 53. Electroencephalogram in FS RECOMMENDATIONS: If the child is presenting with his or her first simple febrile seizure and is otherwise neurologically healthy, an EEG need not normally be performed as part of the evaluation. If at all an EEG is indicated, it is delayed until or repeated after > 2 wk have passed INDICATIONS OF EEG: • If epilepsy is highly suspected An EEG would not predict the future recurrence of febrile seizures or epilepsy even if the result is abnormal • Distinction between ongoing seizure activity and a prolonged postictal period • Intermediate or high risk of recurrence of FS
  54. 54. TREATMENT-FS RECOMENDARTIONS: An antiepileptic therapy continuous or intermittent is not recommended for children with one or more simple febrile seizures If the seizure lasts for > 5 min Then acute treatment with diazepam lorazepam or midazolam is needed Rectal diazepam is often prescribed to be given at the time of recurrence of febrile seizure lasting > 5 min Alternatively buccal or intranasal midazolam may be used Antipyretics do not reduce the risk of having a recurrent febrile seizure
  55. 55. CHOICE OF DRUG ACCORDING TO SEIZURE TYPE AND EPILEPSY SYNDROME
  56. 56. CHOICE OF DRUG: OTHER CONSIDERATIONS  Comparative effectiveness and potential for paradoxical seizure aggravation by some AEDs precipitation of absence seizures and myoclonic seizures by carbamazepine and tiagabine  Comparative tolerability: Increased risk of liver toxicity for valproate therapy in children< 2 yr of age, on polytherapy, and or with metabolic disorders The choice of an AED can also be influenced by the likelihood of occurrence of nuisance side effects such as: • Weight gain (valproate, carbamazepine) • Gingival hyperplasia(phenytoin) • Alopecia (valproate) • Hyperactivity (benzodiazepines,barbiturates, valproate, gabapentin) • Children with behavior problems and/or with attention deficit disorder can become particularly hyperactive with GABAergic drugs such as benzodiazepines and barbiturates or even valproate.
  57. 57. CHOICE OF DRUG: OTHER CONSIDERATIONS  Cost and availability: • Cost of the newer AEDs often precludes their use, particularly in developing countries where costis a major issue. • Generic substitution is generally best avoided if a brand name drug has already proved efficacious.  Ease of initiation of the AED: • AEDs that are started very gradually may not be chosen in situations when there is a need to achieve a therapeutic level quickly- lamotrigine and topiramate • AEDs that have intravenous preparations or that can be started and titrated more quickly may be chosen- valproate, phenytoin, or levetiracetam  Drug interactions:  The presence of comorbid conditions: Avoid : VPA, PB and BZD Safe : OXC,LEV and GBP
  58. 58. CHOICE OF DRUG: OTHER CONSIDERATIONS Phenytoin, Lamotrigine and Valproate are safer Avoid:Levetiracetam Avoid- Valporate Use-Topiramate Adolescent girls of child-bearing potential • Enzyme-inducing AEDs should be avoided because they can interfere with birth control pills • Some AEDs, particularly valproate, can increase risks for fetal malformations so need to be avoided
  59. 59. CHOICE OF DRUG: OTHER CONSIDERATIONS  Coexisting seizures: • In Absence and generalized tonic-clonic seizures broad spectrum AEDs could be used- lamotrigine or valproate • Rather than medications that have a narrow spectrum of efficacy- phenyton  History of prior response to specific AEDs:  Mechanism of drug actions: • avoid combining medications that have similar mechanisms of action-phenytoin and carbamazepine(both work on sodium channel) Lamotrigine and valproate Topiramate and lamotrigine  Ease of use:  Ability to monitor the medication and adjust the dose:  Patient ’s and family ’s preferences:  Genetics and genetic testing: • There strong association between the human leukocyte antigen HLA-B * 1502 allele and severe cutaneous reactions induced by carbamazepine, phenytoin, or lamotrigine in Chinese patients • Mutations of the SCN1A sodium channel gene indicating Dravet syndrome can lead to a seizures exacerbation if lamotrigine is used  Teratogenic profiles: synergistic effects ( different mechanisms of action)
  60. 60. Monotherapy is the rule!!
  61. 61. The principles of monotherapy indicate that a second medication needs to be considered after the first either is pushed as high as tolerated and still does not control the seizures or results in intolerable adverse effects.
  62. 62. In those cases, a second drug is started and the first is tapered and then discontinued. The second drug is then again pushed to the dose that controls the seizure or that results in intolerable side effects.
  63. 63. If the second drug fails monotherapy with a third drug or dual (combination) therapy is considered.
  64. 64. Additional Treatment Non-pharmacological options • Ketogenic diet • Vagal nerve stimulation • Resective surgery • Repetitive transcranial magnetic stimulation • ECT • Mild hypothermia
  65. 65. KETOGENIC DIET • Low carbohydrate, low protein, high fat after fasting to initiate ketosis • Anti-seizure effect of ketosis, acidosis • Main experience with children, especially with multiple seizure types • Long-term effects unknown
  66. 66. Intermittent programmed electrical stimulation of left Vagus nerve 50% reduction of seizures can be expected in up to 30–40% of patients
  67. 67. Focal resection Hemispherectomy Multiple subpial transection Corpus callosotomy Focal resection and hemispherectomy result in a high rate (50-80%) of seizure freedom. Corpus callosotomy result in lower rates (5-10%) of seizure freedom
  68. 68. Additional Treatment pharmacological options:NonAEDs Steroids ACTH Prednisone Intravenous gamma globulin (IVIG)
  69. 69. A prospective, single-blind study demonstrated no difference in effectiveness between high-dose long-duration corticotropin (150 U/m2/day for 3 wk, tapering over 9 wk) and low-dose short- duration corticotropin (20-30 U/day for 2-6 wk, tapering over 1 wk) with respect to spasm cessation and improvement in the patient's EEG. Hypertension was more common with larger doses.
  70. 70. One double-blind, placebo-controlled, crossover study demonstrated no difference between low-dose ACTH (20-30 U/day) and prednisone (2 mg/kg/day) in suppressing clinical spasms and hypsarrhythmic EEG in infants with infantile spasms
  71. 71. Prospective, randomized, single-blinded study demonstrated high-dose ACTH at 150 U/m2/day to be superior to prednisone (2 mg/kg/day) in suppressing clinical spasms and hypsarrhythmic EEG in infants with infantile spasms.
  72. 72. MONITORING AND FOLLOW-UP CBC, LFT & RFT before Starting treatment and every 3-6 month Ca2+,ALP and Vit-D every year First follow-up within 2-4 weeks Subsequent follow-ups every 3-6 months Seizure diary Routine Monitoring not recommended Suspected AED toxicity Managing drug interactions Liver or renal disease and pregnancy Routine laboratory tests Follow-up AED level monitoring
  73. 73. Therapeutic range (In micro gm/mL) Phenytoin 10-20 CBZ 6-12 VPA 50-125 Phenobarbital 10-40
  74. 74. DISCONTINUATION OF AED THERAPY Usual indication of withdrawal: Seizure free >=2 years Normal EEG when AED withdrawal is attempted In benign epilepsy syndrome the duration of therapy can often be as short as 6 months Prolonged period of seizure freedom on treatment is often warranted before AEDs are withdrawn, if withdrawal is attempted at all in the following: •Temporal lobe epilepsy secondary to mesial temporal sclerosis •Lennox-Gastaut syndrome •Severe myoclonic epilepsy Following AEDs withdrawal most relapses occur within the first 6 months
  75. 75. DISCONTINUATION OF AED THERAPY Risk factors which help predicting prognosis after AEDs withdrawal (risk factor for seizure relapse): • Abnormal EEG before medication is discontinued • Remote symptomatic epilepsy • Absences seizure • Those treated with valproate for primary generalized epilepsy • Old age of epilepsy onset • Long duration of epilepsy • Presence of multiple seizure type • Need to use > 2 AEDs
  76. 76. DISCONTINUATION OF AED THERAPY How to discontinue ADEs? AED therapy should be discontinued gradually often over a period of 3-6 months Abrupt discontinuation leads to: • Withdrawal seizure • Status epilepticus Withdrawal seizure is common with: • Phenobarbital • Benzodiazepines Seizures that occur > 2 to 3 mo after AEDs are completely discontinued indicate relapse- Resume treatment A prescription for rectal diazepam to be given at the time of seizures that might occur during and after tapering is warranted
  77. 77. DISCONTINUATION OF AED THERAPY • In meningitis: • In NCC: Acute symptomatic seizures due to active lesions (cystic lesions, granulomas) till such time that they disappear or become inactive (no edema, no enhancement, calcified) – usually for a period of 6 months Remote symptomatic due to inactive calcified lesions presenting with seizures either denovo or as relapses should be treated till a 2 year seizure free period is achieved. Relationship of convulsion with fever Action Before 72 hrs of fever Stop AEDs before discharge After 72 hrs of fever Continue AEDs for 2-3 months
  78. 78. THANK YOU

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