This document discusses the management of seizures. It covers the approach to evaluating a patient with seizures, including common diagnostic tests. It then classifies traditional and newer antiepileptic drugs, describing their mechanisms of action and uses in treating different seizure disorders. The document discusses in detail several commonly used antiepileptic drugs, including phenytoin, carbamazepine, phenobarbital, vigabatrin, lamotrigine, felbamate, gabapentin, pregabalin, topiramate, and valproic acid. It also addresses status epilepticus, drug interactions, teratogenic effects, surgical treatment options, and newer drugs in development.
1.APPROACH TO ACASE OF A SEIZURE2.ANTIEPILEPTIC DRUG CLASSIFICATION3.MECHANISM OF ACTION AT RECEPTORS4.DRUGS IN EACH SEIZURE DISORDER5.INDIVIDUAL DRUG DESCRIPTION 6.STATUS EPILEPTICUS7.SPECIFIC SCENARIOS8.CONCLUSION
FOUR PARTS1.Use ofanti epileptic drugs2.Surgical excision of epileptic foci3.Removal of causative and precipitating factors4.Regulation of physical and mental activity
PHENYTOINOldest non sedativeantiseizure drugMore soluble parenteral drug is fosphenytoinM.O.A- blocks sustained high frequency repetitive firing of action potentials –Na channels – at therapuetic concentrations Inhibits release of serotonin,NEPromotes uptake of dopamineInhibits MAO activityStabilization of membraneReduces calcium permeability
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Accumulates in liver,brain,muslcefat.Elimination is dose dependent.T1/2 -24 hoursWhen oral therapy is started -300mg/day regardless of the body weight.Increased the dose by 25-30 mg in adultsDrug interactions – sulfonamides displace phenytoinHigh affinity for Thyroid binding globulinConc. is with use of phenobarbitone,carbamazepine concentration of phenytoin –isoniazidToxicity – nystagmus,diplopia,ataxia,sedationGingival hyperplasia,hirusitismCoarsening of facial featuresMild peripheral neuropathy OsteomalcaiaCausal relation to hodgkin’ s lymphoma agranulocytosis
CARBAMAZEPINEClosely related toIMIPRAMINEM.O.A –similar to phenytoin – blocks Na channelsPotentiates post synaptic action of GABAInhibits uptake ,release of NEUses – focal seizures,GTCS,trigeminalneuralgia,BPDNot sedativeINDUCES MICROSOMAL enzymesValproic acid its levels, Phenytoin ,phenobarbitone – levelsOnly oral form.15-25mg/kg/d – children 1gm/day -adults
PhenobarbitalOldest of theavailable antiseizure drugs –sedativeDOC in seizures of infantsM.O.A –exact is unknownEnhancement of inhibitory processes,dimintion of excitatory transmissionNa channel blocking at high dosesGABAa receptor actionMay worsen absence ,atonic ,infantile spasmsIn febrile seizures <15ug/ml -ineffective
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VIGABATRINIrreversible inhibitor ofGABA T (degrades GABA)Increases GABA at synaptic sitesInhibits GABA transporterFOCAL seizures,WEST syndromeT1/2 -6-8 hrs 500mg bid2-3 g/dayToxicity -drowsiness,dizziness,weight gain
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LamotrigineSimilar to phenytoinin action Absence attacks in children –voltage gated Ca channelsAdd on treatmentLinear kineticsT1/2 -24 hrs
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FelbamateM.O.A –not knownThirdline drug because of aplasticanemia,hepatitisNMDA receptor blockade via glycine binding siteIncreases phenytoinlevels,valproateDecreases carbamazepineLennox gestaut syndrome
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Gabapentin,PregabalinGABAPENTIN –analog ofGABASpasmolytic,antiseizure drugDoes not act on GABA receptorsAdjunctive drugsNot metabolisedNot bound to plasma proteinsExcreted via renal
EthosuximidePure petit maldrugReduces T TYPE CALCIUM CURRENTS in thalamusInhibits na k ATPaseDepresses cerebral metabolic rateInhibits GABAaminotransferaseNot protein boundDecrease the dose with valproic acid
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Valproic acidSodium salt,orfree acidFatty carboxylic acidBranching,unsaturation – increases lipophilictyEffective agianst absence seizuresEffective in myoclonic seizuresHepatotoxicity90% bound to plasmaproteinsSedation with phenobarbital useBipolar disorders,migraine prophylaxis
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Benzodiazepines6 Lorazepam –longacting than dioazepamDiazpeam –short acitng,GTCS,respiratory depressionClobazam – 1.,5 benzodiazepineNitrazepamClobazateAcetazomaide –mild acidosis in brain,rapidtolernace