Management of seizures
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Management of seizures

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management of seizures is important..

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    Management of seizures Management of seizures Presentation Transcript

    • MANAGEMENT OF SEIZURES
      DR.PRAVEEN NAGULA
    • 1.APPROACH TO A CASE OF A SEIZURE
      2.ANTIEPILEPTIC DRUG CLASSIFICATION
      3.MECHANISM OF ACTION AT RECEPTORS
      4.DRUGS IN EACH SEIZURE DISORDER
      5.INDIVIDUAL DRUG DESCRIPTION
      6.STATUS EPILEPTICUS
      7.SPECIFIC SCENARIOS
      8.CONCLUSION
    • Approach to a case of seizure
    • Investigations
      1.EEG
      2.CT scan
      3.MRI
      4.ROUTINE INVESTIGATIONS- serum electrolytes,blood glucose levels,ABG.
      5.LUMBAR PUCTURE
    • FOUR PARTS
      1.Use of anti epileptic drugs
      2.Surgical excision of epileptic foci
      3.Removal of causative and precipitating factors
      4.Regulation of physical and mental activity
    • Course of a case of EPILEPSY
    • TRADITIONAL AEDs
      1.BROMIDES
      2.PHENOBARBITAL
      3.PHENYTOIN
      4.CARBAMAZEPINE
      5.BENZODIAZEPINES
      6.ETHOSUXIMIDE
      7.PRIMIDONE
      8.VALPROIC ACID
    • NEWER ANTIEPILEPTICs
      1.OXCARBAZEPINE
      2.PREGABALIN
      3.GABAPENTIN
      4.TOPIRAMATE
      5.LAMOTIRIGINE
      6.LEVETIRACETAM
      7.TIAGABINE
      8.FELBAMATE
      9.ZONISAMIDE
      10.FOSPHENYTOIN
    • EXCITATORY GLUTAMATERGIC SYNAPSE
      PHENYTOIN
      CARBAMAZEPINE
      LAMOTRIGINE
      ETHOSUXIMIDE
      LAMOTRIGINE
      GABAPENTIN
      PREGABALIN
      LACOSAMIDE
      RETIGABINE
      GLUTAMATE
      LEVETIRACETAM
      FELBAMATE
      PHENOBARBITAL
      TOPIRAMATE
      LAMOTRIGINE
    • INHIBITORY GABA ergic SYNAPSE
      GABA-T
      VIGABATRIN
      GAT -1
      TIAGABINE
      GABA A
      BENZODIAZEPINES
    • Choice of AEDs by type of adult seizure disorder
    • COMBINATION of AEDs for REFRACTORY seizures
    • PHENYTOIN
      Oldest non sedative antiseizure drug
      More soluble parenteral drug is fosphenytoin
      M.O.A- blocks sustained high frequency repetitive firing of action potentials –Na channels – at therapuetic concentrations
      Inhibits release of serotonin,NE
      Promotes uptake of dopamine
      Inhibits MAO activity
      Stabilization of membrane
      Reduces calcium permeability
    • Accumulates in liver,brain,muslce fat.
      Elimination is dose dependent.
      T1/2 -24 hours
      When oral therapy is started -300mg/day regardless of the body weight.Increased the dose by 25-30 mg in adults
      Drug interactions – sulfonamides displace phenytoin
      High affinity for Thyroid binding globulin
      Conc. is with use of phenobarbitone,carbamazepine
       concentration of phenytoin –isoniazid
      Toxicity – nystagmus,diplopia,ataxia,sedation
      Gingival hyperplasia,hirusitism
      Coarsening of facial features
      Mild peripheral neuropathy Osteomalcaia
      Causal relation to hodgkin’ s lymphoma agranulocytosis
    • PHENYTOIN METABOLISM
    • CARBAMAZEPINE
      Closely related to IMIPRAMINE
      M.O.A –similar to phenytoin – blocks Na channels
      Potentiates post synaptic action of GABA
      Inhibits uptake ,release of NE
      Uses – focal seizures,GTCS,trigeminalneuralgia,BPD
      Not sedative
      INDUCES MICROSOMAL enzymes
      Valproic acid  its levels, Phenytoin ,phenobarbitone –  levels
      Only oral form.
      15-25mg/kg/d – children 1gm/day -adults
    • CARBAMAZEPINE metabolism
    • Phenobarbital
      Oldest of the available antiseizure drugs –sedative
      DOC in seizures of infants
      M.O.A –exact is unknown
      Enhancement of inhibitory processes,dimintion of excitatory transmission
      Na channel blocking at high doses
      GABAa receptor action
      May worsen absence ,atonic ,infantile spasms
      In febrile seizures <15ug/ml -ineffective
    • VIGABATRIN
      Irreversible inhibitor of GABA T (degrades GABA)
      Increases GABA at synaptic sites
      Inhibits GABA transporter
      FOCAL seizures,WEST syndrome
      T1/2 -6-8 hrs
      500mg bid
      2-3 g/day
      Toxicity -drowsiness,dizziness,weight gain
    • Lamotrigine
      Similar to phenytoin in action
      Absence attacks in children –voltage gated Ca channels
      Add on treatment
      Linear kinetics
      T1/2 -24 hrs
    • Felbamate
      M.O.A –not known
      Third line drug because of aplasticanemia,hepatitis
      NMDA receptor blockade via glycine binding site
      Increases phenytoinlevels,valproate
      Decreases carbamazepine
      Lennox gestaut syndrome
    • Gabapentin,Pregabalin
      GABAPENTIN –analog of GABA
      Spasmolytic,antiseizure drug
      Does not act on GABA receptors
      Adjunctive drugs
      Not metabolised
      Not bound to plasma proteins
      Excreted via renal
    • Topiramate
      Substituted monosaccharide
      M.O.A –phenytoin
      Potentiates GABA action
      200- 600 mg/ da
      TIAGABINE –inhibitor of GABA uptake
      LEVETIRACETAM – analog of piracetam ,M.O.A unknown,notmetabolised by cytochrome P450
      Linear kinetcis
    • Ethosuximide
      Pure petit mal drug
      Reduces T TYPE CALCIUM CURRENTS in thalamus
      Inhibits na k ATPase
      Depresses cerebral metabolic rate
      Inhibits GABAaminotransferase
      Not protein bound
      Decrease the dose with valproic acid
    • Valproic acid
      Sodium salt,or free acid
      Fatty carboxylic acid
      Branching,unsaturation – increases lipophilicty
      Effective agianst absence seizures
      Effective in myoclonic seizures
      Hepatotoxicity
      90% bound to plasmaproteins
      Sedation with phenobarbital use
      Bipolar disorders,migraine prophylaxis
    • Benzodiazepines
      6
      Lorazepam –long acting than dioazepam
      Diazpeam –short acitng,GTCS,respiratory depression
      Clobazam – 1.,5 benzodiazepine
      Nitrazepam
      Clobazate
      Acetazomaide –mild acidosis in brain,rapidtolernace
    • Drug interactions
    • Teratogenic effects
      Valproic acid
    • Surgical treatment
    • STATUS EPILEPTICUS
    • Classification of STATUS EPILEPTICUS
    • AEDs In Pregnancy
    • Doses
    • NEWER drugs in pipeline
    • answers
    • REFERENCES
      1.KATZUNG’S 11 th Ed PHARMACOLOGY
      2.LIPPINCOTT ‘S PHARMACOLOGY
      3.MEDICINE UPDATE 2009
      4.HARRISON’S PRINCIPLES OF INTERNAL MEDICINE 17 th Ed
      5.ADAM and VICTOR’S NEUROLOGY,9 th Ed
      6.www.medscape.com
      7.www.ilae.org
      8.www.netterimages.com
    • THANK YOU