Anti-epileptic Drugs PPT

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Classification of Seizures
Partial:  simple or complex
Generalized: absence, tonic, clonic, tonic-clonic, myoclonic, febrile




Pathophysiology of Seizures
The Interictal Spike (paroxysmal depolarization shift)
Increased excitability
 Membrane depolarization, potassium buildup
 Increased excitatory (EAA, glutamate) input
 Decreased inhibitory (GABA) input

Evidence for the Pathophysiology of Seizures
Increased EAA
Increased Excitatory Amino Acid Transmission
Increased sensitivity to EAA
Progressive increase in glutamate release during kindling
Increased glutamate and aspartate at start of seizure
Upregulation of NMDA receptors in kindled rats

Decreased GABA
Decreased binding of GABA and benzodiazepines
Decreased Cl- currents in response to GABA
Decreased glutamate decarboxylase activity (synthesizes GABA)
Interfere with GABA causes seizures

Strategies in Treatment
Stabilize membrane and prevent depolarization by action on ion channels
Increase GABAergic transmission
Decrease EAA transmission

Phenytoin – Toxicity and Adverse Events
Acute Toxicity
High i.v. rate:  cardiac arrhythmias ± hypotension; CNS depression.
Acute oral overdose:  cerebellar and vestibular symptoms and signs:nystagmus, ataxia, diplopia vertigo.

Chronic Toxicity
Folate Deficiency -  megaloblastic anemia
Hypoprothrombinemia and hemorrhage in newborns
Hypersenstivity Reactions – could be severe. SLE, fatal hepatic necrosis, Stevens-Johnson syndrome.
Pseudolymphoma syndrome
Teratogenic

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