This document discusses several antiepileptic drugs including carbamazepine, phenytoin, and sodium valproate. It defines epilepsy as a neurological disorder marked by recurrent seizures. The drugs are classified and their mechanisms of action, pharmacokinetics, clinical uses, and adverse effects are described. Carbamazepine works by blocking sodium channels to prevent seizure spread. Phenytoin also blocks sodium channels and calcium channels. Sodium valproate increases GABA levels in the brain to have an antiseizure effect.

2. ANTIEPILEPSY DRUGS

3. CONTENTS
 Define epilepsy.
 Classification of drugs
 Mechanism of action
 Pharmacokinetics
 Clinical uses
 Adverse effects

4. DEFINE EPILEPSY
A neurological disorder marked by sudden recurrent
episodes of sensory disturbance loss of consciousness or convulsions associated
abnormal electricity activity in brain.
Epilepsy is the third most common neurologic disorder after cerebrovascular and
Alzheimer
Disease.

5. CLASSIFICATION OF DRUGS:
 CARBAMAZEPINE.
 PHYENTOIN.
 SODIUM VALPROATE.

6. CARBAMAZEPINE (TEGRETOL)
MECHANISM OF ACTION:
 Carbamazepine reduces the propagation of abnormal
impulses in the brain by blocking the sodium channel.
 Inhibiting the generation of repetitive action potentials in
the epileptic focus and preventing their spread.

7. PHARMACOKINETICS:
• The rate of absorption of carbamazepine varies widely among patients.
• Complete absorption apparently occur in all peak level are usually achieved
6 to 8 hours after administration.
• Slowly absorption by giving the drug after meal.
• Distribution is slow and volume of distribution 1L/kg.
• The drug is approximately 70% bound to plasma protein.

8.  CLINICAL USES:
• Carbamazepine is also used the partial
seizures and generalized tonic- clonic
seizures.
• Also used bipolar disorder.
 ADVERSE EFFECTS:
• Dizziness.
• Blurred vision.
• Fatigue.
• Hyponatremia.

9.  PHENYTOIN (DILANTIN)
 MECHANISM OF ACTION:
• Phenytoin blocks the voltage gated sodium channels by
selectively binding to the channel in the inactive state and slowing
its rate of recovery.
• At high concentration phenytoin can also block the voltage
dependent Calcium channel and interfere with the release of
mono-aminergic Neurotransmitter.

10.  PHARMACOKINETICS:
• Phenytoin is highly bound to plasma protein.
• Phenytoin is metabolized inactive and excreted in urine.
• The drug is 90% bound to plasma protein.
• The half life of phenytoin varies from 12 to 36 hours.
• At low blood level it takes 5-7 days to reach steady –state level.
• At high level it may be 4-6 weeks before blood level are stable.

11.  CLINICAL USES:
• Phenytoin is used partial seizures.
• It use Status epilepticus.
 ADVERSE EFFECTS:
• Sedation.
• Dizziness.
• Hirsutism.
• Slurred speech.

12.  SODIUM VALPROATE (DEPAKINE)
MECHANISM OF ACTION:
 Sodium valproate block sustained firing of neuron its action against
partial seizures.
 Increase level of GABA in the brain after administration of valproate.
 Effect of valproate to facilitate glutamic acid decarboxylase the
enzyme
 responsible for GABA synthesis inhibitory effect of GABA transporter.
 At high concentration valproate inhibits GABA transaminase in brain
 blocking degradation of GABA.


13.  PHARMACOKINETICS:
 Valproate is well absorbed oral dose with bioavailability greater
than 80%.
 Peak blood levels are observed within 2 hours.
 Valproate acid 90 % bound to plasma protein.
 Its half life 9 to 18 hours.
 Volume of distribution approximately 0.15 L/kg

14.  CLINICAL USES:
 Drug are effective for the partial and primary
generalized epilepsies
 ADVERSE EFFECTS:
 Nausea.
 Vomiting.
 Abdominal pain.
 Weight gain.
 Hair loss.
 Heart burn.

15.  REFERENCE:
 Katzung 12 edition chapter no 24 Anti seizure Drugs
 Lippincot 5 edition chapter no 15 Epilepsy