This document summarizes information about epilepsy and antiepileptic drugs. It defines epilepsy as a neurological disorder causing abnormal brain activity and seizures. It classifies and discusses the mechanisms and pharmacology of various antiepileptic drugs, including their effects on sodium channels, calcium channels, GABA, and glutamate. The document categorizes common antiepileptic drugs and provides details about specific drugs like phenobarbital, primidone, phenytoin, carbamazepine, ethosuximide, valproic acid, and newer drugs; describing their mechanisms of action, uses, pharmacokinetics, and adverse effects.

1. Presented by
Miss. Ashvini Govande
Assistant Professor
Kandhar College of Pharmacy, Kandhar

2.  What is epilepsy
 Classification of epilepsy
 Mechanism of action of epilepsy
 Antiepileptic drug classification
 Mechanism of action of antiepileptic drug
 Pharmacology of drug

3.  Epilepsy is a central nervous system
(neurological) disorder in which brain activity
becomes abnormal, causing seizures or periods of
unusual behavior, sensations, and sometimes loss
of awareness.
 Epilepsy is also known as epileptic seizures or
convulsions.

6.  Antiepileptic are a class of drugs that try and
prevent rapid, repitative, stimulation of brain that
causes seizures activity.
 Mechanism of action of Antiepileptic drug –
 Enhancement of GABA action
 Inhibition of sodium channel function
 Inhibition of calcium channel function
 Other mechanisam include-
 Inhibition of glutamate release
 Block of glutamate receptor

7. Category Drug
Barbiturates Phenobarbitone
Deoxybarbiturate Primidone
Hydantoin Phenytoin, Fosphenytoin
Iminostilbene Carbamazepine, Oxcarbazepine
Succinamide Ethosuximide
Aliphatic carboxylic acid Valproic acid
Benzodiazepines Clonazepam, Diazepam, Lorazepam
Phenyltriazine Lamotrigine
Cyclic GABA analogue GABA pentine
Newer drugs Vigabatrine, Zonisamide,
Topiramate, Tiagabine,
Levetiracetam

9.  Barbituric acid derivatives
 MOA-
 It act on GABA receptors
 Phenobarbital increases the flow of chloride ions
into the neuron which decreases the excitability of
the post-synaptic neuron.
 Uses-
 Anticonvulsant
 Sedative hypnotic properties

10.  Primidone has anticonvulsant activity due to its
two metabolite
1) Phenobarbital
2) Phenylethylmalonamide (PEMA)
 MOA-
 It interactions with voltage-gated sodium channels
which inhibit high-frequency repetitive firing of
action potentials.
 It also increases GABA-mediated chloride flux

11.  Adverse effect –
 Sluggishness, Incoordination, Difficulty in
thinking, Slowness of speech, Faulty judgement,
Drowsiness or coma, Shallow breathing,
Staggering, Severe cases coma and deth.
 Uses-
 Used as anticonvulsant to control grand mal,
psychomotor and focal epileptic seizures.
 First-line therapy for essential tremor along
with propranolol

12.  MOA-
 They blocks sodium channel
 Which reduces hyperexcitability of post synaptic
membrane.
 Uses-
 Anticonvulsant
 Anti-arrhythmic
 Muscle relaxant

13.  Pharmacokinetic-
 Absorption- Well absorbed orally
Bioavailbility is 85%
Food influences absorption
 Distribution- Vol. Of distribution 0.5-1.0L/kg
 Protein binding- 90%
 Metabolism- Hydroxylated in liver by saturable
enzyme system
 Elimination- Drug is excreted in bile as inactive
metabolite which are then reabsorbed from the
intestine and excreted through urine

14.  Adverse effect-
 Rash
 Gum hypertrophy
 Ataxia
 Nystagmus
 Slurred speech
 Confusion
 Drug induced lupus
 Agranulocytosis
 Aplastic anemia
 Hepatitis and anticonvulsant hypersensitivity
syndrome

15.  MOA-
 Carbamazepine is a sodium channel blocker
 It binds preferentially to voltage-gated sodium channels
in their inactive conformation, which prevents repetitive
and sustained firing of an action potential.
 Uses-
 Used to treat partial seizures, tonic-clonic seizures,
 Trigeminal neuralgia
 Psychiatric disorder such as- manic depressive illness
and aggression due to dementia.
 Anticholinergic, Central antidiuretic, antiarrhythmic,
muscle relaxant, antidepressant, sedative and
neuromuscular blocking proprty.

16.  Adverse effect-
 Dizziness, Drowsiness, Unsteadiness, Nausea and
Vomiting.
 Aplastic anemia, Agranulocytosis, Pancytopenia,
Bone marrow depression, Thrombocytopenia,
Leukopenia,Leukocytosis, Eosinopihlia, Acute
intermitent porphyria.
 Contraindication-
 Not used in patient with a history of Bone marrow
depression, Hypersensitivity.
 Drug interaction- with lithium increases risk of
neurotoxicity.

17.  MOA-
 It blocks the calcium channel
 Uses-
 Absence seizures.
 Adverse effect-
 Tiredness, Headache, Gastrointestinal intolerance,
Mood channges, Agitaion, Drowsiness, Inability to
concentrate, Hypersensitivity.

18.  MOA-
 By blocking the excitary glutamate receptor
 By inhibiting GABA metabolism.
 Uses-
 Absence seizures
 Mania and bipolar illness
 Myoclonic and atonic seizures
 Adverse effect-
 Anorexia, Vomiting, Heart burn, Drowsiness,
Ataxia, Tremor, Alopecia, Curling of hair,
increased bleeding tendency, Rashes,
Thrombocytopenia

19.  MOA-
 It potantiate the effect of GABA
 GABA is an inhibitory neurotransmitter.
 Uses-
 Clonazepam is used to treat Myotonic and atonic
seizures, Photosensitive epilepsy, absence seizures,
Lennox-Gastaut syndrome, Akinetic and
myoclonic seizures.
 Lorazepam is used to treat anxiety, status
epilapticus, sedation, anterograde amnesia.

20.  MOA-
 It resembles the action of phenytoin and
carbamazepine in inhibiting voltage sensetive
sodium channel and stabilize membrane.
 Uses-
 Partial seizures, Tonic clonic seizures, Lennox-
Gastaut syndrome

21.  MOA-
 It increases synaptic concentration of GABA
 Enhances GABA response
 Reduces the release of mono-amine
neurotransmitters.
 Uses-
 Postherpetic neuralgia
 Partial seizures

22.  MOA-
 Inhibitor of GABA-transaminase which degrades
GABA
 Uses-
 Partial seizures with or without generalization.
 Adverse effect-
 Behavioural changes, Depression and Psychosis,
Drowsiness, Anemia Motor disturbance.