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Acetazolamide, Sulthiame and Newer Antiepileptics


Not commonly used for treatment of epilepsy. Only effect is due to acidosis produced, being more effective in petit mal epilepsy.


Derivative of sulphonamide. Weak antiepileptic effect mainly due to enzyme inhibiting property. It inhibits metabolism of other antiepileptic drugs, so their action increases, thus can be used in combination.


Vigabatrin, Lamotrigine, GABA  pentin, Topiramate, Tiagabine and Zonisamide are newer drugs, which are 2nd line drugs, used only when patient does not respond to 1st line drugs. They have four properties:

  1. Always given as 2nd line and in combination with other antiepileptic drugs, when patient is not responding. In rare conditions may be used alone
  2. Have wide range of activity, so used in all types of epilepsy
  3. Have minimal plasma protein binding, having less drug interactions.
  4. Do not have enzyme inducing or inhibiting property so have less drug interactions.


Half life 6-8 hours.

Mechanism of Action

Acts by inhibiting GABA transaminase enzyme (responsible for metabolism of GABA) inhibiting it non-competitively.


Broad spectrum –all types of epilepsy, mostly used in patients with seizures and infantile spasms.

Adverse effects

Can cause visual field defects on prolonged administration. So uses are declining.


Start at low dose of 500 mg, which may be increased up to 1500 mg.


Mechanism of Action

As wide range spectrum, can cause

  1. sodium channel blockage
  2. blocks calcium T channels


Mainly metabolized in liver. Longer half life of 24 hours.


All types of epilepsy.

Adverse effects

CNS –in children can cause severe rash, which may even lead to death.

Avoided by giving drug in low doses, 100-300 mg in divided doses.

 GABA Pentin

Mechanism of Action

Interferes with GABA metabolism, synthesis, release and reuptake. Exact mechanism is not known.


Excreted in urine. Half life is 6-8 hours.


In   all types of epilepsy.

Partial seizures, infantile spams. Also used in neuralgias or neuropathic pains.


1.8-4.8 g. Start at low dose

Adverse effects

CNS- drowsiness and sedation


Mechanism of Action

  1. blocks sodium channels directly
  2. blocks calcium T channels
  3. GABA mediated effects – increase in GABA
  4. Inhibitory effects on excitatory neurotransmitters.

Mostly excreted unchanged in urine. Half life is 24-30 hours, thus having a longer half life.

Broad spectrum, so used in all types of epilepsy.

Adverse effects

On prolonged use, increased incidence of urinary calculi or urinary stones.

Advised to take excess of water.

Dose 50-600 mg, start at lower dose.


Mechanism of Action

Mainly by inhibiting the uptake of GABA, increasing the concentration of GABA in brain or in synapses.

Drug is mainly oxidized in liver. About 75% of drug is excreted in faeces. 25% in urine.

Half life is 6-8 hours.

Uses broad range activity

Adverse Effects depression in certain patients.

Dose in range of 16-56 mg. start at lower dose.


Mechanism of Action

Same on sodium channels and GABA.

Has longer half life of about 1-3 days.

Used in all types of epilepsy.

Dose is 100-600 mg. start at lower dose.


Sedative hypnotic not used now, as is an older drug. It is used in patients suffering from head injury as has least respiratory depressant effect.

Now more safer benzodiazepines have been produced (diazepam). Only used in certain cases of status epilepticus.

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