A convulsant is a drug which induces convulsions and/or epileptic seizures, the opposite of an anticonvulsant. These drugs generally act as stimulants at low doses, but are not used for this purpose due to the risk of convulsions and consequent excitotoxicity. Most convulsants are antagonists (or inverse agonists) at either the GABAA or glycine receptors, or ionotropic glutamate receptor agonists. Many other drugs may cause convulsions as a side effect at high doses (e.g. bupropion, tramadol, pethidine, dextropropoxyphene, clomipramine) but only drugs whose primary action is to cause convulsions are known as convulsants. Nerve agents such as sarin which were developed as chemical weapons, produce convulsions as a major part of their toxidrome, but also produce a number of other effects in the body and are usually classified separately.[1][2][3][4]


Some convulsants such as pentetrazol and flurothyl were previously used in shock therapy in psychiatric medicine, as an alternative to electroconvulsive therapy. Others such as strychnine and tetramethylenedisulfotetramine are used as poisons for exterminating pests. Bemegride and flumazenil are used to treat drug overdoses (of barbiturates and benzodiazepines respectively), but may cause convulsions if the dose is too high. Convulsants are also widely used in scientific research, for instance in the testing of new anticonvulsant drugs. Convulsions are induced in captive animals, then high doses of anticonvulsant drugs are administered.[5][6][7]


GABAA receptor antagonists, inverse agonists or negative allosteric modulators
GABA synthesis inhibitors
Glycine receptor antagonists
Ionotropic glutamate receptor agonists
Acetylcholine receptor agonists


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  2. ^ Calabrese EJ. Modulation of the epileptic seizure threshold: implications of biphasic dose responses. Critical Reviews in Toxicology. 2008;38(6):543-56. DOI 10.1080/10408440802014261. PMID 18615309
  3. ^ Johnston GA. Advantages of an antagonist: bicuculline and other GABA antagonists. British Journal of Pharmacology. 2013 May;169(2):328-36. DOI 10.1111/bph.12127. PMID 23425285
  4. ^ de Araujo Furtado M, Rossetti F, Chanda S, Yourick D. Exposure to nerve agents: from status epilepticus to neuroinflammation, brain damage, neurogenesis and epilepsy. Neurotoxicology. 2012 Dec;33(6):1476-90. DOI 10.1016/j.neuro.2012.09.001. PMID 23000013
  5. ^ Löscher W. Animal models of epilepsy for the development of antiepileptogenic and disease-modifying drugs. A comparison of the pharmacology of kindling and post-status epilepticus models of temporal lobe epilepsy. Epilepsy Research. 2002 Jun;50(1-2):105-23. PMID 12151122
  6. ^ Löscher W. Preclinical assessment of proconvulsant drug activity and its relevance for predicting adverse events in humans. European Journal of Pharmacology. 2009 May 21;610(1-3):1-11. DOI 10.1016/j.ejphar.2009.03.025. PMID 19292981
  7. ^ Rubio C, Rubio-Osornio M, Retana-Márquez S, Verónica Custodio ML, Paz C. In vivo experimental models of epilepsy. Central Nervous System Agents in Medicinal Chemistry. 2010 Dec 1;10(4):298-309. PMID 20868357