| Indication | For the treatment of epilepsy and pain associated with true trigeminal neuralgia. |
| Pharmacodynamics | Carbamazepine, an anticonvulsant structurally similar to tricyclic antidepressants, is used to treat partial seizures, tonic-clonic seizures, pain of neurologic origin such as trigeminal neuralgia, and psychiatric disorders including manic-depressive illness and aggression due to dementia. |
| Mechanism of action | Carbamazepine inhibits sustained repetitive firing by blocking use-dependent sodium channels. Pain relief is believed to be associated with blockade of synaptic transmission in the trigeminal nucleus and seizure control with reduction of post-tetanic potentiation of synaptic transmission in the spinal cord. Carbamazepine also possesses anticholinergic, central antidiuretic, antiarrhythmic, muscle relaxant, antidepressant (possibly through blockade of norepinephrine release), sedative, and neuromuscular-blocking properties. |
| Absorption | Not Available |
| Volume of distribution | Not Available |
| Protein binding | Carbamazepine in blood is 76% bound to plasma proteins. |
| Metabolism | Hepatic |
| Route of elimination | Not Available |
| Half life | 25-65 hours |
| Clearance | Not Available |
| Toxicity | Mild ingestions cause vomiting, drowsiness, ataxia, slurred speech, nystagmus, dystonic reactions, and hallucinations. Severe intoxications may produce coma, seizures, respiratory depression, and hypotension |