Primidone is an anticonvulsant of the pyrimidinedione class, the active metabolites of which, phenobarbital (major) and phenylethylmalonamide (PEMA) (minor), are also anticonvulsants. It is used mainly to treat complex partial, simple partial, generalized tonic-clonic seizures, myoclonic, and akinetic seizures and since the 1980s it has been a valuable alternative to propranolol in the treatment of essential tremor. Unlike other anticonvulsants such as carbamazepine and valproic acid, primidone is rarely used in the treatment of bipolar disorder or any other psychiatric problem. It is also not widely used in treatment of neuropathic pain, trigeminal neuralgia, migraine. Primidone has been occasionally used to treat long QT syndrome, cerebral palsy, and athetosis.
Primidone was once a mainstay anticonvulsant in the treatment of partial and generalized seizures and was the treatment of choice for secondarily generalized seizures originating in the temporal lobes, especially when combined with phenytoin, but by the early 1980s, carbamazepine had surpassed it in popularity due to the latter's lower incidence of sedation. As time passed and more and more anticonvulsants came on the market, primidone was pushed further and further away from its former place of prominence and major Western pharmaceutical corporations became less and less interested in manufacturing and selling it. It has largely fallen into disuse in the developed world as more and more anticonvulsants entered the market and has been withdrawn from markets all over the world.
Unlike many other anticonvulsants, primidone works via interactions with voltage-gated sodium channels which inhibit high-frequency repetitive firing of action potentials. It is much less toxic in overdose than phenobarbital. Along with carbamazepine, phenobarbital, and phenytoin, primidone is an inducer of metabolic enzymes in the liver, which means that it accelerates the metabolism of many other pharmaceuticals. Like other anticonvulsants that entered the market before 1989, primidone has been associated with hyperhomocysteinemia, folate deficiency and its various symptoms (birth defects, depression, and megaloblastic anemia), reduced calcium absorption, and various bone diseases. It also shares with most other anticonvulsants the tendency to cause sedation.
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