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Topamax for migraine

Topamax for migraineTopiramate (brand name Topamax ®) is an anticonvulsant drug produced by Ortho-McNeil Neurologics, a division of Johnson & Johnson. It is used to treat epilepsy in both children and adults. In children it is also used for the treatment of Lennox-Gastaut syndrome.

It is approved by the FDA and is prescribed for the prevention of migraine. Some psychiatrists use it for the treatment of bipolar disorder but it is not approved by the FDA for this purpose.

It has investigated the properties of this drug in the treatment of obesity, especially to help reduce the uncontrolled intake, and also as a possible treatment for alcoholism.  However, the manufacturer does not actively promote these uses and like bipolar disorder, it is not indicated in the prospectus.

The drug is also used in clinical trials to treat stress disorder.  A pilot study suggests that topiramate may be effective against spasms.  In May 2006 the website of clinical trials of the National Institute of Health United States, devised a list of several studies sponsored by Ortho-McNeil, proposing to examine the use of topiramate in migraine, cluster headaches and severe headaches.

There are other uses and therapeutic indications of topiramate as treatment for bulimia nervosa, Obsessive-compulsive disorder, treatment of alcoholism, smoking and the treatment of neuropathic pain, including neuralgia.

Pharmacodynamics

From a chemical standpoint, topiramate is a monosaccharide sulfamate replaced by related fructose, which is a relatively rare chemical structure for an anti-convulant. Topiramate is rapidly absorbed after oral administration. Most of the drug (70%) is excreted in urine.

The remainder is extensively metabolized by hydroxylation, hydrolysis and glucuronidation. Six metabolites have been identified in humans, none of which constitutes more than 5% of the administered dose. Topiramate stimulates chloride channels activated by GABA.  In addition, topiramate inhibits excitatory neuro-transmitters through actions on the kainate receptor and AMPA receptors.

There is evidence that topiramate has a specific effect on the kainate receptor GluR5.  It is also a carbonic anhydrase inhibitor, in particular subtypes II and IV, but this action is weak and is unlikely to be involved in the anticonvulsant activity, but it may explain the bad taste and the development of kidney stones during treatment.

Its possible effect as a mood stabilizer seems to occur before anticonvulsant qualities at lower doses. Topiramate inhibits seizures produced by maximal electroshock and pentylenetetrazole, as well as generalized tonic-clonic seizures and partial side of chips in the model, findings that are predictive of a broad spectrum of clinical activities.

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