Letters to the Editor
Oxcarbazepine Treatment of Posttraumatic Stress Disorder
Posttraumatic stress disorder (PTSD) can be a difficult illness, because current treatment options are only partly effective (1). The disorder has been treated with anticonvulsants, based on the evidence that possible neuronal changes in the limbic system occur after exposure to trauma and cause a lowered arousal threshold that leads to reexperiencing symptoms (2). The literature since the 1980s has reported that carbamezapine reduces PTSD reexperiencing symptoms (3–5). I report a case in which a patient with PTSD was tried on numerous medications, including carbamezapine, and successfully treated with oxcarbazepine, which is chemically related to carbamezapine (6).
Mr A, aged 46 years, had a history of chronic PTSD and was treated over the years with several medications, including carbamezapine, valproate, fluoxetine, sertraline, nefazodone, trazodone, paroxetine, clonazepam, and buspirone. He thought that carbamezapine had helped him, but he felt “drugged” and admitted to a lack of compliance caused by frequent blood draws to monitor his carbamezapine serum levels. On initial evaluation, Mr A was taking sertraline 150 mg daily and clonazepam 0.5 mg twice daily. Shortly after passing a significant anniversary date, he experienced frequent nightmares, intrusive thoughts, and flashbacks. His score on the Hamilton Anxiety Rating Scale (HARS) (7) was 23, and his score on the Clinical Global Impression Severity (CGI-S) (8) was 7. His condition left him dysphoric and fatigued, which contributed to occupational impairment. Mr A agreed to a trial of oxcarbazepine, begun at 150 mg twice daily. Initial laboratory tests included a complete blood count, hepatic enzymes, and serum electrolytes, all within normal limits. After 1 week, the oxcarbazepine was raised to 300 mg twice daily, and a serum sodium check was within normal limits. After 2 weeks at 300 mg twice daily, Mr A’s dosage was increased to 450 mg twice daily. At this dosage, he began to experience less frequent and less severe nightmares. His HARS score decreased to 13, and his CGI Global Improvement score was 1. Mr A feels that he has significantly improved in all aspects of functioning since starting oxcarbazepine, especially at work. At 4 months, he maintains his high level of improvement, and his nightmares are infrequent.
Approved in the US in 1999, oxcarbazepine is an anticonvulsant used as an adjunct and as monotherapy to treat partial seizures in adults and as an adjunct to treat partial seizures in children from ages 4 to 16 years (9). The primary mechanism of action appears to be blockage of voltage-dependent sodium channels (9). The drug is structurally related to carbamezapine but is not metabolized to the 10,11-epoxide, which lessens the incidence of side effects associated with carbamezapine (10). Studies have shown oxcarbazepine to be as effective and better tolerated by patients having difficulties with carbamezapine, although this observation pertains to patients with epilepsy (10). Although hematologic and hepatic toxicity have not been reported, hyponatremia has been associated with oxcarbazepine (9). Common side effects related to oxcarbazepine use appear to be dosage-related and include somnolence, dizziness, vomiting, and nausea (11). Oxcarbazepine does not require serum monitoring (12); thus, frequent blood testing is not needed. Because this had been a factor in this patient’s previous noncompliance, and because he had experienced a decrease in his PTSD symptoms while on carbamezapine, he was expected to do well on oxcarbazepine. As with all single-case reports, caution is advised in interpreting results; however, based on this case, further studies done in a controlled fashion may be warranted.
References
1. Nutt DJ. The psychobiology of posttraumatic stress disorder. J Clin Psychiatry 2000; 61 (Suppl 5):24–9.
2. Keck PE, McElroy SL, Friedman LM. Valproate and carbamezapine in the treatment of panic and posttraumatic stress disorder, withdrawal states, and behavioral dyscontrol syndromes. J Clin Psychopharmacol 1992;12 (Suppl):36S–41S.
3. Lipper S, Davidson JRT, Grady TA, Edinger JD, Hammett ER, Mahorney SI, and others. Preliminary study of carbamezapine in post-traumatic stress disorder. Psychosomatics 1986;27:849–54.
4. Wolf ME, Alvai A, Mosnaim AD. Posttraumatic stress disorder in Vietnam veterans clinical and EEG findings; possible therapeutic effects of carbamezapine. Biol Psychiatry 1988;23:642–4.
5. Stewart JT, Bartucci RJ. Posttraumatic stress disorder and partial complex seizures. Am J Psychiatry 1986;143:113–4.
6. Grant SM, Faulds D. Oxcarbezapine: a review of its pharmacology and therapeutic potential in epilepsy, trigeminal neuralgia and affective disorders. Drugs 1992;43:873–88.
7. Hamilton M. The assessment of anxiety states by rating. Br J Med Psychol 1959;32:50–5.
8. National Institute of Mental Health. CGI: Clinical Global Impression. In: Guy W, Bonato RR, editors. Manual for the ECDEU Assessment Battery. Revised 2nd ed. Chevy Chase (MD): National Institute of Mental Health; 1970. 12.1–12.6.
9. McAuley JW, Biederman TS, Smith JC, Moore JL. Newer therapies in the drug treatment of epilepsy. Ann Pharmacother 2002;36:119–28.
10. Fisher RS. Epilepsy. In: Enna SJ, Coyle JT, editors. Pharmacologic management of neurological and psychiatric disorders. New York: McGraw Hill; 1998. p 459–503.
11. Barcs G, Walker EB, Elger CE, Scarmelli A, Stefan H, Sturm Y, and others. Oxcarbazepine placebo-controlled dose ranging trial in refractory partial epilepsy. Epilepsia 2000;41:1597–607.
12. Novartis.Trileptal package insert. East Hanover (NJ): Novartis; 2001.
Timothy Berigan, DDS, MD
Tucson, Arizona
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