uestion:
Does this patient have a history of substance abuse which would make
the use of benzodiazepines problematic due to the risk of dependency and
stimulation of craving for alcohol? uestion:
Does this patient have a history of substance abuse which would make
the use of benzodiazepines problematic due to the risk of dependency and
stimulation of craving for alcohol?
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Trazodone can be helpful at bedtime for sleep, particularly for the nightmares which disturb sleep in PTSD.* SSRI's may cause or exacerbate nightmares,** and we have found trazodone helpful for this, as well.
Benzodiazepines may be helpful for the daytime anxiety of PTSD patients, in addition to the antidepressants that patient is presumably receiving from the previous medication trials. Be on the lookout for SSRI-induced inhibition of benzodiazepine metabolism by cytochrome enzymes, especially fluoxetine and sertraline, if they are on board. The anticonvulsants valproic acid¹ and carbamazepine² are sometimes useful adjuncts for comorbid PTSD, especially for aggression and irritability, but not so much for dissociative experiences. (Be sure to take into consideration cytochrome induction by carbamazepine if the patient is on other drugs that are cytochrome substrates.) Lithium, beta-blockers, and MAOI's may also have a role³, and clonidine and guanfacine are advocated by some. (4) Buspirone has been used but this seems unlikely to be worthwhile after the thorough SSRI trials that would have occurred by this point in the algorithm.
The more severe the depressive symptoms in PTSD, the worse the prognosis with at least some pharmacotherapy (TCA's and MAOI's). There may be differential responsiveness depending on the amount of memory recovery: when the patient recovers long-forgotten memories, s(he) may enter a "flooded stage" of PTSD during which even previously helpful medications may become ineffective. The passage of time, group and individual treatment, and construction of an enhanced network of social support seem to facilitate acceptance of past events.
Some PTSD patients may exhibit a slowed-down appearance which seems like a melancholic depression. However, they may go in and out of these trancelike dissociative states in minutes or hours unlike the autonomousness of melancholic depression. Somatic therapy does not seem to work as well in these patients as it does in true melancholia.
Recommendation #31
¹Fesler FA. Valproate in combat-related PTSD. J Clin Psychiatry 1991;52:361-364.
²Looff D, Grimley P, Kuller F, et al. Carbamazepine for PTSD. J Am Acad Child Adolesc Psychiatry 1995;34(6):03-704.
³Silver JM, Sandberg DP, Hales RE. New approaches in the pharmacotherapy of PTSD. J Clin Psychiatry 1990;519suppl 10):33-38.
(4) Friedman MJ. Current and future drug treatment for PTSD patients. Psychiatric Annals 1998;28(8):461-468.
*Hertzberg MA, Felfman ME, Beckham JC, et al. Trial of trazodone for PTSD using a multiple baseline group design. J Clin Psychopharmacol 1996;16:294-298.
**Lefkifker E, Dannon PW, Iancu I, et al. Nightmares related to fluoxetine treatment. Clin Neuropharmacol 1995;18:90-94.
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Benzodiazepines are best avoided.
Trazodone can be helpful at bedtime for sleep, particularly for the nightmares which disturb sleep in PTSD.* SSRI's may cause or exacerbate nightmares,** and we have found trazodone helpful for this, as well.
The anticonvulsants valproic acid¹ and carbamazepine² are sometimes useful adjuncts for comorbid PTSD, especially for aggression and irritability, but not so much for dissociative experiences. Be sure to take into consideration cytochrome induction by carbamazepine if the patient is on other drugs that are cytochrome substrates. Lithium, beta-blockers, and MAOI's may also have a role.³ Buspirone has been used but this seems unlikely to be worthwhile after the thorough SSRI trials that would have occurred by this point in the algorithm. Clonidine, quanfacine, lithium, beta-blockers, and MAOI's may also be worth considering. (4)
The more severe the depressive symptoms in PTSD, the worse the prognosis with at least some pharmacotherapy (TCA's and MAOI's). There may be differential responsiveness depending on the amount of memory recovery: when the patient recovers long-forgotten memories, s(he) may enter a "flooded stage" of PTSD during which even previously helpful medications may become ineffective. The passage of time, group and individual treatment, and construction of an enhanced network of social support seem to facilitate acceptance of past events.
Some PTSD patients may exhibit a slowed-down appearance which seems like a melancholic depression. However, they may go in and out of these trancelike dissociative states in minutes or hours unlike the autonomousness of melancholic depression. Somatic therapy does not seem to work as well in these patients as it does in true melancholia.
Recommendation #32
¹Fesler FA. Valproate in combat-related PTSD. J Clin Psychiatry 1991;52:361-364.
²Looff D, Grimley P, Kuller F, et al. Carbamazepine for PTSD. J Am Acad Child Adolesc Psychiatry 1995;34(6):03-704.
³Silver JM, Sandberg DP, Hales RE. New approaches in the pharmacotherapy of PTSD. J Clin Psychiatry 1990;519suppl 10):33-38.
(4) Friedman MJ. Current and future drug treatment for PTSD patients. Psychiatric Annals 1998;28(8):461-468.
*Hertzberg MA, Felfman ME, Beckham JC, et al. Trial of trazodone for PTSD using a multiple baseline group design. J Clin Psychopharmacol 1996;16:294-298.
**Lefkifker E, Dannon PW, Iancu I, et al. Nightmares related to fluoxetine treatment. Clin Neuropharmacol 1995;18:90-94.
Show this place in the flowchart.