Posted by Sad Panda on March 15, 2004, at 20:37:07
In reply to esoterica- sleep and trimipramine related, posted by zeugma on March 15, 2004, at 19:44:54
> Trimipramine seemed like a great idea, but then I came across this study that compared its effects on sleep to that of impramine:
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> Depression. 1996;4(1):1-13. Related Articles, Links
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> Trimipramine and imipramine exert different effects on the sleep EEG and on nocturnal hormone secretion during treatment of major depression.
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> Sonntag A, Rothe B, Guldner J, Yassouridis A, Holsboer F, Steiger A.
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> Max Planck Institute of Psychiatry, Department of Psychiatry, Munich, Germany.
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> In a 4-week double-blind clinical trial we compared the effects of the tricyclic antidepressants trimipramine and imipramine on the sleep EEG and on nocturnal bormone secretion in 20 male inpatients with major depression. Both treatments produced rapid significant clinical improvement in depression without severe adverse effects. However, the two drugs had markedly different neurobiologic profiles. Trimipramine enhanced rapid eye movement (REM) sleep and slow wave sleep, whereas imipramine suppressed REM sleep and showed no effect on slow wave sleep. Total sleep time and the sleep efficiency index increased under trimipramine but not under imipramine. Nocturnal cortisol secretion decreased with trimipramine but remained unchanged with imipramine. In contrast to imipramine, trimipramine induced an increase in prolactin secretion compatible with its known antagonism at dopamine (D2) receptors. Imipramine induced a decrease in growth hormone secretion during the first half of the night. Neither of the drugs induced significant changes in plasma testosterone concentration. We conclude that trimipramine is an antidepressant with sleep-improving qualities that possibly acts through inhibition of hypothalamic-pituitary-adrenocortical system activity by a yet unknown mechanism.
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> Publication Types:
> Clinical Trial
> Randomized Controlled Trial
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> PMID: 9160649 [PubMed - indexed for MEDLINE]
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> This suggests that trimipramine would not be a suitable treatment for narcolepsy-related problems, as the symptoms I have are related to sleep-onset REM periods (SOREMPs) and so I need powerful REM suppressants in order to get past the hypnagogic sleep-paralysis phenomena that inevitably disrupt my sleep within minutes of falling asleep. Imipramine is the TCA classically used, but nortriptyline works too, and the mechanism responsible is the amine reuptake blockade. Any of the TCA's should work, given high enough doses- I'll ask my pdoc at my next appointment what he thinks. But it looks like trimipramine is out.
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> There IS some significant research out now suggesting that trimipramine may be a good treatment for primary insomnia:
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> 1: Pharmacopsychiatry. 2002 Sep;35(5):165-74. Related Articles, Links
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> Trimipramine in primary insomnia: results of a polysomnographic double-blind controlled study.
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> Riemann D, Voderholzer U, Cohrs S, Rodenbeck A, Hajak G, Ruther E, Wiegand MH, Laakmann G, Baghai T, Fischer W, Hoffmann M, Hohagen F, Mayer G, Berger M.
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> Department of Psychiatry and Psychotherapy, University of Freiburg, Germany. dieter_riemann@psyallg.ukl.uni-freiburg.de
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> In recent years, sedating antidepressants have been increasingly used to treat primary insomnia. Up to now, only one open pilot study with trimipramine and one double-blind placebo-controlled study with doxepin have provided scientific support for this approach in treating primary insomnia. In order to test the hypothesis that sedating antidepressants are useful in the treatment of primary insomnia, the effect of trimipramine on objectively and subjectively measured parameters of sleep was investigated in a double-blind placebo- and lormetazepam-controlled study in a sample of 55 patients with primary insomnia attending outpatient sleep-disorder clinics. Trimipramine was selected since it has shown positive effects on sleep continuity with a lack of REM sleep suppression in studies on depressed patients and in one pilot study on patients with primary insomnia. Trimipramine at an average dose of 100 mg over a period of 4 weeks significantly enhanced sleep efficiency, but not total sleep time (which had been the primary target variable) compared to placebo as measured by polysomnography. Changes in objective sleep parameters were paralleled by changes in subjective sleep parameters. Trimipramine did not suppress REM sleep. Lormetazepam decreased wake time and sleep stage 3 and increased REM sleep compared to placebo. After switching trimipramine to placebo, sleep parameters returned to baseline. There was no evidence of any rebound effect from trimipramine. Side effects from trimipramine were only marginal. This first double-blind placebo-controlled study with trimipramine suggests its efficacy in the treatment of primary insomnia. However, due to the large intra- and interindividual variance in the parameters of interest before and during treatment a larger sample size would have been necessary to strengthen the validity of our findings.
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> Publication Types:
> Clinical Trial
> Controlled Clinical Trial
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> PMID: 12237787 [PubMed - indexed for MEDLINE]
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>Hi Zeugma,
Trimipramine is a potent H1 & 5-HT2A blocker. It's not as potent as Doxepin at H1 blockade but I believe it's is the most potent of TCA's at 5-HT2A blocking. Imipramine is very weak H1 & 5-HT2a blocker. This probably explains the difference in that sleep study.
Cheers,
Panda.
poster:Sad Panda
thread:324271
URL: http://www.dr-bob.org/babble/20040313/msgs/324778.html