Posted by fachad on May 28, 2002, at 9:48:24
In reply to Unable to sleep yet again!, posted by Angel Girl on May 27, 2002, at 2:13:35
Hi Angel Girl,
I have been around and around with different sleep meds.
For me, as far as pure quality and quantity of sleep, there is nothing better than trimipramine. It is a brand only TCA, Surmontil. If that costs too much for you, doxepin is a cheap generic that is similar, but not quite as good.
Although trimipramine is classed as a TCA, it is actually very unique and different from all other TCAs. It does not inhibit reuptake of either norepenephrine or serotonin. It has very mild dopamine blocking ability.
I will attach some trimipramine abstracts at the end for those who like that sort of thing.
Ambien is very effective at inducing sleep, but worthless in maintaining sleep. It is also a very expensive brand only med. Its main value is that it brings on sleep very reliably and potently with no real side effects.
So, anyway, now I am taking trimipramine 25 mg and Ambien 5 mg and that is a very effective combo for me.
A very important thing about both of these sleep meds is that they do not disturb normal sleep architecture. Benzodiazapines like triazolam and Xanax make you FEEL like you slept well, but if you had been monitored in a sleep lab, the PSG and EEG printout would show that in reality, you did not.
Trimipramine has been shown to produce normal sleep patterns in sleep lab studies.
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Trimipramine for Sleep Abstracts
Drugs 1989;38 Suppl 1:14-6; discussion 49-50 Related Articles, Books, LinkOut
Sleep polygraphic effects of trimipramine in depressed patients. Preliminary report.Mouret J, Lemoine P, Minuit MP, Sanchez P, Taillard J.
Clinical Unit of Biological Psychiatry, Hopital du Vinatier, Lyon, France.
Preliminary results are presented from an ongoing study in hospitalised depressed patients. Changes in sleep parameters were assessed on days 1 to 3 and 12 to 14 of a 4-week study in which patients received trimipramine 150 mg on day 1 and 100 mg thereafter. On days 1 to 3 and 12 to 14, 7 depressed patients had a significantly increased total sleep time and sleep efficiency index and a significantly decreased total wake time and number of intrasleep wake episodes per hour of sleep. Trimipramine treatment had no significant effect on REM sleep, percentage of REM sleep, REM duration and REM sleep stability index. However, a significant increase in REM latency was noted on days 1 to 3 but not on days 12 to 14. These polygraphic data suggest that trimipramine effects a very rapid and maintained sleep improvement in these depressed patients without significant alterations to the parameters of REM sleep.
Drugs 1989;38 Suppl 1:17-24; discussion 49-50 Related Articles, Books, LinkOut
A review of trimipramine. 30 years of clinical use.Lapierre YD.
University of Ottawa, Royal Ottawa Hospital, Canada.
The hybrid chemical structure of trimipramine incorporates an imipramine nucleus and levomepromazine side chain. This structure predicts much of the clinical profile of trimipramine. The initial studies on trimipramine date back nearly 30 years. It now has a well-recognised clinical profile with some characteristics akin to other tricyclic antidepressants (TCA) and others which are quite distinct. It is well established as a highly effective antidepressant with an efficacy profile similar to the other TCAs. Clinically, its anxiolytic and sedative properties distinguish it from most other TCAs. Its effects on sleep architecture are unique and explain some of its unique properties. The side effect profile of trimipramine is in some ways similar to those of the tertiary amine TCAs with a preponderance of anticholinergic and sedative effects. Its cardiotoxic properties are minimal, with some findings suggesting a very favourable profile. Interactions with other drugs, psychotropic or non-psychotropic, are compatible with its pharmacological profile. These are reviewed with its clinical applications in mind. The pharmacokinetic characteristics of trimipramine differ from those of many of the other TCAs. The application of this to clinical situations is addressed. Based on experience using trimipramine, a profile of 'ideal' patient characteristics has been built up. Finally, the use of trimipramine in selected patient populations is reviewed.
Eur J Clin Pharmacol 1989;37(2):145-50 Related Articles, Books, LinkOut
Modulation of sleep by trimipramine in man.Nicholson AN, Pascoe PA, Turner C.
Royal Air Force Institute of Aviation Medicine Farnborough, Hampshire, UK.
We have studied the acute effect of trimipramine (25, 50 and 75 mg) on nocturnal sleep in 6 young men. Fluoxetine (60 mg) and diazepam (10 mg) were included as controls for the potential changes in sleep measures. Trimipramine reduced awake activity, Stage 1 (drowsy) sleep, and the duration of rapid eye movement (REM) sleep. Non-REM (Stage 2) sleep was increased. Residual effects of trimipramine were present the next morning (9 h after ingestion) with impaired coding ability. The effects of trimipramine on sleep and daytime alertness are consistent with its complex pharmacological profile. Reduced wakefulness and sedation are most likely due to synergism between histamine H1, alpha 1-adrenoceptor, and dopamine receptor antagonism. Anticholinergic activity and possibly blockade of alpha 1-adrenoceptors would disturb the balance of transmitter activities which facilitates the optimal appearance of REM sleep. In this way the effects of trimipramine on nocturnal wakefulness and REM sleep are similar to drugs which inhibit the uptake of noradrenaline.
Sleep 1989 Dec;12(6):537-49 Related Articles, Books, LinkOut
Effects on sleep: a double-blind study comparing trimipramine to imipramine in depressed insomniac patients.Ware JC, Brown FW, Moorad PJ Jr, Pittard JT, Cobert B.
Department of Psychiatry and Behavioral Medicine, Eastern Virginia Medical School, Norfolk.
Trimipramine, a sedating tricyclic antidepressant, and imipramine were compared on polysomnographic parameters during a 4-week double-blind trial in depressed patients with insomnia and anxiety. Trimipramine eliminated objective evidence of sleep disturbance. This was not the case with imipramine, although depression improved similarly in both groups. Subjects' sleep appeared unchanged or more disturbed at the end of the treatment with imipramine. For trimipramine, the major changes in sleep parameters occurred during the first week of drug administration and did not parallel the gradual changes seen in the measures of depression. Additionally, trimipramine did not suppress REM sleep even in a subgroup of six trimipramine patients who had short rapid-eye-movement (REM) sleep latencies during the placebo baseline period, even though their depression was alleviated. The data demonstrate that (a) antidepressants may vary in their effects on sleep, even though they have similar effects on depression; (b) REM sleep suppression does not necessarily accompany improvement in depression; and (c) reports of improved sleep by patients undergoing antidepressant therapy may not reflect improvement on objective measures of sleep. The different sleep effects suggest the possibility of different antidepressant pathways.
J Affect Disord 1992 Mar;24(3):135-45 Related Articles, Books, LinkOut
Trimipramine: acute and lasting effects on sleep in healthy and major depressive subjects.Feuillade P, Pringuey D, Belugou JL, Robert P, Darcourt G.
Clinique de Psychiatrie et de Psychologie Medicale, Hopital Pasteur, Nice, France.
The acute effects of trimipramine on sleep EEG patterns were investigated in six depressed inpatients and six healthy volunteers. The effects of long-term administration were then assessed in depressed patients after 4 weeks of treatment. Sedative effects of the drug were more pronounced in healthy subjects while sleep parameters of depressed patients seemed less sensitive to the drug. Chronic effects tended to correct most of the sleep disturbances seen in depressed subjects with respect to the natural organization of sleep. The major sleep effect of trimipramine concerned REM latency which was lengthened in both groups, independently of the treatment protocol.
Eur Arch Psychiatry Clin Neurosci 1994;244(2):65-72 Related Articles, Books, LinkOut
Treatment of primary insomnia with trimipramine: an alternative to benzodiazepine hypnotics?Hohagen F, Montero RF, Weiss E, Lis S, Schonbrunn E, Dressing H, Riemann D, Berger M.
Department of Psychiatry, University of Freiburg, Germany.
A group of 19 middle aged patients suffering from primary insomnia according to the DSM-III-R were treated in a single-blind study with trimipramine, a sedating antidepressant. A total of 15 patients completed the study protocol and were evaluated. The present pilot study aimed at investigating the sleep-inducing properties of trimipramine, and at clarifying the question of whether short- or long-term rebound insomnia occurs after discontinuation of this drug. At four measurement points, i.e. under baseline conditions, under treatment and 4 and 14 days after drug discontinuation, sleep was recorded with an ambulatory-electroencephalogram (EEG) monitoring device in the patient's home environment. Simultaneously, psychometric tests were applied to measure withdrawal symptoms, subjective sleep quality and well-being during daytime. Trimipramine at a mean dose of 166 +/- 48 mg led to a significant increase in sleep efficiency, total sleep time, and stage 2% sleep-period time (SPT), whereas a significant decrease in wake time and stage 1% SPT was noted. Insomniac patients reported an improvement in subjectively perceived sleep quality following trimipramine. Additionally, an improvement in well-being during the daytime occurred. Negative side effects were limited to dry mouth due to the anticholinergic properties of the drug. Discontinuation of trimipramine did not provoke either short- or long-term rebound insomnia in objective and subjective sleep measurements considering mean values of the whole sample, although a subgroup of patients did display total sleep times below baseline values during short- and long-term withdrawal, but generally without a concomitant worsening of sleep quality according to the sleep questionnaire.
Eur Arch Psychiatry Clin Neurosci 1996;246(5):235-9 Related Articles, Books, LinkOut
Trimipramine: a challenge to current concepts on antidepressives.Berger M, Gastpar M.
Klinikum, Albert-Ludwigs-Universitat, Freiburg, Germany.
Although it is chemically a classical tricyclic antidepressant agent, trimipramine shows atypical pharmacological properties. Its well-documented antidepressant action cannot be explained by noradrenaline or serotonin reuptake inhibition or by a down-regulation of beta-adrenoceptors. Furthermore, its receptor affinity profile resembles more that of clozapine, a neuroleptic drug, than that of tricyclic antidepressants. Trimipramine does not reduce, but rather increases, rapid eye movement sleep. It stimulates nocturnal prolactin secretion and inhibits nocturnal cortisol secretion and may act at the level of the hypothalamus on corticotropin-releasing hormone secretion. Trimipramine is of particular value in depressed patients with insomnia, and it has been shown to be effective in the therapy of primary insomnia. As the pharmacological profile indicates, and an open clinical study has shown, trimipramine might also be active as an antipsychotic. The drug is both a tool for increasing our understanding of depression and a potential therapy for several psychiatric disorders.
Depression 1996;4(1):1-13 Related Articles, Books, LinkOut
Trimipramine and imipramine exert different effects on the sleep EEG and on nocturnal hormone secretion during treatment of major depression.Sonntag A, Rothe B, Guldner J, Yassouridis A, Holsboer F, Steiger A.
Max Planck Institute of Psychiatry, Department of Psychiatry, Munich, Germany.
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.
> It seems every night I'm here late, unable to sleep even though I have taken my Triazolam. I've even resorted to also taking a Xanax to help induce sleepiness. All to no avail. :(
>
> Does anybody have any suggestions???
>
> Angel Girl
poster:fachad
thread:107701
URL: http://www.dr-bob.org/babble/20020525/msgs/107821.html