Posted by cassandracomplex on March 24, 2013, at 16:17:20
In reply to PARNATE Disruption Of Circadian Rhythm, posted by vanvog on March 24, 2013, at 1:54:12
Yes, every time I've taken it. It's like the rules of sleep are thrown out the window: sometimes I sleep for 12 to 14 hours and sometimes I wake up 2 hours later and cannot fall asleep again for hours (if I fall asleep again at all). I take Ambien for sleep initiation and Klonopin for night terrors; I have taken Valium in the past for this purpose as well. I used to operate on an entirely artificial sleep schedule: Dexedrine one or two hours before I needed to wake up, my first dose of Parnate two to four hours after that, my second dose of Parnate an hour or two after that, sometimes another dose of Dexedrine in between, and Ambien, Seroquel, and Valium to fall asleep at night. I was on 120 mg of Parnate at this time and have taken from 70 to 120 mg therapeutically. Currently, I am on 70 mg.
The biggest problem for me is that stimulants - well, over-stimulate me. At least Dexedrine and Adderall. I'm not sure about any of the Ritalin analogues or Provigil; by the time I resorted to stimulants, my sleep was so disrupted that my job was in danger and I needed something that worked immediately and effectively. Back then, it was only hypersomnia, but now it's both.
There actually have been some studies on this.
1) Afternoon fatigue and somnolence associated with tranylcypromine treatment.
Joffe RT.
J Clin Psychiatry. 1990 May;51(5):192-3.ABSTRACT
The author examined a series of 23 depressed and 15 obsessive compulsive disorder outpatients who were treated with 40-80 mg/day of tranylcypromine to determine the frequency and clinical features of fatigue and somnolence. Four (all depressed) of the 38 patients experienced hypersomnolence and fatigue in the late afternoon. The somnolence was severe enough to impair their ability to work and drive. Afternoon fatigue and somnolence appear to be important and not uncommon side effects of tranylcypromine treatment.2) Severe daytime somnolence in patients treated with an MAOI.
Teicher MH, Cohen BM, Baldessarini RJ, Cole JO.
Am J Psychiatry. 1988 Dec;145(12):1552-6.ABSTRACT
Eight patients with hypersomnolent, anergic major depression benefited markedly from treatment with relatively high doses of phenelzine or tranylcypromine but experienced intense afternoon somnolence and disrupted sleep. Reducing the dose of monoamine oxidase inhibitor (MAOI) or substituting isocarboxazid sometimes provided relief, but altering the schedule of drugs or meals did not. Bedtime sedation alleviated the disrupted sleep but had little effect on daytime somnolence. The mechanism underlying this side effect is unknown; sleep deprivation, narcolepsy, or hypotension does not account for it. Patients given an MAOI should be assessed for this disturbance and cautioned to avoid risk of injury when it occurs.3) Influence of some monoamine oxidase inhibitors on the sleep-wakefulness cycle of the cat.
Oniani TN, Akhvlediani GR.
Neurosci Behav Physiol. 1988 Jul-Aug;18(4):301-6.ABSTRACT
The influence of some monoamine oxidase inhibitors (phenelzine, transamin [tranylcypromine], nialamide) on the structure of the sleep-wakefulness cycle of the cat was studied. It was shown that these monoamine oxidase inhibitors elicit and increase in slow-wave sleep in the sleep-wakefulness cycle due to complete suppression of paradoxical sleep and significant decrease in wakefulness. After the cessation of the action of the monoamine oxidase inhibitors, a selective rebound of wakefulness is observed against the background of complete or partial absence of paradoxical sleep. The gives grounds for the hypothesis that during partial deprivation of wakefulness under the influence of monoamine oxidase inhibitors an intensification occurs on the accumulation of specific need for this physiological state, the satisfaction of which is accomplished as the result of its rebound in the post-deprivational cycle, i.e., after the termination of the EEG of the synchronizing effect of the monoamine oxidase inhibitors.4) Monoamine oxidase inhibitors in resistant major depression. A double-blind comparison of brofaromine and tranylcypromine in patients resistant to tricyclic antidepressants.
Nolen WA, Haffmans PM, Bouvy PF, Duivenvoorden HJ.
J Affect Disord. 1993 Jul;28(3):189-97.ABSTRACT
In a double-blind study the selective monoamine oxidase-A inhibitor brofaromine was compared with the classical MAOI tranylcypromine in 39 patients with major depression resistant to treatment with tricyclic antidepressants. Concerning efficacy no significant differences were found. Ten out of 22 patients responded to brofaromine and 5 out of 17 patients to tranylcypromine. Adverse effects favoured brofaromine. Although orthostatic hypotension occurred in both groups, severe decrease in blood pressure and dizziness occurred significantly more with tranylcypromine. Both MAOIs caused a decrease in stage 4 and REM sleep and an increase in REM latency. In most patients receiving tranylcypromine REM sleep was completely abolished.5) Effects of tranylcypromine on the sleep of patients with anergic bipolar depression.
Jindal RD, Fasiczka AL, Himmelhoch JM, Mallinger AG, Thase ME.
Psychopharmacol Bull. 2003 Summer;37(3):118-26.ABSTRACT
A significant proportion of patients with bipolar disorder are hypersomnolent. It is not clear if this affects response to treatment because few studies have systematically examined treatment effects on sleep in patients with bipolar depression. Reported herein are the results of what we believe to be the first study of the effects of the monoamine oxidase inhibitor tranylcypromine (average dose=37 mg/day) on the sleep of patients with bipolar depression.Twenty-three patients with anergic bipolar depression completed sleep studies before and after pharmacotherapy. Changes in polysomnographic variables were examined using paired t tests. The patients experienced a 40% reduction in rapid eye movement (REM) sleep time, as well as significant decreases in REM percentage,REM activity, number of REM periods, and REM intensity.REM latency was prolonged by nearly 3-fold. The decrease in REM sleep was accompanied by a modest (8%) reduction in total sleep time and increased "light" sleep. There was no change in sleep continuity indices or slow wave sleep. Correlational analyses suggested that antidepressant response was only weakly associated with changes in REM sleep. These findings indicate that tranylcypromine's effects on REM sleep greatly surpass effects on sleep architecture or sleep maintenance. Moreover, effective treatment of bipolar depression did not "normalize" the hypersomnolence associated with bipolar depression.... and here's an interesting case report:
Partial sleep deprivation to prevent 48-hour mood cycles.
Churchill CM, Dilsaver SC.
Acta Psychiatr Scand. 1990 Apr;81(4):398-9.ABSTRACT
The course of a patient with the phenomenon of 48-h mood cycles, including her response to medication and to systematic partial sleep deprivation, is described. She had only a partial response to tranylcypromine alone. Partial sleep deprivation during the second half of alternate nights successfully prevented depressive mood cycles. Three to four weeks after discontinuing tranylcypromine she lost her ability to sustain this regimen. This case demonstrates an interaction between antidepressant medication and partial sleep deprivation in the prevention of depressive mood cycles.
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URL: http://www.dr-bob.org/babble/20130322/msgs/1040976.html