Posted by zeugma on July 6, 2004, at 16:40:38
In reply to Re: vegetative depression, nortriptyline dosage, posted by SLS on July 6, 2004, at 16:05:58
> Hi Zeugma.
>
> > II began getting hypnagogic/hypnopompic hallucinations (dreamlike states mixed with features of waking consciousness) at the age of 23. At times I have the 'dream within a dream' (false awakening) experience and when I actually wake up, less than 5 minutes have gone by on the clock. As far as I know, the images formed during stage 1 sleep do not have this quality at all; it aapears to be confined to REM states.
>
> > These hallucinations/premature REM events are blocked to varying extents by nortriptyline, buspirone, and Strattera, but not by clonazepam, and of these four medications, only clonazepam is not a strong REM inhibitor.
>
> > When I took Strattera at the same time as clonazepam, and then fell asleep, I did not experience these states, consistent with Strattera's rapid absorption and powerful REM-suppressing effect (for more on this see http://www.sro.org/pdf/863.pdf, which used Strattera's cousin, nisoxetine). When I fell asleep after taking Provigil, I experienced extremely vivid dreams and did not feel rested at all.
>
>
> Have you developed any tolerance to the REM inhibiting effects of these drugs?
>
> When I first took tricyclics and MAOIs, they had a profound effect in reducing or completely abolishing dreaming and presumably REM sleep in me. Upon discontinuation of these drugs, I would experience an intense REM rebound where I would experience the type of waking dreams you described. These things don't happen to me anymore. I wish they did.
>
>
> - Scott
Hi Scott,I haven't developed tolerance to the REM suppressing effects yet. I've only been on nortriptyline for about two years now (I was on it for a year and a half in my early 20's also- maybe that played a role in triggering the REM events at 23? though I had discontinued at 22). Did you find that mood improvement correlated with REM suppression?
I wonder if anyone has investigated poopout in terms of tolerance to REM suppression. From what I've been able to dredge up, it's the initial period of sleep (REM latency) that is crucial for maintainance of response:
: Biol Psychiatry. 1997 Oct 1;42(7):560-7. Related Articles, Links
Maintenance nortriptyline effects on electroencephalographic sleep in elderly patients with recurrent major depression: double-blind, placebo- and plasma-level-controlled evaluation.Reynolds CF 3rd, Buysse DJ, Brunner DP, Begley AE, Dew MA, Hoch CC, Hall M, Houck PR, Mazumdar S, Perel JM, Kupfer DJ.
Mental Health Clinical Research Center for the Study of Late-Life Mood Disorders, University of Pittsburgh Medical Center, Pennsylvania, USA.
Our aim was to contrast the effects of maintenance nortriptyline and placebo on electroencephalographic sleep measures in elderly recurrent depressives who survived 1-year without recurrence of depression. Patients on nortriptyline took longer to fall asleep and did not maintain sleep better than patients on placebo; however, maintenance nortriptyline was associated with more delta-wave production and higher delta-wave density in the first non-REM (NREM) period relative to the second. Nortriptyline levels were positively but weakly related to all-night delta-wave production during maintenance (accounting for 6.6% of the variance in delta-wave counts). Total phasic REM activity increased 100% under chronic nortriptyline relative to placebo, with a robust increase in the rate of REM activity generation across the night. Effective long-term pharmacotherapy of recurrent major depression is associated with enhancement in the rate of delta-wave production in the first NREM period (i.e., delta sleep ratio) and of REM activity throughout the night.
Many of the same people have been working on a theory of depression (or a certain type of depression: there are clearly many types of depression) as linked to abnormal REM/NREM patterns. I had thought this work had been abandoned years ago, with the advent of SSRI's and the total domination of research funded by companies promoting them, but here it is:: Psychiatry Res. 2000 Apr 10;98(2):71-91. Related Articles, Links
Towards a neurobiology of dysfunctional arousal in depression: the relationship between beta EEG power and regional cerebral glucose metabolism during NREM sleep.Nofzinger EA, Price JC, Meltzer CC, Buysse DJ, Villemagne VL, Miewald JM, Sembrat RC, Steppe DA, Kupfer DJ.
Department of Psychiatry, Western Psychiatric Institute and Clinic, 3811 O'Hara Street, Pittsburgh, PA 15213-2593, USA. nofzingerea@msx.upmc.edu
This study sought to clarify the neurobiological basis of variations in one aspect of central nervous system 'arousal' in depression by characterizing the functional neuroanatomic correlates of beta electroencephalographic (EEG) power density during non-rapid eye movement (NREM) sleep. First, nine healthy (n=9) subjects underwent concurrent EEG sleep studies and [18F]2-fluoro-2-deoxy-D-glucose ([18F]FDG) positron emission tomography (PET) scans during their first NREM period of sleep in order to generate hypotheses about specific brain structures that show a relationship between increased beta power and increased relative glucose metabolism. Second, brain structures identified in the healthy subjects were then used as a priori regions of interest in similar analyses from identical studies in 12 depressed subjects. Statistical parametric mapping was used to identify the relationship between beta power and relative regional cerebral glucose metabolism (rCMRglu) during NREM sleep. Regions that demonstrated significant correlations between beta power and relative cerebral glucose metabolism in both the healthy and depressed subjects included the ventromedial prefrontal cortex and the right lateral inferior occipital cortex. During a baseline night of sleep, depressed patients demonstrated a trend toward greater beta power in relation to a separate age- and gender-matched healthy control group. In both healthy and depressed subjects, beta power negatively correlated with subjective sleep quality. Finally, in the depressed group, there was a trend for beta power to correlate with an indirect measure of absolute whole brain metabolism during NREM sleep. This study demonstrates a similar relationship between electrophysiological arousal and glucose metabolism in the ventromedial prefrontal cortex in depressed and healthy subjects. Given the increased electrophysiological arousal in some depressed patients and the known anatomical relations between the ventromedial prefrontal cortex and brain activating structures, this study raises the possibility that the ventromedial prefrontal cortex plays a significant role in mediating one aspect of dysfunctional arousal found in more severely aroused depressed patients.
PMID: 10762734 [PubMed - indexed for MEDLINE]
-z
poster:zeugma
thread:363009
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