Differential effects of amitriptyline and of zimelidine on the sleep electroencephalogram of depressed patients

Shipley, James E.; Kupfer, David J.; Dealy, Robert S.; Griffin, Suzanne; Coble, Patricia A.; McEachran, Ann B.; Grochocinski, Victoria J.

doi:10.1038/clpt.1984.171

Cited by 46 publications

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“…This study confirmed an earlier report of the immediate effects of fluvoxamine on sleep in patients with depression (58). Zimelidine also increases the amount of wakefulness during the night and shows REM-suppressing effects in patients with depression (59,28). Conversely, citalopram appeared to suppress REM sleep and increase REM latency without significant deleterious effects on sleep continuity or wakefulness during the night in a study of patients over 6 weeks of treatment (60).…”

Section: Other Ssrissupporting

confidence: 89%

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The Effects of Antidepressants on Sleep in Patients with Depression

Armitage

2000

Can J Psychiatry

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As assessed by laboratory studies, sleep abnormalities in those with major depressive disorders can be classified as difficulties initiating and maintaining sleep, abnormal sleep architecture, and disruptions in the timing of rapid eye movement (REM) sleep. Sleep initiation and maintenance difficulties include prolonged sleep latency (sleep onset insomnia), intermittent wakefulness and sleep fragmentation during the night, early morning awakenings with an inability to return to sleep, reduced sleep efficiency, and decreased total sleep time. With regard to sleep architecture, abnormalities have been reported in the amounts and distribution of nonrapid eye movement (NREM) sleep stages across the night. These include increased light, stage 1 sleep and reductions in the amount ofdeep, slow-wave (stages 3 and 4) sleep. REM sleep disturbances in patients with depression include a short latency (65 minutes) to the first REM sleep, a prolonged first REM sleep period, and increased total REM sleep time, particularly in the first one-half of the night (1-3).Sleep disturbances are generally more prevalent among inpatients with depression (80%), whereas only 40% to 60% of outpatients show sleep abnormalities (4). A recent metaanalysis, however, indicated that no single sleep variable reliably distinguished patients with depression from healthy controls Manuscript

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Section: Other Ssrissupporting

confidence: 89%

“…Clomipramine and desipramine are 2 ofthe most potent REM-suppressing TCAs, followed by imipramine and nortriptyline (25)(26)(27)(28)(29). Clomipramine, desipramine, and amitriptyline also significantly increase stage I sleep and decrease sleep efficiency over baseline levels (29).…”

Section: Tricyclicsmentioning

confidence: 99%

The Effects of Antidepressants on Sleep in Patients with Depression

Armitage

2000

Can J Psychiatry

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“…It has been postulated that the anticataplectic action of tricyclics is mediated by REM suppression. In previous studies, short-term administration of large doses of zimelidine produced some degree of REM suppression in animals (24) and in human depressed patients (25). However, in the present study, no REM suppression was seen during nocturnal or diurnal sleep recordings except for the first morning nap.…”

Section: Physiopathology Of Cataplexycontrasting

confidence: 51%

Serotoninergic Reuptake Mechanisms in the Control of Cataplexy

Montplaisir

1986

Sleep

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Summary: Zimelidine, a selective inhibitor of serotonin (5-HT) reuptake in the CNS, was administered to narcoleptic patients. This medication has a potent anticataplectic action without improving daytime somnolence. These results suggest that 5-HT neuronal systems are involved in the physiopathology of cataplexy. Zimelidine, however, has no anticholinergic effect, so it is unlikely that cholinergic mechanisms thought to be important in animal cataplexy would playa major role in human cataplexy. In addition, zimelidine had no effect on nocturnal sleep patterns of these patients which is surprising considering the importance of 5-HT neuronal systems in sleep physiology. A 5-HT hypothesis of cataplexy is formulated, and the mechanisms of action of other anticataplectic agents are discussed.Key Words: Narcolepsy-Cataplexy-Serotonin-Zimelidine-Myoclonus.Narcoleptic patients complain of two major symptoms, namely, excessive daytime sleepiness (EDS) and cataplexy. Clinical data suggest that different mechanisms are involved in these two symptoms. In most patients, EDS and cataplexy do not develop simultaneously, and there is no correlation between the intensity of the two symptoms. Pharmacological studies also suggest that different mechanisms are involved. For instance, drugs known to improve EDS have little or no effect on cataplexy, and, conversely, most anticataplectic medications do not relieve the complaint of EDS (1).In humans, EDS most likely involves dopaminergic mechanisms in the central nervous system (CNS). For instance, low concentrations of free dopamine (DA) (2) and of homovanillic acid (HVA) (3), the main metabolite of DA, were found in the cerebrospinal fluid (CSF) of narcoleptic patients. In addition, psychostimulants effective to treat daytime sleepiness selectively decrease DA reuptake (4).The pathophysiology of cataplexy is more controversial. In humans, most data come from pharmacological studies (5). Although there is no controlled study comparing the potency of various anticataplectic agents, our clinical experience indicates that chlorimipramine is the most effective medication. Among anticataplectic agents, chlorimipramine also happens to be the most potent 5-HT reuptake blocker (6). We hypothesize that this mechanism is responsible for the anticataplectic action of this medication. However, chlorimipramine has also a strong anticholinergic action, and desmethylchlorimipramine, its main metabolite, is a norepinephrine (NE) reuptake blocker in the CNS. The anticholinergic

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“…administration, there is evidence of tolerance with some measures of REM activity during long-term treatment, particularly in patients [33,36] . However, little is known about the long-term effects on sleep in healthy volunteers.…”

Section: Discussionmentioning

confidence: 99%

Sleep Laboratory Study on Single and Repeated Dose Effects of Paroxetine, Alprazolam and Their Combination in Healthy Young Volunteers

et al. 2005

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Aims: To evaluate the potential interaction of 20 mg paroxetine and 1 mg alprazolam (early morning once-daily administration) on polysomnographic (PSG) sleep and subjective sleep and awakening quality, both after a single intake and after reaching a steady-state concentration. Methods: Twenty-two (11 for the PSG) healthy young volunteers of both sexes with no history of sleep disturbances (Pittsburgh Sleep Quality Index <5) participated in a double-blind, double-dummy, placebo-controlled, repeated-dose, 4-period, cross-over study. All volunteers received all 4 treatment sequences: paroxetine–alprazolam placebo (PAP); paroxetine placebo–alprazolam (PPA); paroxetine–alprazolam (PA), and paroxetine placebo–alprazolam placebo (PLA), in a randomized order. Each treatment was administered over 15 consecutive days, with a treatment-free interval of 7 days prior to the subsequent study period. In each experimental period, one PSG sleep study was performed on the 1st night (single-dose effects) and another study was performed on the 15th night (repeated-dose effects). Additionally, two other PSG studies were assessed: an adaptation recording, and a control night recording. All-night PSG recordings were obtained following standard procedures. Each 30-second period was scored according to the criteria of Rechtschaffen and Kales by means of an automatic sleep analysis system: Somnolyzer 24x7^TM. A self-rating scale for sleep and awakening quality and early morning behavior was completed no later than 15 min after awakening over the 15 days of each experimental intervention. General lineal models (treatment/time) were applied separately to each variable. Results: (1) No significant effects were observed in any sleep variables when control nights were compared with the 1st night with PLA. (2) Sleep continuity: After PAP a clear awakening effect was seen both in the first and second evaluations, mainly in wake time, movement time, number of awakenings and stage-1 duration. After PPA an evident hypnotic effect was observed on night 1. This effect was mainly observed in maintenance variables and slightly in sleep initiation variables; it had decreased by night 15. After PA an intermediate behavior in the variables related to sleep continuity was seen, highlighting the absence of the tolerance phenomenon observed when PPA was administered alone. (3) Sleep architecture: The most important effects in REM sleep were observed after PAP; an increase in REM latency and decreases in REM sleep. PAP also induced decreases in the number of non-REM and REM periods and increases in the average duration of non-REM periods and sleep cycles. PA presented a similar pattern to PAP, and PPA similar to PLA. In relation to non-REM sleep, PA showed more stage-2 and less slow-wave sleep (SWS). (4) Subjective perception: No significant differences were observed between treatments while they were being taken, but impairments in subjective sleep quality, awaking quality, latency and efficiency were seen, mainly after PA but also after PPA discon...

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Differential effects of amitriptyline and of zimelidine on the sleep electroencephalogram of depressed patients

Cited by 46 publications

References 0 publications

The Effects of Antidepressants on Sleep in Patients with Depression

The Effects of Antidepressants on Sleep in Patients with Depression

Serotoninergic Reuptake Mechanisms in the Control of Cataplexy

Sleep Laboratory Study on Single and Repeated Dose Effects of Paroxetine, Alprazolam and Their Combination in Healthy Young Volunteers

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