The effects of antidepressants on sleep in patients with depression.

This paper reviews sleep disturbances in patients with major depressive disorders and the effects of different classes of antidepressants on sleep. It is clear from the studies reviewed that not all antidepressants improve sleep, and, indeed, some worsen sleep disturbances in patients with depression. Whether sleep is improved or further disrupted is of high clinical significance, because persistent sleep problems elevate the risk of relapse, recurrence, or suicide, as well as the need for augmenting medications.     

The effects of trazodone on sleep disturbances induced by brofaromine.

The effects of trazodone on subjective and objective sleep parameters were compared to those of placebo in a double-blind design in seven patients who developed insomnia during treatment with the selective and reversible MAO-A inhibitor, brofaromine. Trazodone significantly increased deep sleep and altered the architecture of sleep in these patients. Subjectively, patients reported a better and deeper sleep. No negative interactions between brofaromine and trazodone were observed and side-effects were minimal. A low dose of trazodone may be a safe and effective agent in the treatment of MAO-I induced insomnia.     

The effects of antidepressants on sleep: a review

Sleep disturbances are a frequent complication of depressive disorders and their treatment. Familiarity with the interaction among sleep, depression, and antidepressant medications may assist the clinician in selecting agents to suit the needs of individual patients. The authors review the current knowledge of changes in sleep architecture associated with particular antidepressant agents and with depressive illness, as well as the theoretical relevance of such changes to the antidepressant effect. Articles for review were found through a Medline search on the terms "polysomnography," "sleep," "antidepressants," and "insomnia" in English-language papers published from 1966 through March 2000. Additional articles were found in the reference lists of relevant papers.     

The link between sleep and depression: The effects of antidepressants on EEG sleep

The assumption that sleep dysregulation is more than a mere epiphenomenon of depression is based on several observations: sleep disturbances are strongly associated with the depressive state; a number of sleep manipulations can alleviate symptoms of depression in some patients; and the majority of antidepressants bring about remarkable changes in sleep polygraphic variables. An obvious question is whether changes in sleep physiological processes are intimately involved in the pathogenesis and recovery from depression. One way to elucidate the link between sleep and depression is to examine whether the influence of antidepressants on sleep is related to clinical improvement in depressives. For that purpose, the effects of antidepressants on EEG sleep and their importance for the treatment of depression are summarized against the background of two existing hypotheses concerning the link between sleep and depression: one hypothesis concerning the role of REM; the other concerning the role of non-REM sleep. EEG sleep studies on the use of antidepressants in depressives have not produced clear evidence of the involvement of REM sleep or non-REM sleep in the mechanisms underlying clinical change. Furthermore, the role of sleep physiological mechanisms during treatment with antidepressants is still unclear. To interpret the effects of antidepressants on EEG sleep in terms of sleep physiological processes more fundamental sleep research is necessary. Also, more comparative studies of antidepressants with similar therapeutic effects but different pharmacological profiles are needed in both healthy and depressed subjects to further quantify the impact of EEG sleep modification in the recovery from depression and to differentiate between pharmacological and sleep-related aspects.     

The jitteriness syndrome in panic disorder patients treated with antidepressants

The jitteriness syndrome (jitteriness, shakiness, increased anxiety, and insomnia) can develop with low doses of tricyclic antidepressants in patients who are sensitive to these drugs. The authors review the antidepressant treatment of 180 patients. Only those with panic attacks had jitteriness, usually during the first week of treatment. Desipramine was associated with a much higher frequency of jitteriness than was imipramine. Tolerance to jitteriness occurred with continued treatment, but fewer patients with jitteriness responded to treatment, apparently because of difficulties in increasing the dose. Characteristics of the jitteriness syndrome in panic disorder patients are consistent with noradrenergic hypotheses of panic anxiety. The clinical and theoretical implications of these findings are discussed.     

Occurrence of myoclonus in patients treated with cyclic antidepressants

Myoclonus associated with cyclic antidepressant therapy has been considered to be a rare phenomenon. Ninety-eight patients who were to begin receiving cyclic antidepressant therapy were prospectively evaluated for myoclonus. Thirty patients experienced clinically insignificant drug-associated myoclonus. Nine patients had clinically significant myoclonus. The myoclonus was reversible with the discontinuation of therapy but tended to persist if medication changes were not made. None of the tested clinical variables were able to predict which patients would develop myoclonus.     

One-year seizure prognosis in epilepsy patients treated with antidepressants

To investigate the clinical effects of antidepressants on seizure frequency of patients with epilepsy treated with antiepileptic drugs, we retrospectively evaluated the 1-year course of seizure frequency. One hundred twenty-one patients with epilepsy treated with antidepressants and 300 patients with epilepsy not treated with antidepressants (controls) were the subjects of this study. Seizure frequency over the 1-year period of administration of antidepressants was retrospectively evaluated and compared with that for controls. In the patients with epilepsy taking antidepressants, seizure frequencies at four observation points (1, 3, 6, and 12 months after starting antidepressants) were equivalent to those of the control group. There was no significant difference in seizure frequency between first- and second-generation antidepressants. Patients with epilepsy treated with antiepileptic drugs can take antidepressants without a significant risk of exacerbation of seizures. Most antidepressants can be used for psychiatric treatment of patients with epilepsy.     

The effects of lamotrigine on sleep in patients with epilepsy

PURPOSE: The older antiepileptic drugs (AEDs) have a variety of effects on sleep, including marked reduction in REM, slow-wave sleep (SWS) and sleep latency, and increased percentage of light sleep. The effects of the newer AEDs on sleep are unknown. Our purpose was to study the effect of lamotrigine (LTG) on sleep. METHODS: Ten adults with focal epilepsy, in whom the decision was made to add LTG to either phenytoin (PHT) or carbamazepine (CBZ) for control of seizures, were the subjects of this study. Patients underwent pre- and posttreatment polysomnography (PSG) and completed sleep questionnaires. Polygraphic variables and Epworth Sleepiness Scale (ESS) scores, a subjective measure of sleep propensity, were compared by using the Wilcoxon sign rank test. RESULTS: Seven patients were taking CBZ, and three were treated with PHT. All subjects were titrated to an LTG dose of 400 mg/day. Treatment with LTG produced a significant decrease in SWS and an increase in stage 2 sleep percentage. No significant difference in ESS or any of the other polygraphic variables was observed. However, LTG treatment was associated with a reduction in arousals and stage shifts and an increase in REM periods. No subjects reported insomnia with treatment. CONCLUSIONS: LTG appears to be less disruptive to sleep than some of the older AEDs.     

Spontaneous treatment discontinuation in panic disorder patients treated with antidepressants

OBJECTIVE: We examined the relationships between long-term treatment response, side-effects and drug discontinuation in panic disorder (PD)-agoraphobia. METHOD: A total of 326 patients were naturalistically treated with antidepressants and followed for a period of 3 years. All patients were evaluated by means of the Panic Disorder/Agoraphobia Interview and the Longitudinal Interview Follow-up Examination (LIFE-UP). RESULTS: A total of 179 patients interrupted pharmacological treatment. Among them, 26.8% were not traceable; 36.9% had deemed further contact with the psychiatrist unnecessary because of remission. Other reasons for interruption were: ineffectiveness (18.4%), side-effects (10.6%) and personal reasons (7.3%). Patients who interrupted pharmacological treatment because of symptom remission remained in the study for a longer period than those patients who interrupted their treatment because of inefficacy. CONCLUSION: In the long-term treatment of PD with antidepressants, a high percentage of patients who have achieved symptom remission tend to default from further treatment; adherence to long-term treatment with antidepressants was predicted by severe and long-lasting symptomatology.     

Increased libido in three men treated with trazodone

Two sexual side effects associated with trazodone have been reported: priapism in men and increased libido in women. This report describes three depressed men who had increased libido while receiving trazodone. Possible mechanisms are suggested. Research is needed to explore trazodone's usefulness in treating disorders of sexual desire.     

A prospective naturalistic study of 326 panic-agoraphobic patients treated with antidepressants

OBJECTIVE: How far the results of randomized controlled studies apply to everyday care cannot be judged without regular measurements of outcomes in daily practice. We report on systematic data from a 3-year naturalistic prospective study on panic disorder-agoraphobic (PDA) patients treated with antidepressants in a setting of routine clinical practice. Our aim is to describe the evolution of PDA in relation to the treatments employed, and to explore demographic and clinical characteristics that might be predictive of outcome. METHODS: 326 DSM-III-R PDA patients treated with antidepressants in a setting of routine clinical practice were included in a 3-year naturalistic prospective study. We utilized structured and semi-structures instruments, including the Structured Clinical Interview for Diagnosis and the Longitudinal Interview Follow-up Examination. The main antidepressants used were imipramine (39%), clomipramine (28.5%) and paroxetine (23.3%); only 9% of patients received other antidepressants. RESULTS: 147 patients (45.1%) stayed on medication throughout the entire period of the follow-up. Of those who interrupted the treatment, 38% stayed in remission. The probability of achieving at least one remission during the 3-year follow-up period was 96.5% for PD and 95.9% for Agoraphobia. Relapses after a period of at least 2 months of complete remission were also common, and the probability of presenting at least one relapse during the 3-years follow-up period was 67.1% for PD and 39% for Agoraphobia. The longest period of remission of PD is associated with low severity, medium-lasting course in patients with an onset of the illness in young adulthood. Less severe agoraphobia associated with moderately severe panic attacks appears to confer a better control of phobic behavior. All three major drugs were reasonably well tolerated (only 9% dropped out because of side effects), with sexual dysfunction and increased appetite being the most common side effects at the last evaluation; in the first phase of the treatment anticholinergic effects and jitteriness were more common with TCAs. CONCLUSION: Both classical antidepressants and paroxetine emerge as a useful treatment in the long-term management of PDA; paroxetine appears particularly useful in PDA patients because it was significantly less likely to induce jitteriness, thereby reducing barriers to compliance.     

Sex differences in cognitive estimation during sleep deprivation: effects of stimulant countermeasures

Stimulant medications restore simple alertness during sleep loss, but it is not clear how they affect complex executive functions, particularly in light of sex differences in cerebral organization. The effectiveness of caffeine, modafinil, dextroamphetamine, or placebo for sustaining performance on the Biber Cognitive Estimation Test (BCET) was compared in 29 men and 25 women following 46 hr of sleep deprivation. Stimulants had differential effects on BCET performance as a function of the sex of the subjects. Women receiving placebo or caffeine scored significantly worse than males, while modafinil and dextroamphetamine were effective at sustaining BCET performance of men and women.     

The effects of antidepressants on sexual functioning in depressed patients: a review

Sexual dysfunction has long been noted as both a symptom of depressive illness and as a side effect of many of the medications used to treat depression. Although most people suffering from a major depressive illness would like to be sexually active, half experience a decrease in desire or sexual performance. Antidepressant medications often interfere with several parts of the sexual response. This review compares data from different types of research into the effect of antidepressant medications on the sexual response: case reports, chart reviews, and single- and double-blind studies with and without active control medications. From this review, it is clear that antidepressants of most classes interfere with human sexual functioning, with the notable exceptions of bupropion and nefazodone.     

Monosymptomatic hypochondriasis treated with tricyclic antidepressants

The authors report on two patients with disabling monosymptomatic hypochondriasis who responded to tricyclic antidepressants. They include a brief review of the literature on this uncommon debilitating illness.     

帕罗西汀联合曲唑酮治疗抑郁症患者睡眠障碍效果观察

目的：探讨帕罗西汀联合曲唑酮治疗抑郁症患者睡眠障碍的临床效果。方法回顾性分析我院门诊106例抑郁症患者的临床资料,根据治疗方法不同分为治疗组和对照组各53例,对照组患者给予帕罗西汀治疗,治疗组在对照组治疗基础上加用曲唑酮,比较2组治疗6周后临床疗效、睡眠质量以及不良反应发生情况。结果治疗6周后治疗组总有效率88.68％,对照组75.47％,2组比较差异有统计学意义（ P＜0.05）;治疗3周和6周后治疗组患者睡眠质量良好率均显著高于对照组（ P＜0.05）;治疗组总不良反应发生率15.09％,与对照组的18.88％比较,差异无统计学意义（ P＞0.05）。结论帕罗西汀联合曲唑酮治疗抑郁症睡眠障碍患者可显著提高睡眠质量,效果显著,且安全性高。     

曲唑酮治疗海洛因戒断症状临床研究

目的：观察曲唑酮对海洛因依赖稽延性戒断症状的疗效。方法：采用双盲对照法，用曲唑酮或安慰剂分别治疗海洛因依赖临床脱毒后存在的稽延性戒断症状的患者。结果：曲唑酮较安慰剂能明显减轻患者的稽延性戒断症状、情绪障碍及对毒品的心理渴求，且无严重不良反应。结论：曲唑酮对海洛因依赖稽延性戒断症状有效。