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Query: UMLS:C0917801 (insomnia)
 10,606 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

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.
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PMID:The effects of trazodone on sleep disturbances induced by brofaromine. 1057 43

The bi-directional nature of the neurovegetative symptoms of depression, as well as the differential response to antidepressant medications, underscore the existence of possible subtypes of this disorder. This study surveyed 56 physicians practicing psychiatry in Hawaii for opinions regarding the most effective antidepressant medication for the following symptoms: hypersomnia vs. insomnia, psychomotor agitation vs. retardation, and gain vs. loss of appetite or weight. Fluoxetine was found to be the drug of choice for weight and appetite gain, hypersomnia, and psychomotor retardation. Mirtazapine was viewed as most effective for weight and appetite loss. Trazodone was found most effective for insomnia and nefazodone for psychomotor agitation. It is concluded that subtyping of depression should be investigated at the symptom level and the generalizability of the effects of each specific compound should be tested.
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PMID:The relationship between type of antidepressant and neurovegetative symptoms in adult unipolar nonpsychotic depression: an opinion survey. 1178 64

Utilizing polysomnography (PSG) and psychometry, objective and subjective sleep and awakening quality was investigated in 11 drug-free patients (five females, six males) aged 35-75 years (mean age 54.1 +/- 11.4) suffering from nonorganic insomnia (F 51.0) related to a depressive episode (F 32) or recurrent depressive disorder (F 33). as compared with 11 age- and sex-matched normal controls (five females, six males) aged 36-75 years (mean age 53.0 +/- 13.5). PSG demonstrated decreased sleep efficiency, total sleep time (TST), total sleep period (TSP) and sleep stage S2, as well as increased wakefulness during TSP, early morning awakening, sleep latency to S1, S2, S3 and sleep stage S1 in depressed patients. Subjective sleep quality and the total score of the Self-Assessment of Sleep and Awakening Quality Scale (SSA) were deteriorated as were morning and evening well being, drive, mood and fine motor activity right. Evening and morning blood pressure, the O2 desaturation index and periodic leg movement (PLM) index were increased. In a subsequent acute, placebo-controlled cross-over design study, the acute effects of 100 mg of trazodone, a serotonin reuptake inhibitor with a sedative action due to 5-HT2 and alpha1 receptor blockade, were investigated in the patients. As compared with placebo, trazodone induced an increase in sleep efficiency (primary target variable), TST, TSP and SWS (S3 + S4), as well as a decrease in wakefulness during the TSP, early morning awakening and S2. There was no change in rapid eye movement (REM) sleep with the exception of an increase in the REM duration in minutes. Trazodone also caused an improvement in subjective sleep quality, affectivity, numerical memory and somatic complaints. All respiratory variables remained within normal limits. Critical flicker frequency and moming diastolic blood pressure were decreased. The present study demonstrated that depression induced significant changes in objective and subjective sleep and awakening quality, which were counteracted by 100 mg of trazodone, thus suggesting a key-lock principle in the treatment of depression.
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PMID:Insomnia in depression: differences in objective and subjective sleep and awakening quality to normal controls and acute effects of trazodone. 1181 1

Patients with chronic pain often suffer from sleep disturbances, specifically decreased deep sleep, and thus may get into a vicious circle which maintains their pain condition. Utilizing polysomnography and psychometry, objective and subjective sleep and awakening quality was investigated in 11 patients with nonorganic insomnia (F51.0) related to somatoform pain disorder (SPD; F45.4) as compared with age- and sex-matched healthy controls of the Siesta normative database. Patients demonstrated a markedly deteriorated Pittsburgh Sleep Quality Index, a decreased Quality of Life Index, slightly increased self-reported anxiety (Zung SAS) and depression scores (Zung SDS), as well as an increased Epworth Sleepiness Scale and International Restless Legs Syndrome Scale score. Subjective sleep and awakening quality was markedly reduced, while somatic complaints were increased. Polysomnographic evaluation by a recently developed automatic sleep classifier (Somnolyzer 24 x 7) based on the rules of Rechtschaffen and Kales demonstrated reduced slow-wave sleep (SWS), the target variable in the present study, a decreased stage shift index, increased SWS latency and stage 4 sleep (S4) latency and an increased frequency of shifts from S2 to wakefulness (W) in patients as compared with controls. Minimal oxygen saturation was found decreased, periodic leg movements (PLMs) were increased. In the morning, patients showed deteriorated well-being, drive, mood and wakefulness. There were no significant noopsychic or psychophysiological differences between patients and controls (except for a reduced numerical memory and a slightly increased morning diastolic blood pressure in patients). Subsequent evaluation of the acute effects of 100 mg of a controlled-release formulation of trazodone (Trittico retard) in the patients demonstrated an increase in the target variable SWS, accompanied by a reduction in the number of awakenings and stage shifts. It normalized the frequency of shifts from S2 to W and reduced the frequency of shifts from W to S1, from S1 to S2, as well as from any stage to S1 and S2. Trazodone, however, also significantly reduced the total sleep period and S2 and increased the latency to S1. Moreover, the drug increased the reduced minimal O(2 )saturation, reduced the arousal index and the PLMs-in-wake index and normalized the increased morning diastolic blood pressure. In conclusion, our study demonstrated that SPD induced significant changes in subjective and objective sleep and awakening quality, which were partially mitigated by trazodone therapy. The data on the target variable SWS support our hypothesis of a key-lock principle in the diagnosis and drug treatment of sleep disorders. Our study provided the first evidence on the usefulness of the Somnolyzer 24 x 7 and the Siesta database in clinical practice.
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PMID:Insomnia in somatoform pain disorder: sleep laboratory studies on differences to controls and acute effects of trazodone, evaluated by the Somnolyzer 24 x 7 and the Siesta database. 1583 86

Insomnia and depression are widespread diseases causing deterioration of life's quality and increasing morbidity and mortality of cardiovascular diseases. Both of them and certain antidepressants adversely affect physiological structure of sleep, while others restore it. The latter drugs must be preferred in therapy of depression accompanying insomnia, and some of them may be effective in treatment of insomnias without depression. Most antidepressants cause REM-reduction, generally with increased serotonin-function. Selective H1-antagonists readily induce sleep, and also the inhibition of cholinergic neurons in the general arousal networks promotes sleep. Sleep continuity is improved by the rise of synaptic level of serotonin. Among tricyclic antidepressants trimipramine and amitriptyline are the best to improve sleep. However, the former has low antidepressant effect and the latter has many adverse side effects. Selective serotonin reuptake inhibitors, except paroxetine, improve sleep only at the time and to the extent of restoring depression. Paroxetine has beneficial effect on sleep at the beginning of the treatment. Mirtazapine is the first-line sleep promoter among atypical antidepressants, however, its effect on increasing appetite markedly limits its application. Trazodone causes hangover, and mianserin may induce restless legs. Insomnias without depression demand lower dose of antidepressants than depression.
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PMID:[Effects of antidepressants on sleep]. 1678 Jan 85

Trazodone is one of the most commonly prescribed medicines for treating depression and insomnia. However, the pharmacological mechanism of action underlying trazodone's unique effects is unclear. Despite its nanomolar affinity for 5HT(2A) receptors, histamine(1) receptors and alpha(1) adrenoceptors the drug is given at high doses to achieve clinical efficacy suggesting that other target activities may also contribute to its effects. Here we report that trazodone inhibits recombinant T-type calcium channels (Ca(v)3.1, Ca(v)3.2 and Ca(v)3.3) in whole-cell patch-clamp studies at therapeutically relevant concentrations (IC(50)=43 microM, 45 microM, 23 microM, respectively). Inhibition was not use-dependent and showed only moderate voltage-dependence. Tonic block of Ca(v)3.1 channels held at negative membrane potentials suggested drug interaction with channels in the resting state. The major metabolite of trazodone, m-chlorophenylpiperazine, showed comparable potency on Ca(v)3.3 channels (IC(50)=35 microM) and was less active on Ca(v)3.1 channels (IC(50)=317 microM). We also demonstrate trazodone's inhibitory effects on native T-type calcium currents recorded from subthalamic neurons in a patch-clamp rat brain slice assay (approximately 30% inhibition at 100 microM). Our data suggest that T-type calcium channel antagonism may contribute to the pharmacology of trazodone and its reported neurological effects.
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PMID:Trazodone inhibits T-type calcium channels. 1761 Sep 10

Caffeine is the world's most popular stimulant and is known to disrupt sleep. Administration of caffeine can therefore be used in healthy volunteers to mimic the effects of insomnia and thus to test the hypnotic effects of medication. This study assessed the effects of caffeine on sleep architecture and electroencephalography (EEG) spectrum alone and in combination with two different sleep-promoting medications. Home polysomnography was performed in 12 healthy male volunteers in a double-blind study whereby subjects received placebo, caffeine (150 mg), caffeine plus zolpidem (10 mg) and caffeine plus trazodone (100 mg) at bedtime in a randomised crossover design. In addition to delaying sleep onset, caffeine decreased total sleep time (TST), sleep efficiency (SE) and stage 2 sleep without significantly altering wake after sleep onset or the number of awakenings. Zolpidem attenuated the caffeine-induced decrease in SE and increased spindle density in the caffeine plus zolpidem combination compared with placebo. Trazodone attenuated the decrease in SE and TST, and it also increased stage 3 sleep, decreased the number of awakenings and decreased the spindle density. No significant changes in rapid eye movement (REM) sleep were observed, neither was any significant alteration in slow wave activity nor other EEG spectral measures, although the direction of change was similar to that previously reported for caffeine and appeared to 'normalise' after trazodone. These data suggest that caffeine mimics some, but not all of the sleep disruption seen in insomnia and that its disruptive effects are differentially attenuated by the actions of sleep-promoting compounds with distinct mechanisms of action.
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PMID:Effects on sleep stages and microarchitecture of caffeine and its combination with zolpidem or trazodone in healthy volunteers. 1935 1

Trazodone Contramid(R) once-a-day (TzCOAD) is a reformulation of trazodone hydrochloride that controls the release of trazodone over 24 hours. A standard effect size analysis (Cohen's d) determined which items of the 17-item Hamilton Depression Rating Scale (HAMD-17) and the Montgomery-Asberg Depression Rating Scale (MADRS) showed the greatest improvement in patients with major depressive disorder (MDD), following up to 8 weeks of therapy with TzCOAD. An additional insomnia analysis assessed whether the efficacy of TzCOAD is influenced by improvements in insomnia or baseline severity of insomnia. The analyses used data from a randomized study of 412 patients receiving 150-375 mg TzCOAD (N = 206) or placebo (N = 206). The results of the Cohen's d analysis on the modified intent-to-treat population (LOCF) showed HAMD items with the greatest improvement were insomnia items (middle (-0.35), late (-0.24)), feelings of guilt (-0.24), and depressed mood (-0.23); for MADRS items they were reduced sleep (-0.31), inner tension (-0.22), reported sadness (-0.21), and suicidal thoughts (-0.21). An analysis of covariance showed no significant interaction between improvements in the HAMD Bech-6 core symptoms of depression and the baseline MADRS reduced sleep item or early changes in the HAMD-17 sleep disturbance factor. These results suggest that the antidepressant efficacy was independent of the baseline severity of insomnia and of the improvement in insomnia. Overall, the results elucidate the efficacy components and tolerability characteristics previously demonstrated for TzCOAD monotherapy for patients with MDD at the recommended daily dose of 300 mg.
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PMID:The efficacy and tolerability of once-daily controlled-release trazodone for depressed mood, anxiety, insomnia, and suicidality in major depressive disorder. 2058 90

Sleep disorders are among the most common in the general population. Insomnia is a serious clinical and social problems. The prevalence of insomnia in developed countries is estimated at 10-35% (40%). The effective treatment of insomnia, it is essential to proper diagnosis and treatment of the primary causes. When choosing an antidepressant for a patient with sleep disorders should be taken into account the effectiveness of antidepressant, sedative activity profile, good tolerability and possible administration evening dose. Trazodone is an sedative antidepressant, acting quickly, efficiently, safely, with a small number of adverse reactions and proven effective in the treatment of insomnia.
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PMID:[Efficacy of trazodone in the treatment of insomnia]. 2064 16

Offering a new perspective on sleep state misperception, we discuss a patient who presented with sleep state misperception and was ultimately diagnosed with delusional disorder. A 60-year-old woman with chief complaints of insomnia, agitation, and suicidal ideation, was admitted to an inpatient psychiatric ward. Based on information from her family and a mental state examination, her primary diagnosis was sleep state misperception. She was treated with Trazodone. Because she was unresponsive to the treatment, a full psychiatric evaluation and wrist actigraphy report were undertaken, resulting in a revised diagnosis of delusional disorder. She was started on Olanzapine and, after 6 weeks was discharged with good improvement. Sleep state misperception might be considered not just as a sleep disorder, but also as a psychiatric disorder with psychotic symptoms. Further research is recommended.
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PMID:Insomnia treatment by olanzapine. Is sleep state misperception a psychotic disorder? 2067 99


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