Temazepam's efficacy in patients with sleep onset insomnia.

Roehrs, Timothy; Lamphere, James; Paxton, C; Wittig, R; Zorick, Frank; Roth, T.

doi:10.1111/j.1365-2125.1984.tb02405.x

Cited by 17 publications

(6 citation statements)

References 8 publications

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“…The prevalence of rebound insomnia was found to be significantly lower in all benzodiazepines compared to triazolam [52,[60][61][62][63][64][65][66][67][68][69] and was lower than that with triazolam. Thus, similarly to rebound anxiety, the risk seems related to benzodiazepine elimination half-life and potency [20,23] and independent form the length of treatment [1].…”

Section: Rebound Symptoms After Benzodiazepine Discontinuationmentioning

confidence: 75%

Acute and Persistent Withdrawal Syndromes Following Discontinuation of Psychotropic Medications

Cosci

Chouinard

2020

Psychother Psychosom

187

184

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Studies on psychotropic medications decrease, discontinuation, or switch have uncovered withdrawal syndromes. The present overview aimed at analyzing the literature to illustrate withdrawal after decrease, discontinuation, or switch of psychotropic medications based on the drug class (i.e., benzodiazepines, nonbenzodiazepine benzodiazepine receptor agonists, antidepressants, ketamine, antipsychotics, lithium, mood stabilizers) according to the diagnostic criteria of Chouinard and Chouinard [Psychother Psychosom. 2015; 84 (2): 63-71], which encompass new withdrawal symptoms, rebound symptoms, and persistent post-withdrawal disorders. All these drugs may induce withdrawal syndromes and rebound upon discontinuation, even with slow tapering. However, only selective serotonin reuptake inhibitors, serotonin noradrenaline reuptake inhibitors, and antipsychotics were consistently also associated with persistent post-withdrawal disorders and potential high severity of symptoms, including alterations of clinical course, whereas the distress associated with benzodiazepines discontinuation appears to be shortlived. As a result, the common belief that benzodiazepines should be substituted by medications that cause less dependence such as antidepressants and antipsychotics runs counter the available literature. Ketamine, and probably its derivatives, may be classified as at high risk for dependence and addiction. Because of the lag phase that has taken place between the introduction of a drug into the market and the description of withdrawal symptoms, caution is needed with the use of newer antidepressants and antipsychotics. Within medication classes, alprazolam, lorazepam, triazolam, paroxetine, venlafaxine, fluphenazine, perphenazine, clozapine, and quetiapine are more likely to induce withdrawal. The likelihood of withdrawal manifestations that may be severe and persistent should thus be taken into account in clinical practice and also in children and adolescents.

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Section: Rebound Symptoms After Benzodiazepine Discontinuationmentioning

confidence: 75%

Acute and Persistent Withdrawal Syndromes Following Discontinuation of Psychotropic Medications

Cosci

Chouinard

2020

Psychother Psychosom

187

184

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“…Post-randomization, patients were required to visit the clinic at the end of weeks 1, 2, 4 and 6 and to return for follow-up visits 14 and 28 days after last dose. Efficacy and safety assessments conducted at each visit included the HAM-D (17-item using the SIGH-D, Williams, 1988), Clinical Global Impressions - Severity of Illness (CGI-S) and Improvement (CGI-I, Guy, 1976) (Guy, 1976), the Clinical Global Impression of Improvement (CGI-I, 18), the Quick Inventory of Depressive Symptomatology (self-reported, QIDS-SR, Rush et al, 2003), the Cognitive and Physical Function Questionnaire (CPFQ, Fava et al, 2009), the Morning Sleep Questionnaire (Roehrs et al, 1984, captured by Clinphone Plc, Nottingham, UK), the Columbia Suicidality Severity Rating Scale (CSSRS, Posner et al, 2011), and the Massachusetts General Hospital Sexual Functioning Questionnaire (MSFQ, Fava et al, 1998; Labbate and Lare, 2001). The Discontinuation-Emergent Signs and Symptoms (DESS, Fava, 2006) scale was administered at the end of double-blind treatment and the 14 day follow-up visit.…”

Section: Efficacy Studiesmentioning

confidence: 99%

Full central neurokinin-1 receptor blockade is required for efficacy in depression: evidence from orvepitant clinical studies

et al. 2013

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Full, persistent blockade of central neurokinin-1 (NK1) receptors may be a potential antidepressant mechanism. The selective NK1 antagonist orvepitant (GW823296) was used to test this hypothesis. A preliminary positron emission tomography study in eight male volunteers drove dose selection for two randomized six week studies in patients with major depressive disorder (MDD). Displacement of central [(11)C]GR205171 binding indicated that oral orvepitant doses of 30-60 mg/day provided >99% receptor occupancy for ≥24 h. Studies 733 and 833 randomized patients with MDD and 17-item Hamilton Depression Rating Scale (HAM-D)≥22 to double-blind treatment with orvepitant 30 mg/day, orvepitant 60 mg/day or placebo (1:1:1). Primary outcome measure was change from baseline in 17-item HAM-D total score at Week 6 analyzed using mixed models repeated measures. Study 733 (n=328) demonstrated efficacy on the primary endpoint (estimated drug-placebo differences of 30 mg: -2.41, 95% confidence interval (CI) (-4.50 to -0.31) p=0.0245; 60 mg: -2.86, 95% CI (-4.97 to -0.75) p=0.0082). Study 833 (n=345) did not show significance (estimated drug-placebo differences of 30 mg: -1.67, 95% CI (-3.73 to 0.39) p=0.1122; 60 mg: -0.76, 95% CI (-2.85 to 1.32) p=0.4713). The results support the hypothesis that full, long lasting blockade of central NK1 receptors may be an efficacious mechanism for the treatment of MDD.

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“…Temazepam produced a number of improvements in the objective sleep of both osteoarthritic patients and controls. Several studies have reported a reduction in sleep latency following nocturnal temazepam administration (Beary et af., 1984;Roehrs et al, 1984). It is hardly surprising that temazepam did not reduce sleep latency in this study, since it was given only five min before bedtime.…”

Section: Discussionmentioning

confidence: 74%

Temazepam as a hypnotic in osteoarthritic patients

Leigh

Hindmarch

Bird

et al. 1987

Human Psychopharmacology

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PThe effects of nocturnal temazepam elixir on 14 male osteoarthritic patients and 16 age-and sex-matched healthy controls were investigated in a double-blind parallel groups study. Temazepam produced a number of significant changes in objective sleep. In the osteoarthritic patients temazepam reduced the duration of awakenings, percentage stage 0, percentage stage 1, percentage stages (0+1) and increased percentage stage 2 and REM latency. In the controls temazepam reduced the duration of awakenings, percentage stage 0, percentage stages (0+1) and increased percentage stage 2, sleep efficiency and REM latency. During the drug period, seven out of 15 subjects receiving temazepam reported improved sleep, compared with one out of 15 placebo subjects. There was no evidence to suggest that temazepam caused any unwanted side-effects or affected the duration of morning stiffness in osteoarthritic patients. Temazepam produced no significant impairment of early morning psychomotor performance or significant withdrawal effects in either patients or controls.

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Temazepam's efficacy in patients with sleep onset insomnia.

Cited by 17 publications

References 8 publications

Acute and Persistent Withdrawal Syndromes Following Discontinuation of Psychotropic Medications

Acute and Persistent Withdrawal Syndromes Following Discontinuation of Psychotropic Medications

Full central neurokinin-1 receptor blockade is required for efficacy in depression: evidence from orvepitant clinical studies

Temazepam as a hypnotic in osteoarthritic patients

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