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Treatment of residual insomnia after CBT for PTSD: case studies.

Insomnia is one of the most common symptoms of posttraumatic stress disorder (PTSD). Evidence suggests that insomnia may persist for many PTSD patients after other symptoms have responded to cognitive-behavioral therapy (CBT). The present article reports the effects of administering a five-session cognitive-behavioral insomnia treatment to 5 patients who responded to CBT for PTSD yet continued to report insomnia. Insomnia treatment was associated with improvements on subjective sleep measures (Pittsburgh Sleep Quality Index, Insomnia Severity Index, and Beliefs and Attitudes about Sleep Scale) and self-monitored sleep efficiency and related measures in 4 of 5 cases. Results highlight issues specific to treating insomnia in trauma populations and future directions for examining treatment of insomnia associated with PTSD.

Adult↗

Zopiclone and triazolam in insomnia associated with generalized anxiety disorder: a placebo-controlled evaluation of efficacy and daytime anxiety.

In a double-blind placebo-controlled study, following a 1 week washout, 75 outpatients suffering from generalized anxiety disorder with severe insomnia as the target symptom were randomly assigned to 4 weeks of treatment with zopiclone 7.5 mg, triazolam 0.5 mg or placebo at bedtime. Zopiclone was significantly better than placebo on most sleep parameters. Triazolam tended to be superior to placebo, but its superiority was significant only on the sleep induction factor. Triazolam-treated patients presented significantly more day-time-interdose anxiety than zopiclone as assessed by the weekly HARS and Clinical Global Assessment of Anxiety. Although daytime-interdose anxiety was observed with both drugs, this treatment emergent symptom was more frequent and severe with triazolam. Side-effects were of a mild to moderate intensity for both zopiclone and triazolam; however, taste perversion frequently appeared with zopiclone. Although both drugs share similar pharmacological properties and bind to benzodiazepine receptors, they differ significantly with respect to side-effects and daytime anxiety.

Adult↗

Cognitive Behavior vs Bright Light Therapy for Insomnia in Women Undergoing Chemotherapy for Breast Cancer: A Randomized Clinical Trial.

IMPORTANCE: Women receiving chemotherapy for breast cancer experience insomnia and fatigue, which impair quality of life. To date, no randomized clinical trial (RCT) has evaluated the use of cognitive behavior therapy for insomnia (CBT-I) and bright light therapy (BLT) both alone and in combination, and few have evaluated the use of either during chemotherapy. OBJECTIVE: To determine the main effects of CBT-I and BLT on insomnia and fatigue symptoms in women undergoing chemotherapy for breast cancer. DESIGN, SETTING, AND PARTICIPANTS: Sleep, Cancer, Rest (SleepCARE) was a 6-week, 2 × 2 factorial, superiority, parallel RCT conducted at 5 metropolitan and regional hospitals in Australia from January 22, 2021, to August 21, 2024. Participants were women (aged ≥18 years) receiving chemotherapy for early or metastatic breast cancer. INTERVENTIONS: Two brief interventions were administered: CBT-I and BLT alone (using light glasses at 1500 lux) and in combination, creating 4 groups (CBT-I alone, BLT alone, CBT-I plus BLT, and sleep hygiene education [SHE]). All interventions included SHE. The interventions lasted 6 weeks and included a 1:1 consultation session, emails sent once or twice per week, and a midpoint call for all groups, as well as light glasses for the BLT groups. MAIN OUTCOMES AND MEASURES: Dual primary outcomes were Insomnia Severity Index (ISI) scores and Patient-Reported Outcomes Measurement Information System (PROMIS)-Fatigue T scores. Both are patient-reported outcome measures and measure insomnia and fatigue symptoms, respectively. Assessments occurred via surveys administered at baseline and at the midpoint (3 weeks), postintervention (6 weeks), and follow-up (3 months and 6 months) periods. Modified intention-to-treat analyses used latent growth models. RESULTS: Of the 219 women enrolled (mean [SD] age, 50.7 [10.8] years; 54 [26.9%] with metastatic cancer), 55 were randomized to CBT-I, 55 to BLT, 52 to CBT-I plus BLT, and 57 to SHE. A total of 208 women (95.0%) with any data at any time point were analyzed. Insomnia symptoms (ISI score mean difference [MD], -2.19 [95% CI, -3.33 to -1.05] points; P = .002) but not fatigue symptoms (PROMIS-Fatigue score MD, -0.90 [95% CI, -3.08 to 1.28] points; P = .52) improved more in the CBT-I groups compared with the non-CBT-I groups. The BLT groups (compared with the non-BLT groups) did not differ in insomnia symptoms (ISI score MD, -0.88 [95% CI, -2.02 to 0.26] points; P = .26) or fatigue symptoms (PROMIS-Fatigue score MD, -0.71 [95% CI, -2.89 to 1.47] points; P = .52). Comparable results emerged in the high-adherence subgroup and in the subgroups with high initial insomnia and fatigue symptoms. However, exploratory subgroup analyses in women with metastatic breast cancer showed that BLT (vs non-BLT) improved insomnia symptoms (ISI score MD, -2.87 [95% CI, -5.06 to -0.67] points; P = .01) and fatigue symptoms (PROMIS-Fatigue score MD, -5.16 [95% CI, -9.57 to -0.76] points; P = .02). CONCLUSIONS AND RELEVANCE: In the SleepCARE RCT of CBT-I and BLT administered for 6 weeks to women receiving chemotherapy for breast cancer, CBT-I improved insomnia but not fatigue compared with SHE or BLT. BLT did not produce greater improvements in fatigue or insomnia symptoms compared with non-BLT treatment. The study findings indicate that brief CBT-I, but not BLT, may reduce insomnia symptoms among women receiving chemotherapy for breast cancer. TRIAL REGISTRATION: ANZCTR Identifier: ACTRN12620001133921.

Humans↗

[Withdrawal reactions after clomipramine].

Abrupt or gradual discontinuation of tricyclic antidepressants may precipitate withdrawal symptoms. The most common of these are general somatic or gastrointestinal distress, anxiety and agitation, sleep disturbance, akathisia, parkinsonism, paradoxical behavioral activation and mania. There are very few reports of withdrawal reactions following discontinuation of clomipramine since it has not been in use in the US until recently. 2 patients with withdrawal symptoms following discontinuation of clomipramine are presented. A 45-year-old man had general somatic symptoms, including headache, myalgia, weakness, fatigue (flu-like syndrome) and nervousness and insomnia after clomipramine, 75 mg/d, had been discontinued abruptly. All symptoms disappeared without treatment after 3 days. A 47-year-old woman presented mainly with severe insomnia, anxiety, agitation, jitteriness and tension after discontinuing a low dose of 25 mg/d of clomipramine. Symptoms disappeared after she started self-treatment with 50 mg/d of the drug. It is important to differentiate withdrawal symptoms from relapse of the primary psychiatric disorder.

Anxiety↗

Nasal dilator strip therapy for chronic sleep maintenance insomnia: a case series.

Sleep-disordered breathing (SDB) is a salient factor in chronic sleep maintenance insomnia. However, many insomnia patients with comorbid SDB may not be interested initially in receiving treatment with continuous positive airway pressure or oral appliance therapy. As an interim pathway, we used Breathe Right nasal dilator strip (NDS) therapy to introduce these patients to the relationship between insomnia and SDB. We hypothesized that NDS-associated improvements might motivate patients to pursue comprehensive SDB therapies. In this open label trial, three men with chronic sleep maintenance insomnia were treated with an educational session about SDB coupled with nightly NDS therapy. At 4-week follow-up, global insomnia severity, difficulty staying asleep, difficulty falling back asleep when awakened, total number of awakenings, and wake time after sleep onset systematically improved. Following NDS therapy, all three insomnia patients elected to pursue comprehensive SDB treatment at local sleep centers.

Case-Control Studies↗

An investigation of monitoring for sleep-related threat in primary insomnia.

In Study 1, individuals with primary insomnia (n=32) and good sleepers (n=38), recruited from a university population, completed a semi-structured interview. The interview assessed monitoring for sleep-related threat, negative thoughts and safety behaviours, at night and during the day. Compared to good sleepers, individuals with insomnia reported more frequent monitoring at night and during the day, more negative thoughts associated with monitoring at night and during the day, and the use of more safety behaviours associated with monitoring at night. A path analysis showed that the total monitoring frequency was significantly positively related to the score for total negative thoughts, which in turn, was significantly positively related to the total number of safety behaviours used. Study 2 aimed to test the generalisability of these findings in a clinical sample of individuals with primary insomnia (n=23). The results indicated that the clinical sample also engaged in monitoring for sleep-related threat, experienced negative thoughts and used safety behaviours. Further, more severe insomnia was associated with more negative thoughts and the use of more safety behaviours associated with monitoring at night. Together, these results are consistent with the proposal that monitoring for sleep-related threat functions to maintain insomnia by triggering negative thoughts and the use of safety behaviours. Future research is required to verify the proposed causal status of monitoring, using prospective designs and experimental manipulations.

Adaptation, Psychological↗

An internet-based randomized, placebo-controlled trial of kava and valerian for anxiety and insomnia.

The herbal extracts kava and valerian are the leading dietary supplements used in the self-management of anxiety and insomnia, respectively. There is limited evidence to support their effectiveness for these common symptoms. The Internet has been used to a limited extent for research, but it is not known whether randomized controlled trials can be conducted entirely using Internet technology. We performed a randomized, double-blind, placebo-controlled trial using a novel Internet-based design to determine if kava is effective for reducing anxiety and if valerian is effective for improving sleep quality. E-mail recruitment letters and banner advertisements on websites were used to recruit a large pool of interested participants (1551) from 45 states over an 8-week period. Participants were first asked to read study information, complete an online informed consent process, and undergo electronic identity verification. In order to be eligible for the study, participants were required to have 1) anxiety as documented by scores of at least 0.5 standard deviations above the mean on the State-Trait Anxiety Inventory State subtest (STAI-State) on 2 separate occasions, and 2) insomnia, defined as a "problem getting to sleep or staying asleep over the past 2 weeks." We randomly assigned 391 eligible participants to 1 of the following 3 groups, and mailed 28 days' supply: kava with valerian placebo (n = 121), valerian with kava placebo (n = 135), or double placebo (n = 135). The primary outcome measures were changes from baseline in anxiety (STAI-State questionnaire) and insomnia (Insomnia Severity Index [ISI]) compared with placebo. Participants receiving placebo had a 14.4 point decrease in anxiety symptoms on the STAI-State score and an 8.3 point decrease in insomnia symptoms on the ISI. Those receiving kava had similar reductions in STAI-State score (2.7 point greater reduction in placebo compared with kava; 95% confidence interval [CI], -0.8 to +6.2). Those receiving valerian and placebo had similar improvements in sleep (0.4 point greater reduction in the placebo than the valerian group; 95% CI, -1.3 to +2.1). Results were similar when limited to the 83% of participants who adhered to study compounds for all 4 weeks. Neither kava nor valerian relieved anxiety or insomnia more than placebo. This trial demonstrates the feasibility of conducting randomized, blinded trials entirely via the Internet.

Adult↗

Treatment of sleep dysfunction and psychiatric disorders.

Patients with neurologic disorders commonly experience sleep dysfunction and psychiatric disorders. The most common sleep dysfunction is insomnia, which is a primary symptom in 30% to 90% of psychiatric disorders. Insomnia and fatigue are prominent symptoms of anxiety disorders and major depression, including patients who are treated but have residual symptoms. Anxiety and depressive disorders account for 40% to 50% of all cases of chronic insomnia. It is also recognized that primary insomnia and other primary sleep disorders produce symptoms that are similar to those reported by patients with psychiatric disorders. A clinician must judge whether sleep deprivation causes mood disturbance or whether depressive or anxiety disorder represents the primary reason for sleep dysfunction. When insomnia is comorbid with mild to moderate depression, therapy should begin with bedtime dosing of sedating antidepressants such as mirtazapine, nefazodone, or tricyclic antidepressants, which are preferred because of their sedative effects, although side effects may limit their usefulness. Intervention for chronic insomnia is similar in nonpsychiatric and psychiatric patients. Behavioral therapies, particularly cognitive behavioral therapy, and lifestyle changes show significant long-term efficacy as treatments for chronic insomnia. Sedative hypnotic agents are the most studied agents to treat insomnia, particularly those that are active through the benzodiazepine receptor-GABA complex, such as benzodiazepines, eszopiclone, zaleplon, and zolpidem. The new melatonin-receptor agonist ramelteon has not yet been studied in psychiatric patients. Prescription of adjunctive trazodone 50 to 150 mg is a common clinical practice to treat comorbid insomnia during antidepressant therapy, but published data are surprisingly limited when considered against the frequent usage of trazodone. Although there has been insufficient research on the use of atypical antipsychotic agents in severe insomnia, psychiatrists use quetiapine, olanzapine, or other agents to lessen agitation that disrupts sleep onset or maintenance. When insomnia or hypersomnia continues even as mood, anxiety, or thought disorders improve with standard therapy, the physician should consider the potential presence of underlying sleep disorders.

Journal Article↗

Evaluation of the safety and efficacy of quazepam for the treatment of insomnia in psychiatric outpatients.

BACKGROUND: This study was conducted to further evaluate the safety and efficacy of the benzodiazepine hypnotic quazepam within the context of a clinical practice setting of psychiatric outpatients who had insomnia. METHOD: A total of 2,813 adult, psychiatric outpatients were evaluated in an open-label study design. Each subject was instructed to take one 15-mg quazepam tablet each night at bedtime for 7 consecutive nights and was given a questionnaire to be completed at home upon arising each morning. RESULTS: Insomnia improved after 1 night of treatment with 15 mg of quazepam. Eighty-five percent of patients rated their quality of sleep as fair-to-excellent after 1 week of treatment. Similar efficacy outcomes also were observed on the second through sixth nights of treatment. Improvement occurred for patients who had an initial sleep latency complaint or unsatisfactory duration of sleep and for those who either had difficulty in staying asleep or complained of early morning awakening. The mean number of insomnia complaints was significantly (p < .001) reduced after the first and the seventh nights of treatment both in the population of all evaluable patients and in a subset of patients with more severe insomnia. CONCLUSION: This open-label study in 2,813 outpatients provided evidence that quazepam reduces the complaints of insomnia in a difficult-to-treat psychiatric population after 1 night and after 7 nights of treatment. Quazepam was well tolerated, even when coadministered with psychotherapeutic medications, some of which can cause insomnia.

Adolescent↗

[Insomnia and hallucinations caused by vascular lesions of the pontine].

Small ischemic vascular lesions or hemorrhages provide a pathological model useful for the study of sleep disturbances in human due to lesions in the pontine tegmentum. We present 7 patients, 4 men and 3 women, with severe insomnia and hallucinations due to small vascular lesions of the pontine tegmentum. Nocturnal-sleep and/or 24-h polygraphic studies were done on all patients, as were neurophysiological and image studies; pathological studies were performed in one patient. Insomnia affected both non-REM and REM sleep, appeared in the acute phase and tended to improve with time. The patients tolerated insomnia with no serious effects on general health. Insomnia was not affected by administration of L-tryptophan with or without carbidopa. Hallucinations were mainly visual, but were also auditory in 2 cases; they were unrelated to the occurrence of normal or dissociated REM sleep. Imaging studies, and autopsy in 1 case, revealed damage to the pontis centralis caudalis and pontis centralis oralis nuclei, which appeared to be responsible for insomnia. The relationship between visual and/or auditory hallucinations and sleep disturbances remain speculative.

Aged↗

Relationship between regional cerebral blood flow and separate symptom clusters of major depression: a single photon emission computed tomography study using statistical parametric mapping.

This study examined the relationship between resting regional cerebral blood flow (rCBF) patterns in patients with major depressive disorder (MDD) and specific symptom clusters derived from ratings on the Hamilton Rating Scale for Depression (HRSD) and the Mini Mental State Examination. We hypothesized that the functional activity in frontal, parietal, anterior cingulate, basal ganglia and limbic regions would be related to specific symptom domains. Fifteen patients fulfilling DSM-IV criteria for MDD who were off all psychotropic medications for >4 weeks and 15 normal volunteers were recruited. Single photon emission computed tomography (SPECT) images were obtained after (99m)Tc-ECD injection, and correlations between rCBF patterns and symptom severity ratings were calculated on a voxel-by-voxel basis, using statistical parametric mapping (SPM). Severity of depressive mood was inversely correlated with rCBF in the left amygdala, lentiform nucleus, and parahippocampal gyrus, and directly correlated with rCBF in the right postero-lateral parietal cortex (p < 0.001, uncorrected for multiple comparisons). Insomnia severity was inversely correlated with rCBF in the right rostral and subgenual anterior cingulate cortices, insula and claustrum. Anxiety severity was directly correlated with rCBF in the right antero-lateral orbitofrontal cortex, while cognitive performance was directly correlated with rCBF in the right postero-medial orbitofrontal cortex and in the left lentiform nucleus. Our findings confirmed the prediction that separate symptom domains of the MDD syndrome are related to specific rCBF patterns, and extend results from prior studies that suggested the involvement of anterior cingulate, frontal, limbic and basal ganglia regions in the pathophysiology of MDD.

Adolescent↗

[Nocturnal awakenings as a function of age in insomniacs (author's transl)].

The effect of ageing on the sleep of insomniacs was studied by comparing objective insomnia characteristics from polygraphic recordings made during two successive nights in two groups of different ages : 14 patients aged 19 to 39 years (mean 31 years) and 11 aged 42 to 65 years (mean 50 years). All of them had severe insomnia causing them to request consultation for sleep disorders. Their only clinical symptom was chronic primary insomnia, persisting following withdrawal of hypnotics, no other physical (particularly no sleep apnea) or psychological disorder being present. Parameters studied during the first and the second night were the number and duration of intra-sleep awakenings, and the proportions of the sleep and wakefulness periods.

Adult↗

Attempts to control unwanted thoughts in the night: development of the thought control questionnaire-insomnia revised (TCQI-R).

The attempted control of intrusive, uncontrollable thoughts has been implicated in the maintenance of a range of psychological disorders. The current paper describes the refinement of the Thought Control Questionnaire Insomnia (TCQI; Behav. Cogn. Psychoth. 29 (2001)) through its administration to a sample (n=385) including good sleepers and individuals with insomnia. Several items with poor psychometric properties were discarded, resulting in a 35-item revised TCQI. Factor analysis revealed six factors; aggressive suppression, cognitive distraction, reappraisal, social avoidance, behavioural distraction, and worry. The attempted management of unwanted thoughts was compared across individuals with insomnia and good sleepers, and the impact of these strategies on sleep quality, anxiety and depression was investigated. With the exception of cognitive distraction, individuals with insomnia, relative to good sleepers, more frequently used every thought control strategy. The strategies of aggressive suppression and worry, in particular, appeared to be unhelpful, with the use of these strategies predicting sleep impairment, anxiety and depression. The strategy of cognitive distraction appeared to be helpful, with the use of this strategy predicting better sleep quality.

Adaptation, Psychological↗

Eight weeks of non-nightly use of zolpidem for primary insomnia.

CONTEXT: Intermittent use (i.e., a few nights per week) of hypnotic medication is often recommended for the treatment of chronic insomnia despite an absence of efficacy and safety data using this regimen. STUDY OBJECTIVES: To evaluate the clinical efficacy and safety of intermittent pharmacotherapy for chronic insomnia. DESIGN AND SETTING: Randomized, double-blind, placebo-controlled, parallel groups, clinical trial at six sleep research sites. PATIENTS: One hundred-sixty-three (115 women, 48 men; mean age 44.1+ SE. 0.9 years), DSM-IV-defined primary insomnia patients were randomized, 134 patients completed the study. INTERVENTIONS: Eight weeks of treatment with either zolpidem 10 mg or placebo. Patients were instructed to take medication when they felt they needed it, but at least three and no more than five times per week. MAIN OUTCOME MEASURES: Investigator and Patient Global Ratings were the primary outcome variables. Secondary measures from daily questionnaires to assess efficacy, rebound insomnia and drug taking behavior. RESULTS: The Investigator's Global Rating indicated that intermittent use of zolpidem produced a significantly better therapeutic effect and significantly reduced insomnia severity throughout the 8-week study relative to placebo. Zolpidem was found to be effective in initiating and maintaining sleep on nights taken, as compared to placebo, based upon the Patient's Global Ratings and all subjective sleep variables. No evidence of rebound insomnia was found on nights that zolpidem was not taken. The number of nights a pill was taken did not differ between groups, nor did frequency of pill taking change in either group across the duration of the study. There were no significant effects of treatment upon quality of life or neurocognitive measures. CONCLUSIONS: Zolpidem 10 mg is effective in treating insomnia when used intermittently, without evidence of discontinuation effects or increased frequency of pill taking.

Analysis of Variance↗

Wernicke encephalopathy-like symptoms as an early manifestation of Creutzfeldt-Jakob disease in a chronic alcoholic.

A case of Creutzfeldt-Jakob disease (CJD) with presenting Wernicke encephalopathy (WE)-like symptoms and severe insomnia is presented. An 80-year-old alcoholic man with a 6 month history of tremors, ataxia, memory loss and confabulation, developed profound insomnia, confusion, and delirium with vivid hallucinations. Polysomnography revealed a marked reduction of sleep time, with central-type sleep apnea. Neither myoclonus nor periodic synchronous discharge (PSD) was observed. An autopsy revealed diffuse spongiform changes and astrocytosis throughout the cerebral gray matter, with severe involvement of the mammillary bodies and thalamus. Prion protein (PrP) immunostaining was positive in kuru plaques in the cerebellum, PrP polymorphism at codon 129 was heterozygous Met/Val, and proteinase K resistant PrP (PrP(res)) was demonstrated by Western blotting. The lack of necrotizing lesions in the mammillary bodies, thalamus, and periaqueductal gray matter could rule out WE. The data suggest that the present case of CJD is consistent with PrP(res) type 2 (CJD M/V 2), but was unique in the lack of some typical CJD signs and the presence of signs of WE and sleep abnormalities.

Aged↗

Valerian-hops combination and diphenhydramine for treating insomnia: a randomized placebo-controlled clinical trial.

CONTEXT: Insomnia is a prevalent health complaint associated with daytime impairments, reduced quality of life, and increased health-care costs. Although it is often self-treated with herbal and dietary supplements or with over-the-counter sleep aids, there is still little evidence on the efficacy and safety of those products. OBJECTIVE: To evaluate the efficacy and safety of a valerian-hops combination and diphenhydramine for the treatment of mild insomnia. DESIGN AND SETTING: Multicenter, randomized, placebo-controlled, parallel-group study conducted in 9 sleep disorders centers throughout the United States. PATIENTS: A total of 184 adults (110 women, 74 men; mean age of 44.3 years) with mild insomnia. INTERVENTIONS: (1) Two nightly tablets of standardized extracts of a valerian (187-mg native extracts; 5-8:1, methanol 45% m/m) and hops (41.9-mg native extracts; 7-10:1, methanol 45% m/m) combination for 28 days (n = 59), (2) placebo for 28 days (n = 65), or (3) 2 tablets of diphenhydramine (25 mg) for 14 days followed by placebo for 14 days (n = 60). OUTCOME MEASURES: Sleep parameters measured by daily diaries and polysomnography, clinical outcome ratings from patients and physicians, and quality of life measures. RESULTS: Modest improvements of subjective sleep parameters were obtained with both the valerian-hops combination and diphenhydramine, but few group comparisons with placebo reached statistical significance. Valerian produced slightly greater, though nonsignificant, reductions of sleep latency relative to placebo and diphenhydramine at the end of 14 days of treatment and greater reductions than placebo at the end of 28 days of treatment. Diphenhydramine produced significantly greater increases in sleep efficiency and a trend for increased total sleep time relative to placebo during the first 14 days of treatment. There was no significant group difference on any of the sleep continuity variables measured by polysomnography. In addition, there was no alteration of sleep stages 3-4 and rapid eye movement sleep with any of the treatments. Patients in the valerian and diphenhydramine groups rated their insomnia severity lower relative to placebo at the end of 14 days of treatment. Quality of life (Physical component) was significantly more improved in the valerian-hops group relative to the placebo group at the end of 28 days. There were no significant residual effects and no serious adverse events with either valerian or diphenhydramine and no rebound insomnia following their discontinuation. CONCLUSIONS: The findings show a modest hypnotic effect for a valerian-hops combination and diphenhydramine relative to placebo. Sleep improvements with a valerian-hops combination are associated with improved quality of life. Both treatments appear safe and did not produce rebound insomnia upon discontinuation during this study. Overall, these findings indicate that a valerian-hops combination and diphenhydramine might be useful adjuncts in the treatment of mild insomnia.

Adult↗

Assessment and diagnosis of insomnia in non-pharmacological intervention studies.

A number of non-pharmacologic interventions have been developed and studied for the treatment of primary insomnia in adults. Fifty-four non-pharmacological intervention studies published over the last 20 years were reviewed to determine how primary insomnia was assessed and to characterize patients participating in the studies. The main objectives were to inform clinicians who look to the literature for information on the treatment of insomnia about selection and diagnosis of participants, and to examine differences between clinic-based and research-based studies. Mean age for all patients was 47 years; 65% were women. Studies typically used interview procedures to assess participants. The most common exclusion criteria overall was insomnia secondary to medical illness or psychiatric disorder. Methods for assessing these criteria varied widely across studies. Inclusion most commonly required a 6-month duration of insomnia, and sleep difficulty at least 3 nights per week. There were significant differences between clinic- and research-based studies in the screening assessments, exclusion criteria, and participant drop-out rate. The heterogeneity in assessment and diagnosis complicates comparison across studies. Some studies were more likely to include severe insomnia sufferers and/or individuals with secondary insomnia. Comprehensive assessment and complete reporting of research methods is essential to determining the relative efficacy and clinical utility of interventions. Clinicians should be aware of the differences across studies from research vs. clinical settings. To enhance the generalizability of research-based studies to clinical practice, careful screening and description of study participants is essential. When participants are well-described, research-based studies can be useful and informative to clinicians.

Adult↗

Long-lasting insomnia induced by preoptic neuron lesions and its transient reversal by muscimol injection into the posterior hypothalamus in the cat.

In order to analyse the role of the anterior hypothalamus in the regulation of the sleep-waking cycle we made bilateral neuronal lesions at different levels of the anterior hypothalamus in cats, by means of microinjections of a cell-specific neurotoxin:ibotenic acid. These lesions resulted in severe insomnia in eight cats. This insomnia was characterized by a large decrease or even disappearance of paradoxical sleep and deep slow wave sleep and, to a lesser extent, by a decrease of light slow wave sleep, for 2-3 weeks. In the other five animals, we observed a large reduction of deep slow wave sleep (0-40% of control level), but a less intensive decrease of time spent in paradoxical sleep (50-75% of control level) and no marked effect on light slow wave sleep. During the first 3-6 postoperative days we also noticed hyperthermia in all cats; thereafter, the animals presented only a slight increase in brain temperature which did not appear to trigger the sleep impairment. Histological analysis of the different lesions revealed that the insomnia could be attributed to neuronal cell body destruction in the mediobasal part of the anterior hypothalamus covering; the medial preoptic area and a narrow portion of the lateral preoptic area as well as a restricted part of the anterior hypothalamic nucleus. In order to investigate the putative role of the posterior hypothalamic structures in the mechanism of insomnia after lesion of the mediobasal preoptic area neurons we injected an agonist of GABA into the ventrolateral part of the posterior hypothalamus to locally depress the neuronal activity. The bilateral intracerebral microinjection of muscimol (0.5-5 micrograms) induced a transient intensive hypersomnia (slow wave sleep and paradoxical sleep). These findings indicate that neuronal cell loss in the mediobasal preoptic area induced a long lasting insomnia. Thus, it may be hypothesized that the integrity of this structure is necessary for sleep appearance. Finally, our data are in keeping with an intrahypothalamic regulation of the sleep-waking cycle.

Animals↗