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Primary Insomnia (primary + insomnia)
Selected AbstractsSensory gating in primary insomniaEUROPEAN JOURNAL OF NEUROSCIENCE, Issue 11 2010Ilana S. Hairston Abstract Although previous research indicates that sleep architecture is largely intact in primary insomnia (PI), the spectral content of the sleeping electroencephalographic trace and measures of brain metabolism suggest that individuals with PI are physiologically more aroused than good sleepers. Such observations imply that individuals with PI may not experience the full deactivation of sensory and cognitive processing, resulting in reduced filtering of external sensory information during sleep. To test this hypothesis, gating of sensory information during sleep was tested in participants with primary insomnia (n = 18) and good sleepers (n = 20). Sensory gating was operationally defined as (i) the difference in magnitude of evoked response potentials elicited by pairs of clicks presented during Wake and Stage II sleep, and (ii) the number of K complexes evoked by the same auditory stimulus. During wake the groups did not differ in magnitude of sensory gating. During sleep, sensory gating of the N350 component was attenuated and completely diminished in participants with insomnia. P450, which occurred only during sleep, was strongly gated in good sleepers, and less so in participants with insomnia. Additionally, participants with insomnia showed no stimulus-related increase in K complexes. Thus, PI is potentially associated with impaired capacity to filter out external sensory information, especially during sleep. The potential of using stimulus-evoked K complexes as a biomarker for primary insomnia is discussed. [source] The effectiveness of acupuncture and reflexology in primary insomniaFOCUS ON ALTERNATIVE AND COMPLEMENTARY THERAPIES AN EVIDENCE-BASED APPROACH, Issue 2005CA McCullough [source] Sleep and Headache Disorders: Clinical Recommendations for Headache ManagementHEADACHE, Issue 2006Jeanetta C. Rains PhD Clinical practice points were drawn from a review of sleep and headache disorders published in the regular issue of Headache (released in tandem with this supplement). The recommendations include: (1) Sleep as well as psychiatric disorders tend to become prevalent in more complex and severe headache patterns and regulation of sleep and mood may favorably impact headache threshold; (2) Specific headache patterns, irrespective of headache diagnosis, are suggestive of a potential sleep disorder (eg, "awakening" or morning headache, chronic daily headache); (3) Sleep disorders most implicated with headache include obstructive sleep apnea, primary insomnia, and circadian phase abnormalities, and treatment of such sleep disorders may improve or resolve headache; (4) Inexpensive screening tools (eg, sleep history interview, headache/sleep diary, validated questionnaires, prediction equations) aid identification of patients warranting polysomnography; and (5) Pharmacologic and behavioral therapies are effective in the regulation of sleep and are compatible with usual headache care. [source] Next-day cognition, psychomotor function, and driving-related skills following nighttime administration of eszopicloneHUMAN PSYCHOPHARMACOLOGY: CLINICAL AND EXPERIMENTAL, Issue 5 2008Julia Boyle Abstract Objective To evaluate next-day driving ability, as assessed by brake reaction time (BRT), and cognitive/psychomotor function following nighttime administration of 3,mg eszopiclone. Methods Two randomized, double-blind, placebo-controlled, cross-over studies were performed in healthy volunteers (n,=,32) and patients with primary insomnia (n,=,32). Study participants received nighttime dosing of 3,mg eszopiclone or placebo. BRT and a psychometric test battery were used to assess the next-day effects of eszopiclone treatment. Results In both studies, driving ability and measures of cognitive and psychomotor function were not impaired the morning after eszopiclone, as compared to placebo. All eszopiclone subjects reported improved ease in getting to sleep and quality of sleep with no significant changes in behavior upon awakening. A significant increase in next-day feelings of sedation was reported in healthy volunteers, but not in patients with primary insomnia, following eszopiclone treatment relative to placebo. Sleep induction, maintenance, duration, and efficiency, as assessed by PSG, were significantly improved following eszopiclone treatment in patients with insomnia. Conclusions Nighttime administration of 3,mg eszopiclone improved objective and subjective sleep measures in patients with insomnia (and subjective sleep measures in healthy patients) and did not impair next-day driving-related skills or measures of cognition in either study population relative to placebo. Copyright © 2008 John Wiley & Sons, Ltd. [source] Dose-response effects of zaleplon as compared with triazolam (0·25 mg) and placebo in chronic primary insomniaHUMAN PSYCHOPHARMACOLOGY: CLINICAL AND EXPERIMENTAL, Issue 8 2000Christopher L Drake Abstract The effects of two nights of treatment with the short-acting benzodiazepine receptor agonist zaleplon, triazolam, or placebo was assessed in chronic primary insomniacs using two concurrent, multi-center, randomized, double-blind, Latin Square crossover studies. Study 1 (n = 47) compared zaleplon (10 and 40 mg) to triazolam (0·25 mg) and placebo. Study 2 (n = 36) compared zaleplon (20 and 60 mg) to triazolam (0·25 mg) and placebo. For each study, polysomnographically recorded sleep parameters and patient reports of sleep quality were collected during baseline and two consecutive nights during the four treatment phases in each study. All doses of zaleplon produced significant decreases in latency to persistent sleep. Although no minimally effective dose could be determined, dose-response effects were apparent. Triazolam 0·25 mg produced a decrease in latency to persistent sleep that was comparable to that of zaleplon 10 mg. Only the triazolam dose and the 60 mg dose of zaleplon produced significant increases in total sleep time over placebo. Zaleplon 40 and 60 mg and triazolam produced decreases in the percentage of REM sleep compared to placebo. Patient reports of efficacy were consistent with objective findings. In addition, all doses of zaleplon tended to increase while triazolam decreased the percentage of stage 3/4 sleep. There was no evidence of residual daytime impairment for any of the zaleplon doses, however, triazolam administration produced significant impairment in performance on a digit copying test. A higher number of adverse events were seen with the 40 and 60 mg doses of zaleplon compared to triazolam (0·25) and placebo. At higher doses, zaleplon is more effective than triazolam at reducing latency to persistent sleep in chronic insomnia and is not associated with the decrease in slow-wave sleep or residual impairment observed with triazolam. However, increases in total sleep time were apparent only at doses which produced concomitant increases in the number of adverse events. In contrast, triazolam (0·25 mg) produced increases in total sleep time (,25 min) and decreases in latency to persistent sleep at a dose of 0·25 mg. Copyright © 2000 John Wiley & Sons, Ltd. [source] The Role of Benzodiazepines in the Treatment of InsomniaJOURNAL OF AMERICAN GERIATRICS SOCIETY, Issue 6 2001Meta-Analysis of Benzodiazepine Use in the Treatment of Insomnia PURPOSE: To obtain a precise estimate of the efficacy and common adverse effects of benzodiazepines for the treatment of insomnia compared with those of placebo and other treatments. BACKGROUND: Insomnia, also referred to as disorder of initiating or maintaining sleep, is a common problem and its prevalence among older people is estimated to be 23% to 34%.1 The total direct cost in the United States for insomnia in 1995 was estimated to be $13.9 billion.2 The complaint of insomnia in older people is associated with chronic medical conditions; psychiatric problems, mainly depression, chronic pain, and poor perceived general condition;1,3,4 and use of sleep medications.5 Thus in most cases, insomnia is due to some other underlying problem and is not just a consequence of aging.6 Accordingly, the management of insomnia should focus on addressing the primary problem and not just short-term treatment of the insomnia. Benzodiazepines belong to the drug class of choice for the symptomatic treatment of primary insomnia.7 This abstract will appraise a meta-analysis that compared the effect of benzodiazepines for short-term treatment of primary insomnia with placebo or other treatment. DATA SOURCES: Data sources included articles listed in Medline from 1966 to December 1998 and the Cochrane Controlled Trials Registry. The medical subject heading (MeSH) search terms used were "benzodiazepine" (exploded) or "benzodiazepine tranquillizers" (exploded) or "clonazepam,""drug therapy,""randomized controlled trial" or "random allocation" or "all random,""human," and "English language." In addition, bibliographies of retrieved articles were scanned for additional articles and manufacturers of brand-name benzodiazepines were asked for reports of early trials not published in the literature. STUDY SELECTION CRITERIA: Reports of randomized controlled trials of benzodiazepine therapy for primary insomnia were considered for the meta-analysis if they compared a benzodiazepine with a placebo or an alternative active drug. DATA EXTRACTION: Data were abstracted from 45 randomized controlled trials representing 2,672 patients, 47% of whom were women. Fifteen studies included patients age 65 and older and four studies involved exclusively older patients. Twenty-five studies were based in the community and nine involved inpatients. The duration of the studies ranged from 1 day to 6 weeks, with a mean of 12.2 days and median of 7.5 days. The primary outcome measures analyzed were sleep latency and total sleep duration after a sleep study, subjects' estimates of sleep latency and sleep duration, and subjects' report of adverse effects. Interrater reliability was checked through duplicate, independent abstraction of the first 21 articles. Overall agreement was between 95% and 98% (kappa value of 0.90 and 0.95 accordingly) for classification of the studies and validity of therapy, and 76% (kappa value of 0.51) for study of harmful effects. A scale of 0 to 5 was used to rate the individual reports, taking into account the quality of randomization, blinding, follow-up, and control for baseline differences between groups. Tests for homogeneity were applied across the individual studies and, when studies were found to be heterogeneous, subgroup analysis according to a predefined group was performed. MAIN RESULTS: The drugs used in the meta-analysis included triazolam in 16 studies; flurazepam in 14 studies; temazepam in 13 studies; midazolam in five studies; nitrazepam in four studies; and estazolam, lorazepam, and diazepam in two studies each. Alternative drug therapies included zopiclone in 13 studies and diphenhydramine, glutethimide, and promethazine in one study each. Only one article reported on a nonpharmacological treatment (behavioral therapy). The mean age of patients was reported in 33 of the 45 studies and ranged between 29 and 82. SLEEP LATENCY: In four studies involving 159 subjects, there was sleep-record latency (time to fall asleep) data for analysis. The pooled difference indicated that the latency to sleep for patients receiving a benzodiazepine was 4.2 minutes (95% CI = (,0.7) (,9.2)) shorter than for those receiving placebo. Patient's estimates of sleep latency examined in eight studies showed a difference of 14.3 minutes (95% CI = 10.6,18.0) in favor of benzodiazepines over placebo. TOTAL SLEEP DURATION: Analysis of two studies involving 35 patients in which total sleep duration using sleep-record results was compared indicated that patients in the benzodiazepine groups slept for an average of 61.8 minutes (95% CI = 37.4,86.2) longer than those in the placebo groups. Patient's estimates of sleep duration from eight studies (566 points) showed total sleep duration to be 48.4 minutes (95% CI = 39.6,57.1) longer for patients taking benzodiazepines than for those on placebo. ADVERSE EFFECTS: Analysis of eight studies (889 subjects) showed that those in the benzodiazepine groups were more likely than those in the placebo groups to complain of daytime drowsiness (odds ratio (OR) 2.4, 95% confidence interval (CI) = 1.8,3.4). Analysis of four studies (326 subjects) also showed that subjects in the benzodiazepine groups were more likely to complain of dizziness or lightheadedness than the placebo groups. (OR 2.6, 95% CI = 0.7,10.3). Despite the increased reported side effects in the benzodiazepine groups, drop-out rates were similar in the benzodiazepine and placebo groups. For patient reported outcome, there was no strong correlation found for sleep latency data, (r = 0.4, 95% CI = (,0.3) (,0.9)) or for sleep duration (r = 0.2, 95% CI = ,0.8,0.4) between benzodiazepine dose and outcome. COMPARISON WITH OTHER DRUGS AND TREATMENTS: In three trials with 96 subjects, meta-analysis of the results comparing benzodiazepines with zopiclone, did not show significant difference in sleep latency in the benzodiazepine and placebo groups, but the benzodiazepine groups had increased total sleep duration (23.1 min. 95% CI = 5.6,40.6). In four trials with 252 subjects, the side effect profile did not show a statistically significant difference (OR 1.5, CI 0.8,2.9). There was only one study comparing the effect of behavioral therapy with triazolam. The result showed that triazolam was more effective than behavioral therapy in decreasing sleep latency, but its efficacy declined by the second week of treatment. Behavioral therapy remained effective throughout the 9-week follow-up period. There were four small trials that involved older patients exclusively, with three of the studies having less than 2 weeks of follow-up. The results were mixed regarding benefits and adverse effects were poorly reported. CONCLUSION: The result of the meta-analysis shows that the use of benzodiazepines results in a decrease in sleep latency and a significant increase in total sleep time as compared with placebo. There was also a report of significantly increased side effects, but this did not result in increased discontinuation rate. There was no dose-response relationship for beneficial effect seen with the use of benzodiazepines, although the data are scant. Zopiclone was the only alternative pharmacological therapy that could be studied with any precision. There was no significant difference in the outcome when benzodiazepines were compared with zopiclone. There was only one study that compared the effect of benzodiazepines with nonpharmacological therapy; thus available data are insufficient to comment. [source] Sleep-related attentional bias in patients with primary insomnia compared with sleep experts and healthy controlsJOURNAL OF SLEEP RESEARCH, Issue 2 2008KAI SPIEGELHALDER Summary Sleep-related attentional bias has been proposed to be an important factor in the development and maintenance of primary insomnia. In this study, a newly introduced mixed modality (visual auditory) task and an emotional Stroop task were used to investigate attentional processes in patients with primary insomnia, sleep experts and healthy controls (n = 20 per group). The sleep expert group served as second control group to control for effects of frequency of concept usage (FOCU). The results of the emotional Stroop task showed a sleep-related attentional bias in the insomnia group in comparison with the expert group. However, no significant differences were detected in the other group comparisons and in the mixed modality task. The difference between insomnia patients and sleep experts in the emotional Stroop task indicates that FOCU is not the underlying process of sleep-related attentional bias. Insomnia patients seem to be more emotionally, cognitively or procedurally affected by sleep-related stimuli than sleep experts. The findings suggest that a desensitization of sleep-related stimuli might be used therapeutically, thus extending the current cognitive behavioral treatments for primary insomnia. [source] Latest news and product developmentsPRESCRIBER, Issue 13-14 2008Article first published online: 29 JUL 200 NSAIDs stroke risk NSAIDs have been linked with an increased risk of stroke in an epidemiological study from The Netherlands (Arch Intern Med 2008;168: 1219-24). Nine years' follow-up of 7636 older persons (mean age 70) identified 807 strokes. The risk of stroke was significantly increased for current use of nonselective NSAIDs (hazard ratio 1.72 for all strokes) and COX-2 selective NSAIDs (HR 2.75 for all strokes; HR 4.54 for ischaemic stroke). Increased risk was found for several individual NSAIDs but was statistically significant only for naproxen (HR 2.63) and the withdrawn rofecoxib (HR 3.38). HPV vaccine chosen The DoH has chosen GlaxoSmithKline's Cervarix HPV vaccine for the national immunisation campaign beginning in September. Cervarix is a bivalent vaccine conferring immunity against HPV16 and 18, which account for 70 per cent of cervical cancers worldwide. Its competitor, Gardasil, is a quadrivalent vaccine additionally protecting against HPV6 and 11, which cause 90 per cent of genital warts. The procurement process assessed the vaccines against ,a wide range of criteria such as their scientific qualities and cost effectiveness'. The DoH has not revealed what it will pay for Cervarix. Melatonin for insomnia Lundbeck has introduced melatonin (Circadin) as monotherapy for the short-term treatment of primary insomnia characterised by poor quality of sleep in patients who are aged 55 or over. The dose is 2mg once daily two hours before bed-time and after food for three weeks. A course costs £10.77. Fesoterodine launched Pfizer has introduced feso-terodine (Toviaz), a prodrug for tolterodine (Detrusitol), for the treatment of symptoms of overactive bladder. Treatment is initiated at a dose of 4mg per day and increased to 8mg per day according to response. The full therapeutic effect may not occur until after two to eight weeks; treatment should be re-evaluated after eight weeks. A month's treatment at either dose costs £29.03, the same as sustained-release tolterodine (Detrusitol XL). Intensive glycaemic control for T2D? Two large trials of intensive glycaemic control in patients with type 2 diabetes have conflicting implications for clinical practice. The ACCORD study (N Engl J Med 2008;358:2545-9) found that treating patients at high CVD risk to a target HbA1c of <6.0 per cent was associated with a 22 per cent increased risk of death and no reduction in macrovascular end-points compared with a target of 7.0-7.9 per cent. The ADVANCE study compared treating to a standard (HbA1c 7.3 per cent) or low (HBA1c 6.5 per cent) target. More intensive glycaemic control significantly reduced microvascular end-points, primarily due to a reduction in nephropathy. There was no difference in the risk of retinopathy or macrovascular end-points. Nicorandil as ulcer cause The potassium-channel activator nicorandil (Ikorel) may be associated with gastro-intestinal ulceration but is frequently overlooked as a possible cause, warns the MHRA in its latest Drug Safety Update (2008;1:Issue 11). Ulceration may affect any portion of the gastro-intestinal tract from the mouth to the perianal area, and it is frequently severe and may cause perforation. Ulcers due to nicorandil are refractory to treatment and only resolve on withdrawal of the drug. Withdrawal should be carried out under the supervision of a cardiologist. , This issue of Drug Safety Update also includes an overview of safety issues with natalizumab (Tysabri) for multiple sclerosis. Atypical antipsychotics diabetes risk ,small' The excess risk of diabetes due to treatment with an atypical antipsychotic is small compared with older anti-psychotics, say UK researchers (Br J Psychiatry 2008;192:406-11). Their meta-analysis of 11 studies found that, compared with the use of first-generation antipsychotics in patients with schizophrenia, the over-all increased risk of diabetes with atypicals was 32 per cent. Risperidone was associated with lowest excess risk (16 per cent), followed by quetiapine (Seroquel) and olanzapine (Zyprexa; 28 per cent) then clozapine (39 per cent). Most studies had method-ological limitations. Copyright © 2008 Wiley Interface Ltd [source] Circadin: a new option in sleep disordersPROGRESS IN NEUROLOGY AND PSYCHIATRY, Issue 8 2008Mark Greener Circadin - a prolonged-release formulation containing 2mg melatonin - offers a promising short-term treatment for primary insomnia that is characterised by poor sleep quality in patients aged 55 years or over. Medical writer, Mark Greener, reviews this new addition to the sleep treatment armamentarium. Copyright © 2008 Wiley Interface Ltd [source] | ||||||||||