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Sleep Initiation and Maintenance Disorders: HELP
Articles by Atul Malhotra
Based on 7 articles published since 2008
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Between 2008 and 2019, A. Malhotra wrote the following 7 articles about Sleep Initiation and Maintenance Disorders.
 
+ Citations + Abstracts
1 Editorial Connecting insomnia, sleep apnoea and depression. 2017

Grandner, Michael A / Malhotra, Atul. ·Sleep and Health Research Program, Department of Psychiatry, University of Arizona College of Medicine, Tucson, Arizona, USA. · Division of Pulmonary, Critical Care, and Sleep Medicine, Department of Medicine, University of California San Diego, San Diego, California, USA. ·Respirology · Pubmed #28556352.

ABSTRACT: -- No abstract --

2 Review Sleep in Chronic Obstructive Pulmonary Disease: Evidence Gaps and Challenges. 2016

Jen, Rachel / Li, Yanru / Owens, Robert L / Malhotra, Atul. ·Clinical Investigator Program, Department of Medicine, University of British Columbia, Vancouver, BC, Canada V5Z 1M9; Division of Pulmonary, Critical Care and Sleep Medicine, University of California, San Diego, La Jolla, CA 92037, USA. · Department of Otorhinolaryngology-Head and Neck Surgery, Sleep Medicine Center, Beijing Tongren Hospital, Capital Medical University, Beijing 100730, China. · Division of Pulmonary, Critical Care and Sleep Medicine, University of California, San Diego, La Jolla, CA 92037, USA. ·Can Respir J · Pubmed #27445564.

ABSTRACT: Chronic obstructive pulmonary disease (COPD) prevalence is rising to epidemic proportions due to historical smoking trends, the aging of the population, and air pollution. Although blaming the victims has been common in COPD, the majority of COPD worldwide is now thought to be nonsmoking related, that is, caused by air pollution and cookstove exposure. It is increasingly appreciated that subjective and objective sleep disturbances are common in COPD, although strong epidemiological data are lacking. People with obstructive sleep apnea (OSA) plus COPD (the so-called overlap syndrome) have a high risk of cardiovascular death, although again mechanisms are unknown and untested. This review aims to draw attention to the problem of sleep in COPD, to encourage clinicians to ask their patients about symptoms, and to stimulate further research in this area given the large burden of the disease.

3 Article Restless legs syndrome status as a predictor for lower physical function. 2014

Zhang, Chunbai / Li, Yanping / Malhotra, Atul / Ning, Yi / Gao, Xiang. ·From The Channing Division of Network Medicine (C.Z., Y.L., X.G.) and Division of Sleep Medicine (C.Z., A.M.), Department of Medicine, Brigham and Women's Hospital and Harvard Medical School, Boston, MA · the Department of Epidemiology and Community Health (Y.N.), Virginia Commonwealth University, Richmond · the Department of Nutrition (X.G.), Harvard School of Public Health, Boston, MA · and School of Public Health (XG), Peking Union Medical College, Beijing, China. ·Neurology · Pubmed #24598708.

ABSTRACT: OBJECTIVE: To examine the potential long-term impact of restless legs syndrome (RLS) and other common sleep complaints on subsequent physical function (PF), we conducted a longitudinal analysis of 12,556 men in the Health Professionals Follow-up Study. METHODS: We used a set of questions recommended by the International RLS Study Group to assess RLS in 2002. We asked questions regarding other sleep complaints--insomnia, sleep fragmentation, and excessive daytime sleepiness--in 2004. We used the Physical Function (PF-10) survey of the Short Form-36 Health Survey to characterize PF in 1996 and 2008. We examined the 2008 PF-10 scores across categories of baseline RLS (2002), adjusted for age, 1996 PF-10 score, and other potential confounders. RESULTS: The participants with RLS at baseline had significantly lower PF-10 score 6 years later than those without RLS (mean difference = -2.32, p = 0.01), after adjusting for potential confounders. The magnitude of difference in PF-10 score for RLS symptoms ≥ 15 times/month vs no RLS was more than that of a 5-year increase of age or moderate amount of smoking. Having daily daytime sleepiness and sleep duration ≥ 9 hours/day were associated with lower mean PF value than not having these symptoms (p < 0.05 for both). CONCLUSIONS: RLS and other sleep complaints are associated with lower PF. Our findings need to be replicated by more longitudinal studies including women and populations of other social and cultural backgrounds. It is important to understand whether RLS is an independent risk factor or a marker for other unknown risk factors for disability.

4 Article Repeated melatonin supplementation improves sleep in hypertensive patients treated with beta-blockers: a randomized controlled trial. 2012

Scheer, Frank A J L / Morris, Christopher J / Garcia, Joanna I / Smales, Carolina / Kelly, Erin E / Marks, Jenny / Malhotra, Atul / Shea, Steven A. ·Medical Chronobiology Program, Division of Sleep Medicine, Department of Medicine, Brigham and Women's Hospital, Boston, Massachusetts, USA. fscheer@rics.bwh.harvard.edu ·Sleep · Pubmed #23024438.

ABSTRACT: STUDY OBJECTIVES: In the United States alone, approximately 22 million people take beta-blockers chronically. These medications suppress endogenous nighttime melatonin secretion, which may explain a reported side effect of insomnia. Therefore, we tested whether nightly melatonin supplementation improves sleep in hypertensive patients treated with beta-blockers. DESIGN: Randomized, double-blind, placebo-controlled, parallel-group design. SETTING: Clinical and Translational Research Center at Brigham and Women's Hospital, Boston. PATIENTS: Sixteen hypertensive patients (age 45-64 yr; 9 women) treated with the beta-blockers atenolol or metoprolol. INTERVENTIONS: Two 4-day in-laboratory admissions including polysomnographically recorded sleep. After the baseline assessment during the first admission, patients were randomized to 2.5 mg melatonin or placebo (nightly for 3 weeks), after which sleep was assessed again during the second 4-day admission. Baseline-adjusted values are reported. One patient was removed from analysis because of an unstable dose of prescription medication. MEASUREMENTS AND RESULTS: In comparison with placebo, 3 weeks of melatonin supplementation significantly increased total sleep time (+36 min; P = 0.046), increased sleep efficiency (+7.6%; P = 0.046), and decreased sleep onset latency to Stage 2 (-14 min; P = 0.001) as assessed by polysomnography. Compared with placebo, melatonin significantly increased Stage 2 sleep (+41 min; P = 0.037) but did not significantly change the durations of other sleep stages. The sleep onset latency remained significantly shortened on the night after discontinuation of melatonin administration (-25 min; P = 0.001), suggesting a carryover effect. CONCLUSION: n hypertensive patients treated with beta-blockers, 3 weeks of nightly melatonin supplementation significantly improved sleep quality, without apparent tolerance and without rebound sleep disturbance during withdrawal of melatonin supplementation (in fact, a positive carryover effect was demonstrated). These findings may assist in developing countermeasures against sleep disturbances associated with beta-blocker therapy. CLINICAL TRIAL INFORMATION: his study is registered with ClinicalTrials.gov, identifier: NCT00238108; trial name: Melatonin Supplements for Improving Sleep in Individuals with Hypertension; URL: http://www.clinicaltrials.gov/ct2/show/NCT00238108.

5 Article A possible method to predict response to non-pharmacological insomnia therapy. 2011

Campana, Lisa M / Clifford, Gari D / Trinder, John / Pittman, Stephen D / Malhotra, Atul. ·Boston University, Boston, MA, USA. lcampana@bu.edu ·J Clin Sleep Med · Pubmed #21897773.

ABSTRACT: STUDY OBJECTIVES: To determine if electrocardiographic parameters are predictive of response to non-pharmacological insomnia therapy. DESIGN: Secondary analysis of heart rate parameters from a double blind, randomized, sham-controlled trial at multiple study sites. SETTING: Six sites in the United States were used for the data collection. PARTICIPANTS: One hundred ninety-eight healthy subjects with no sleep disorders. INTERVENTIONS: Subjects were studied on 2 consecutive nights, a baseline night and a therapy night. On the therapy night, subjects were phase advanced 4 h and randomized to receive either sham or vestibular stimulation, an experimental therapy for insomnia. MEASUREMENTS AND RESULTS: ECG data were recorded and analyzed for the 5-min periods preceding and following sleep onset. Analyses were conducted on those who did and did not respond to therapy, as defined by latency from bedtime to persistent sleep (LPS). Responders to therapy were found to have higher low-frequency (LF) power at baseline during wakefulness than non-responders, and responders had higher high-frequency (HF) power during therapy than non-responders on therapy. Furthermore, responders > 35 y had elevated LF power at baseline than non-responders > 35 y (p < 0.05). No differences were seen in the sham group in identical analyses, ruling out a nonspecific effect of sleep onset. CONCLUSIONS: Heart rate variability analyses indicate that differences exist between those who respond to insomnia therapy and those that do not, particularly in an older subset of subjects. Further research into the use of ECG and other physiological parameters to stratify response to therapeutic interventions is warranted.

6 Article The effect of vestibular stimulation in a four-hour sleep phase advance model of transient insomnia. 2010

Krystal, Andrew D / Zammit, Gary K / Wyatt, James K / Quan, Stuart F / Edinger, Jack D / White, David P / Chiacchierini, Richard P / Malhotra, Atul. ·Duke University School of Medicine, Durham, NC 27710, USA. kryst001@mc.duke.edu ·J Clin Sleep Med · Pubmed #20726278.

ABSTRACT: STUDY OBJECTIVES: To determine if vestibular stimulation is an effective therapy for transient insomnia in a sleep phase advance model. DESIGN: Multi-site, double-blind, randomized, parallel-group, sham-controlled trial SETTING: This study was carried out at 6 sites in the United States. PARTICIPANTS: 198 healthy normal sleepers. INTERVENTIONS: Bilateral electrical stimulation of the vestibular apparatus of the inner ear via electrodes on the skin of the mastoid process at a frequency of 0.5 Hz vs. sham stimulation. RESULTS: We did not find a significant effect of treatment on our primary outcome variable, latency to persistent sleep onset (LPS). However, our planned analysis identified that the mean latency to sleep onset on the multiple sleep latency test was a significant covariate. This led us to carry out post hoc analyses, which showed a significant effect of treatment on LPS in those subjects with a mean MSLT sleep onset latency > or = 14 minutes. CONCLUSIONS: Vestibular stimulation did not have a therapeutic effect in a model of transient insomnia in the overall population studied. However, this study provides preliminary evidence that vestibular stimulation may shorten sleep onset latency compared with sham therapy in the subset of subjects with mean MSLT sleep onset latency > or = 14 minutes.

7 Article Trazodone increases arousal threshold in obstructive sleep apnoea. 2008

Heinzer, R C / White, D P / Jordan, A S / Lo, Y L / Dover, L / Stevenson, K / Malhotra, A. ·Sleep Medicine Division, Brigham and Women's Hospital, Harvard Medical School, Boston, MA, USA. rheinzer@post.harvard.edu ·Eur Respir J · Pubmed #18256066.

ABSTRACT: A low arousal threshold is believed to predispose to breathing instability during sleep. The present authors hypothesised that trazodone, a nonmyorelaxant sleep-promoting agent, would increase the effort-related arousal threshold in obstructive sleep apnoea (OSA) patients. In total, nine OSA patients, mean+/-sd age 49+/-9 yrs, apnoea/hypopnoea index 52+/-32 events.h(-1), were studied on 2 nights, one with trazodone at 100 mg and one with a placebo, in a double blind randomised fashion. While receiving continuous positive airway pressure (CPAP), repeated arousals were induced: 1) by increasing inspired CO(2) and 2) by stepwise decreases in CPAP level. Respiratory effort was measured with an oesophageal balloon. End-tidal CO(2 )tension (P(ET,CO(2))) was monitored with a nasal catheter. During trazodone nights, compared with placebo nights, the arousals occurred at a higher P(ET,CO(2)) level (mean+/-sd 7.30+/-0.57 versus 6.62+/-0.64 kPa (54.9+/-4.3 versus 49.8+/-4.8 mmHg), respectively). When arousals were triggered by increasing inspired CO(2) level, the maximal oesophageal pressure swing was greater (19.4+/-4.0 versus 13.1+/-4.9 cm H(2)O) and the oesophageal pressure nadir before the arousals was lower (-5.1+/-4.7 versus -0.38+/-4.2 cm H(2)O) with trazodone. When arousals were induced by stepwise CPAP drops, the maximal oesophageal pressure swings before the arousals did not differ. Trazodone at 100 mg increased the effort-related arousal threshold in response to hypercapnia in obstructive sleep apnoea patients and allowed them to tolerate higher CO(2) levels.