Peter R. Buchanan

Increased sexual desire with exogenous testosterone administration in men with obstructive sleep apnea: a randomized placebo‐controlled study

Testosterone (T) deficiency, sexual dysfunction, obesity and obstructive sleep apnea (OSA) are common and often coexist. T prescriptions have increased worldwide during the last decade, including to those with undiagnosed or untreated OSA. The effect of T administration on sexual function, neurocognitive performance and quality of life in these men is poorly defined. The aim of this study was to examine the impact of T administration on sexual function, quality of life and neurocognitive performance in obese men with OSA. We also secondarily examined whether baseline T might modify the effects of T treatment by dichotomizing on baseline T levels pre‐specified at 8, 11 and 13 nmol/L. This was a randomized placebo‐controlled study in which 67 obese men with OSA (mean age 49 ± 1.3 years) were randomized to receive intramuscular injections of either 1000 mg T undecanoate or placebo at baseline, week 6 and week 12. All participants were concurrently enrolled in a weight loss program. General and sleep‐related quality of life, neurocognitive performance and subjective sexual function were assessed before and 6, 12 and 18 weeks after therapy. T compared to placebo increased sexual desire (p = 0.004) in all men, irrespective of baseline T levels. There were no differences in erectile function, frequency of sexual attempts, orgasmic ability, general or sleep‐related quality of life or neurocognitive function (all p = NS). In those with baseline T levels below 8 nmol/L, T increased vitality (p = 0.004), and reduced reports of feeling down (p = 0.002) and nervousness (p = 0.03). Our findings show that 18 weeks of T therapy increased sexual desire in obese men with OSA independently of baseline T levels whereas improvements in quality of life were evident only in those with T levels below 8 nmol/L. These small improvements would need to be balanced against potentially more serious adverse effects of T therapy on breathing.

Spectral EEG analysis and sleepwalking defense: unreliable scientific evidence.

I a recent publication in JCSM,1 Drs. Cartwright and Guilleminault suggest that spectral analysis of the sleep EEG can be used to support a defense of sleepwalking in criminal cases. In particular the authors point to 3 publications that concluded that the sleep of sleepwalkers is defi ned by frequent arousals during SWS (slow wave sleep) as well as—or as a result of—lower % of SWA (slow wave activity).2-4 However, the authors of the study most often referred to have themselves concluded that spectral analysis of the sleep EEG in sleepwalkers is not suitable for forensic use. Gadreau and colleagues2 write: “ Given the likelihood that results of our study could be used in medico-legal settings, it is worth noting that the presence or absence of a decrease of SWA early in the night and of awakenings from SWS in a given individual does not conclusively establish or refute a tendency toward sleepwalking” (pages 4-5). The issue of frequent arousals and changes in SWS% in sleepwalkers as forensic evidence has also been previously reviewed in detail5 and was the subject of a series of letters to the editor of Sleep Medicine Reviews between Drs. Cartwright and Pressman in 2007-8 that readers might fi nd of interest.6-9 As noted by Drs. Cartwright and Guilleminault, establishing a current diagnosis of sleepwalking for a defendant is not the same as establishing that the defendant was sleepwalking during the commission of a crime. Nevertheless, this article suggests that spectral analysis of sleep recorded months or years after the incident offense can be used to support such a sleepwalking defense. There are 3 scientifi c publications currently available that conclude that arousals from SWS sleep and hypersynchronous delta waves are not diagnostic for sleepwalking.10-12 These published scientifi c studies analyzed arousals and SWS using standard visual methods and have reported a lack of statistical sensitivity and especially specifi city as diagnostic markers. Further, there are now more than 7 published studies that report arousals indexes for patients with sleepwalking (see Table 1 in ref. 10). While they are often elevated compared to normal controls there is signifi cant interstudy variability and there is no specifi c cutoff statistically or otherwise to assist in making the diagnosis. Additionally, the Spectral EEG Analysis and Sleepwalking Defense: Unreliable Scientifi c Evidence Mark R. Pressman, Ph.D., F.A.A.S.M.1; Mark Mahowald, M.D., F.A.A.S.M.2; Carlos Schenck, M.D.2; Michel Cramer Bornemann, M.D., F.A.A.S.M.3; Dev Banerjee, M.D.4; Michael Howell, M.D.2; Peter Buchanan, M.D.4; Alon Avidan, M.D., M.P.H., F.A.A.S.M.5 1Lankenau Medical Center and Lankenau Institute for Medical Research, Jefferson Medical School, Villanova School of Law, Villanova, PA; 2University of Minnesota, Minneapolis, MN; 3Sleep Medicine Services, HealthEast Care Systems of Minnesota, Minneapolis, MN; 4NHMRC Centre for Integrated Research and Understanding of Sleep (CIRUS), Woolcock Institute of Medical Research, Sydney, Australia; 5UCLA Sleep Disorders Center, Department of Neurology David Geffen School of Medicine at UCLA, UCLA, Los Angeles, CA

Alcohol, sleepwalking and violence: lack of reliable scientific evidence.

Sir, The recent Letter to the Editor by Drs Ebrahim and Fenwick (2012) challenges one sentence in a 2010 article published in Brain (Siclari et al. , 2010) stating that, because of the lack of reliable evidence, alcohol-induced sleepwalking should not be allowed as a defence to criminal acts. This, in turn, refers to an article published 22 years ago (Mahowald et al. , 1990). Drs Ebrahim and Fenwick express concern that defendants who have allegedly committed criminal acts while severely intoxicated with alcohol are potentially being denied a valid defence. In our opinion, claims of alcohol-induced sleepwalking violence or sleep sex …

Z Drug zombies: Parasomnia, drug effect or both?

In this issue of SMR Mark Pressman1 addresses the perplexing problem of sleep driving, particularly as it relates to use of zolpidem and zopiclone. His argument can be summarised into two major points. Firstly, the symptoms of the two conditions sleepwalking sleep driving (i.e., sleep driving as an uncommon variant of the non-REM parasomnia sleepwalking) and Z drug affected driving are qualitatively different phenomena. Secondly, Z drug affected driving appears to occur more commonly than sleepwalking sleep driving, and may be an under-acknowledged public and individual health hazard. The article suggests guidelines, based on current knowledge and informed speculation, which may help to identify and better understand the inherently dangerous activity of driving while under the influence of an hypnotic. Dr Pressman proposes that there is an incorrect lumpingtogether of these driving behaviours and teases out important differentiating features between the major aetiological categories. On the one hand, he draws upon the common descriptions of sleepwalking (and its variants) which have the typical background of genetic predisposition,2 priming factors (stress, sleep deprivation)3 and acute precipitating events (touch, noise) to remind us of the behavioural features that fit a diagnosis of the non-REM parasomnia sleepwalking (and by implication the sleep driving variant of sleepwalking). It is notable there has been very meagre and only indirect documentation of such “true” sleep driving sleepwalking episodes in the literature. There have been useful recent attempts to more readily reproduce more generally reported non-REM parasomnia behaviour in the sleep laboratory, and in other controlled experimental conditions looking at the semiology of parasomnias and like behaviours.3–6 This approach holds promise to advance the science of parasomnias but we are yet to see any direct method for studying sleepwalking sleep driving specifically. However it does appear that non-REM parasomnia research is gaining some critical momentum that has been hitherto lacking (this article, and others,2–4 plus the recent award by the AASM to Drs Mahowald and Schenck for their pioneering work in the parasomnia field may stimulate further research).5 In Australia a recent survey of sleep physicians has indicated that the lack of evidence for conventional pharmacotherapy of non-REM parasomnias is worrying to clinicians and this concern will hopefully translate into a well-structured trial of therapy.7,8 Additionally Pressman draws upon governmental and other data sources to present a description of Z drug impaired driving behaviour that carries an only superficial resemblance to the behaviour presented as characteristic of “true” sleepwalking sleep driving. What is seen both at the roadside and supported by observations from controlled experimental conditions is that Z drug-associated driving is behaviour attributable to CNS

Alcohol and Sleep Review: Flawed Design, Methods, and Statistics Cannot Support Conclusions

N A RECENT publication, Ebrahim and colleagues state in their abstract that they have provided an assessment of “all known scientific studies of the effects of alcohol on the nocturnal sleep of healthy volunteers” (Ebrahim et al., 2013, p. 539). Our review of this article found it to be seriously flawed by research design and statistical problems. Ebrahim and colleagues (2013) selected 20 published articles concerned with the effects of alcohol on sleep in humans. Numerous articles were excluded from consideration. Within these articles are 38 groups of subjects based on other criteria such as sex or dose of alcohol administered. Although all sleep stages were addressed, Ebrahim and colleagues (2013) focus on the effects of alcohol on slow-wave sleep (SWS); variously known as or abbreviated as SWS, deep sleep, Stages 3 + 4. Current nomenclature combines stages 3 and 4 sleep and renames them “N3”(Iber et al., 2007). As noted in their conclusion, One area of debate and sometimes controversy has been the issue of the impact of alcohol on SWS. For the first time, all the available data are presented here and based on the findings from all available studies, and in the majority, alcohol clearly increases SWS in the first part of sleep at all doses, across gender and ages. Data for the impact of alcohol on total night SWS display a dose dependent effect with low doses showing no clear trend, moderate doses show a trend toward an increase in SWS and with high doses there is a significant and clear effect of increasing total SWS. This effect is consistent across gender and age groups. (Ebrahim et al., 2013, pp. 547–548)

Neuropharmacology of obstructive sleep apnea and central apnea

There has been limited progress in the development of effective pharmacotherapy for sleep apnea. A range of agents has been utilized, but there has been lack of or only modest benefit in the treatment of OSA and CSA using these agents. Anumber of drug therapies are limited as well by significant side effects. The promise of serotonergic drug therapy is yet to be realized, and further developments await the full exploration and understanding of the complex interplay of the various and often counteractive 5-HT receptor subtypes in the CNS and PNS that in concert may affect upper airway patency in sleep and wake states. It is possible that effective OSA drug treatment may necessitate combination drug therapies, for example so that excitatory stimulation of upper airway dilator muscles in sleep is combined with pharmacological inhibitory actions on constrictor/relaxant mechanisms.

Supine awake oximetry as a screening tool for daytime hypercapnia in super-obese patients

Evidence‐based screening tools are required for detection of daytime hypercapnia in high‐risk patient populations.

Positive-pressure treatment of obstructive sleep apnea syndrome.

Publisher Summary Continuous positive airway pressure (CPAP) is applied in the established treatment of first choice for moderate to severe obstructive sleep apnea syndrome (OSAS). Studies have provided information on different aspects of usage and compliance of CPAP therapy. The chapter presents the data with emphasis on the practical use of CPAP therapy in clinical management of OSAS patients. Positive airway pressure (PAP) is the treatment of first choice for obstructive sleep apnea (OSA) of moderate or greater severity in adults. Applied through a facial interface it is a very effective and safe method of preventing the upper-airway obstructions characteristic of OSA. There remain issues of imperfect patient acceptance and compliance with continuous PAP, uncertainties regarding the role of CPAP in mild OSA, and the desired cardiovascular benefits of CPAP. Techniques of diagnosing OSA and initiating CPAP in a timely and economic manner continue to evolve.