Jeremy Mercer

Bio: Jeremy Mercer is an academic researcher from Flinders University. The author has contributed to research in topics: Polysomnography & Population. The author has an hindex of 10, co-authored 15 publications receiving 714 citations. Previous affiliations of Jeremy Mercer include Repatriation General Hospital.

Poor long-term patient compliance with the tennis ball technique for treating positional obstructive sleep apnea.

Abstract: Study Objectives:Little is known regarding long-term patient compliance with the tennis ball technique (TBT), one of the original simple methods of positional therapy (i.e., avoiding the supine pos...

Accurate position monitoring and improved supine-dependent obstructive sleep apnea with a new position recording and supine avoidance device

Abstract: Study Objectives:Approximately 30% of obstructive sleep apnea (OSA) patients have supine-predominant OSA, and simply avoiding supine sleep should normalise respiratory disturbance event rates. Howe...

Insomniacs' perception of wake instead of sleep.

Abstract: Study objectives To establish if insomniacs' underestimation of sleep time is due to reduced ability to discriminate between sleeping and waking states. Design Two night's home polysomnography were compared to sleep diaries. Five laboratory nights employed a series of recorded questions regarding perception of prior sleep-wake state, which were presented during sustained wake and interrupted Stage 2 and REM sleep. Setting Sleep laboratory and participants' homes. Participants Fourteen insomniacs were compared to 8 good sleepers. Mean age for both groups was 58 years. Interventions N/A. Measurements and results A signal detection theory analysis was applied to participants' responses to questions presented overnight in the laboratory concerning judgement of prior sleep-wake state and confidence in their decision. Insomniacs had reduced sleep-wake discriminability in addition to a greater bias toward reporting prior wakefulness in the laboratory compared to good sleepers. These measures correlated significantly with the degree of underestimation of total sleep and overestimation of wake recorded at home. Conclusions Insomniacs' underestimation of total sleep time is the product of prior sleep being misperceived as wake time upon awakening overnight. This misperception may play a role in the perpetuation of insomnia.

Central Sleep Apnea on Commencement of Continuous Positive Airway Pressure in Patients With a Primary Diagnosis of Obstructive Sleep Apnea-Hypopnea

Abstract: Introduction: Central sleep apnea (CSA) may occur in patients with snor- ing and obstructive sleep apnea-hypopnea (OSAH) during commencement of continuous positive airway pressure (CPAP) therapy. The presence of CSA may limit the effectiveness of CPAP therapy. The aims of this study were to assess the prevalence of CSA amongst patients starting CPAP for OSAH and to identify possible predictors of this condition. Methods: We reviewed the polysomnograms (PSGs) and clinical re- cords of 99 consecutive patients with a primary diagnosis of OSAH who were referred for an in-laboratory CPAP titration study. Patients with a CSA Index of ≥5 per hour at or near (±1 cm H 2 O) prescribed CPAP level formed the CSA-CPAP group. The remaining patients made up the noCSA-CPAP group. Demographic, baseline and CPAP titration PSG variables were compared between the 2 two groups. Results: 13 subjects (13.1%) had CSA-CPAP. Patients with and without CSA-CPAP did not differ with respect to age or body mass index. 46% of patients with CSA-CPAP had CSA on their baseline PSGs compared with 8% in the noCSA-CPAP group (p <0.01). CSA-CPAP patients also had a higher apnea-hypopnea index (72.1 vs. 52.7 p = 0.02), a higher arousal index (43.3 vs. 29.2 p <0.01), and a higher mixed apnea index (6.8 vs. 1.3 p = 0.03), on their baseline PSGs. Therapeutic CPAP could not be determined in 2 CSA-CPAP patients due to a very high frequency (of severe) central apneas. In the remaining 11, the CPAP prescription to eliminate obstructive events was higher than in the noCSA-CPAP group (11.0 vs. 9.3 p = 0.08). AHI was greater both at or near prescribed CPAP (48.8 vs. 6.7 p <0.01) and overall (47.4 vs. 14.9 p <0.01). A history of ischemic heart disease or heart failure was more frequent amongst pa- tients with CSA-CPAP than those without (p = 0.03). Conclusion: A significant minority of patients with a primary diagnosis of OSAH have either emergence or persistence of CSA on CPAP. Risk factors include male sex, history of cardiac disease, and CSA on base- line PSG.

Noninvasive cardiovascular markers of acoustically induced arousal from non-rapid-eye-movement sleep.

Abstract: STUDY OBJECTIVES Changes in cardiovascular measures such as heart rate (HR) and pulse transit time (PTT) have been advocated as sensitive markers of autonomic arousal from sleep. In animal studies, alerting stimuli produce particularly marked skin vascular responses. We hypothesized that changes in skin vascular conductance would provide more sensitive markers of autonomic arousal during sleep compared to central cardiovascular response measures such as HR and PTT. DESIGN Cardiovascular responses to auditory-induced arousals were recorded during overnight sleep studies. SETTING Sleep disorders unit in a 270-bed teaching hospital. PARTICIPANTS Eleven young healthy male subjects. INTERVENTIONS Throughout ovemight sleep studies, auditory tones (5-second duration, 54-90 decibels, 22-56 per subject) were presented during non-rapid-eye-movement sleep. Beat-by-beat HR, PTT, laser-Doppler fingertip skin blood flow (SBF) and finger and ear photoplethysmogram pulse wave amplitudes (PWA) were measured in the 20 seconds preceding and 30 seconds following each tone and compared to control measurements obtained during 50-second periods of recording with no stimulus (no tone, 6-22 per subject). Electroencephalographic (EEG) arousals were scored according to standard criteria (American Sleep Disorders Association) into no discemible, 3- to 10-second duration, or 10- to 15-second duration arousals. Poststimulus cardiovascular measurements were expressed as a percentage of the prestimulus mean and response magnitudes quantified from peak responses and the area under the poststimulus response curve. The ability of each cardiovascular response measure to discriminate EEG arousals (EEG changes lasting more than 3 seconds) was assessed from the area under the receiver operating characteristic (ROC) curve. MEASUREMENTS AND RESULTS There were no significant changes in any cardiovascular parameter during control recordings. In contrast to all other parameters, finger PWA and SBF decreased following tones that produced no discernible EEG arousal (P < 0.05). A significant HR rise and decreases in all cardiovascular measures occurred with greater than 3-second arousals, with longer duration arousals generally exhibiting larger responses. Conventional EEG arousals (greater than 3 seconds) were relatively poorly detected from HR responses (ROC area HR rise 0.80 +/- 0.04) compared to changes in SBF (0.85 +/- 0.02), PTT (0.85 +/- 0.03) and finger PWA (0.90 +/- 0.01). CONCLUSIONS Decreases in skin vascular conductance (finger PWA and SBF) provide sensitive markers of autonomic arousal during sleep. They are at least as sensitive as PTT for detecting conventionally scored EEG arousals and may be more sensitive in detecting "subcortical" arousals.

A Primer of Signal Detection Theory; Table of D' and β

Abstract: Contents: Foreword. Preface. What Are Statistical Decisions? Non-Parametric Measures of Sensitivity. Gaussian Distributions of Signal and Noise With Equal Variances. Gaussian Distributions of Signal and Noise With Unequal Variances. Conducting a Rating Scale Experiment. Choice Theory Approximations to Signal Detection Theory. Threshold Theory. The Laws of Categorical and Comparative Judgement. Appendices: Answers to Problems. Logarithms. Integration of the Expression for the Logistic Curve. Computer Programmes for Signal Detection Analysis. Tables.

Obstructive sleep apnoea syndrome

Abstract: Obstructive sleep apnoea syndrome (OSAS) is a common clinical condition in which the throat narrows or collapses repeatedly during sleep, causing obstructive sleep apnoea events. The syndrome is particularly prevalent in middle-aged and older adults. The mechanism by which the upper airway collapses is not fully understood but is multifactorial and includes obesity, craniofacial changes, alteration in upper airway muscle function, pharyngeal neuropathy and fluid shift towards the neck. The direct consequences of the collapse are intermittent hypoxia and hypercapnia, recurrent arousals and increase in respiratory efforts, leading to secondary sympathetic activation, oxidative stress and systemic inflammation. Excessive daytime sleepiness is a burden for the majority of patients. OSAS is also associated with cardiovascular co-morbidities, including hypertension, arrhythmias, stroke, coronary heart disease, atherosclerosis and overall increased cardiovascular mortality, as well as metabolic dysfunction. Whether treating sleep apnoea can fully reverse its chronic consequences remains to be established in adequately designed studies. Continuous positive airway pressure (CPAP) is the primary treatment modality in patients with severe OSAS, whereas oral appliances are also widely used in mild to moderate forms. Finally, combining different treatment modalities such as CPAP and weight control is beneficial, but need to be evaluated in randomized controlled trials. For an illustrated summary of this Primer, visit: http://go.nature.com/Lwc6te.

Royal Australian and New Zealand College of Psychiatrists clinical practice guidelines for the management of schizophrenia and related disorders

Abstract: Objectives:This guideline provides recommendations for the clinical management of schizophrenia and related disorders for health professionals working in Australia and New Zealand. It aims to encou...

Role of arousals in the pathogenesis of obstructive sleep apnea

Abstract: Arousal is believed to be needed for upper airway opening in obstructive hypopneas-apneas, without compelling evidence to support this notion. The association may be incidental. I studied the temporal relation between arousal and opening and impact of arousal on flow response at opening in 82 patients (apnea-hypopnea index, 46 +/- 35/hour). Obstructive apneas-hypopneas were induced by dial-down of continuous positive airway pressure. Obstructions and hypopneas occurred in 44 and 56% of dial-downs, respectively. When arousal occurred (83% of dial-downs), the temporal relation between arousal and opening was inconsistent between and within patients. Frequency of opening without or before arousal increased with milder obstructions (p < 10(-9)) and with delta power of EEG (p < 10(-6)). Time of opening was unaffected by whether arousal occurred before or after opening (18.0 +/- 9.8 vs. 18.1 +/- 10.5 seconds). Flow response was already excessive when opening occurred without or before arousal (180 +/- 148% of initial flow decline) and was considerably higher when arousal occurred (267 +/- 154%, p < 10(-10)). Flow undershoot after first ventilatory response was greater if arousal occurred (p < 0.01). It is concluded that arousals are incidental events that occur when thresholds for arousal and for arousal-independent opening are close. They are not needed to initiate opening or to obtain adequate flow and they likely increase the severity of the disorder by promoting greater ventilatory instability.

(Mis)perception of Sleep in Insomnia: A Puzzle and a Resolution

Abstract: Insomnia is prevalent, causing severe distress and impairment. This review focuses on illuminating the puzzling finding that many insomnia patients misperceive their sleep. They overestimate their sleep onset latency (SOL) and underestimate their total sleep time (TST), relative to objective measures. This tendency is ubiquitous (although not universal). Resolving this puzzle has clinical, theoretical, and public health importance. There are implications for assessment, definition, and treatment. Moreover, solving the puzzle creates an opportunity for real-world applications of theories from clinical, perceptual, and social psychology as well as neuroscience. Herein we evaluate 13 possible resolutions to the puzzle. Specifically, we consider the possible contribution, to misperception, of (1) features inherent to the context of sleep (e.g., darkness); (2) the definition of sleep onset, which may lack sensitivity for insomnia patients; (3) insomnia being an exaggerated sleep complaint; (4) psychological distress causing magnification; (5) a deficit in time estimation ability; (6) sleep being misperceived as wake; (7) worry and selective attention toward sleep-related threats; (8) a memory bias influenced by current symptoms and emotions, a confirmation bias/belief bias, or a recall bias linked to the intensity/recency of symptoms; (9) heightened physiological arousal; (10) elevated cortical arousal; (11) the presence of brief awakenings; (12) a fault in neuronal circuitry; and (13) there being 2 insomnia subtypes (one with and one without misperception). The best supported resolutions were misperception of sleep as wake, worry, and brief awakenings. A deficit in time estimation ability was not supported. We conclude by proposing several integrative solutions.