Purpose A high prevalence of depressive symptomatology has been reported amongst sufferers of obs... more Purpose A high prevalence of depressive symptomatology has been reported amongst sufferers of obstructive sleep apnea (OSA), but it remains unclear as to whether this is due to their OSA or other factors associated with the disorder. The current study aimed to assess the incidence and aetiology of depression in a community sample of individuals presenting to the sleep laboratory for diagnostic assessment of OSA. Methods Forty-five consecutive individuals who presented to the sleep laboratory were recruited; of those, 34 were diagnosed with OSA, and 11 were primary snorers with no clinical or laboratory features of OSA. Nineteen control subjects were also recruited. Patients and controls completed the Beck Depression Inventory, the Profile of Mood States (POMS), and the Epworth Sleepiness Scale to assess their mood and sleepiness, prior to their polysomnography. Results All patients reported significantly more depressive symptoms compared with healthy controls, regardless of their degree of OSA. There were no significant differences between OSA patients and primary snorers on any of the mood and self-rated sleepiness measures. Depression scores were not significantly associated with any of the nocturnal variables. Regression analysis revealed that the POMS fatigue subscale explained the majority of the variance in subjects' depression scores. Conclusions Fatigue was the primary predictor of the level of depressive symptoms in patients who attended the sleep laboratory, regardless of the level of severity of sleepdisordered breathing. When considering treatment options, practitioners should be aware of the concomitant occurrence of depressive symptoms and fatigue in patients presenting with sleep complaints, which may not be due to a sleep disorder. Sleep Breath (2011) 15:439-445
Study Objectives: To determine whether cerebral metabolite changes may underlie abnormalities of ... more Study Objectives: To determine whether cerebral metabolite changes may underlie abnormalities of neurocognitive function and respiratory control in OSA. Design: Observational, before and after CPAP treatment. Participants: 30 untreated severe OSA patients, and 25 age-matched healthy controls, all males free of comorbidities, and all having had detailed structural brain analysis using voxel-based morphometry (VBM). Measurements and Results: Single voxel bilateral hippocampal and brainstem, and multivoxel frontal metabolite concentrations were measured using magnetic resonance spectroscopy (MRS) in a high resolution (3T) scanner. Subjects also completed a battery of neurocognitive tests. Patients had repeat testing after 6 months of CPAP. There were significant differences at baseline in frontal N-acetylaspartate/choline (NAA/Cho) ratios (patients [mean (SD)] 4.56 [0.41], controls 4.92 [0.44], P = 0.001), and in hippocampal choline/creatine (Cho/Cr) ratios (0.38 [0.04] vs 0.41 [0.04], P = 0.006), (both ANCOVA, with age and premorbid IQ as covariates). No longitudinal changes were seen with treatment (n = 27, paired t-tests), however the hippocampal differences were no longer significant at 6 months, and frontal NAA/Cr ratios were now also significantly different (patients 1.55 [0.13] vs control 1.65 [0.18] P = 0.01). No significant correlations were found between spectroscopy results and neurocognitive test results, but significant negative correlations were seen between arousal index and frontal NAA/Cho (r = −0.39, corrected P = 0.033) and between % total sleep time at SpO2 < 90% and hippocampal Cho/Cr (r = −0.40, corrected P = 0.01). Conclusions: OSA patients have brain metabolite changes detected by MRS, suggestive of decreased frontal lobe neuronal viability and integrity, and decreased hippocampal membrane turnover. These regions have previously been shown to have no gross structural lesions using VBM. Little change was seen with treatment with CPAP for 6 months. No correlation of metabolite concentrations was seen with results on neurocognitive tests, but there were significant negative correlations with OSA severity as measured by severity of nocturnal hypoxemia.
Drowsiness is a major risk factor for motor vehicle and occupational accidents. Real-time objecti... more Drowsiness is a major risk factor for motor vehicle and occupational accidents. Real-time objective indicators of drowsiness could potentially identify drowsy individuals with the goal of intervening before an accident occurs. Several ocular measures are promising objective indicators of drowsiness; however, there is a lack of studies evaluating their accuracy for detecting behavioral impairment due to drowsiness in real time. In this study, eye movement parameters were measured during vigilance tasks following restricted sleep and in a rested state (n = 33 participants) at three testing points (n = 71 data points) to compare ocular measures to a gold standard measure of drowsiness (OSLER). The utility of these parameters for detecting drowsiness-related errors was evaluated using receiver operating characteristic curves (ROC) (adjusted by clustering for participant) and identification of optimal cutoff levels for identifying frequent drowsiness-related errors (4 missed signals in a minute using OSLER). Their accuracy was tested for detecting increasing frequencies of behavioral lapses on a different task (psychomotor vigilance task [PVT]). Ocular variables which measured the average duration of eyelid closure (inter-event duration [IED]) and the ratio of the amplitude to velocity of eyelid closure were reliable indicators of frequent errors (area under the curve for ROC of 0.73 to 0.83, p &amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;lt; 0.05). IED produced a sensitivity and specificity of 71% and 88% for detecting ≥ 3 lapses (PVT) in a minute and 100% and 86% for ≥ 5 lapses. A composite measure of several eye movement characteristics (Johns Drowsiness Scale) provided sensitivities of 77% and 100% for detecting 3 and ≥ 5 lapses in a minute, with specificities of 85% and 83%, respectively. Ocular measures, particularly those measuring the average duration of episodes of eye closure are promising real-time indicators of drowsiness.
Mobile phone exposure-related effects on the human electroencephalogram (EEG) have been shown dur... more Mobile phone exposure-related effects on the human electroencephalogram (EEG) have been shown during both waking and sleep states, albeit with slight differences in the frequency affected. This discrepancy, combined with studies that failed to find effects, has led many to conclude that no consistent effects exist. We hypothesised that these differences might partly be due to individual variability in response, and that mobile phone emissions may in fact have large but differential effects on human brain activity. Twenty volunteers from our previous study underwent an adaptation night followed by two experimental nights in which they were randomly exposed to two conditions (Active and Sham), followed by a full-night sleep episode. The EEG spectral power was increased in the sleep spindle frequency range in the first 30 min of non-rapid eye movement (non-REM) sleep following Active exposure. This increase was more prominent in the participants that showed an increase in the original study. These results confirm previous findings of mobile phone-like emissions affecting the EEG during non-REM sleep. Importantly, this low-level effect was also shown to be sensitive to individual variability. Furthermore, this indicates that previous negative results are not strong evidence for a lack of an effect and, given the far-reaching implications of mobile phone research, we may need to rethink the interpretation of results and the manner in which research is conducted in this field.
Sleep loss, widespread in today's society and associated with a number of clinical conditions, ha... more Sleep loss, widespread in today's society and associated with a number of clinical conditions, has a detrimental effect on a variety of cognitive domains including attention. This study examined the sequelae of sleep deprivation upon BOLD fMRI activation during divided attention. Twelve healthy males completed two randomized sessions; one after 27 h of sleep deprivation and one after a normal night of sleep. During each session, BOLD fMRI was measured while subjects completed a cross-modal divided attention task (visual and auditory). After normal sleep, increased BOLD activation was observed bilaterally in the superior frontal gyrus and the inferior parietal lobe during divided attention performance. Subjects reported feeling significantly more sleepy in the sleep deprivation session, and there was a trend towards poorer divided attention task performance. Sleep deprivation led to a down regulation of activation in the left superior frontal gyrus, possibly reflecting an attenuation of top-down control mechanisms on the attentional system. These findings have implications for understanding the neural correlates of divided attention and the neurofunctional changes that occur in individuals who are sleep deprived.
Study Objectives: Previous studies have demonstrated that as little as 18 hours of sleep deprivat... more Study Objectives: Previous studies have demonstrated that as little as 18 hours of sleep deprivation can cause deleterious effects on performance. It has also been suggested that sleep deprivation can cause a “tunnel-vision” effect, in which attention is restricted to the center of the visual field. The current study aimed to replicate these behavioral effects and to examine the electrophysiological underpinnings of these changes. Design: Repeated-measures experimental study. Patients or Participants: Nineteen professional drivers (1 woman; mean age = 45.3 ± 9.1 years). Interventions: Two experimental sessions were performed; one following 27 hours of sleep deprivation and the other following a normal night of sleep, with control for circadian effects. Measurements & Results: A tunnel-vision task (central versus peripheral visual discrimination) and a standard checkerboard-viewing task were performed while 32-channel EEG was recorded. For the tunnelvision task, sleep deprivation resulted in an overall slowing of reaction times and increased errors of omission for both peripheral and foveal stimuli (P < 0.05). These changes were related to reduced P300 amplitude (indexing cognitive processing) but not measures of early visual processing. No evidence was found for an interaction effect between sleep deprivation and visual-field position, either in terms of behavior or electrophysiological responses. Slower processing of the sustained parvocellular visual pathway was demonstrated. Conclusions: These findings suggest that performance deficits on visual tasks during sleep deprivation are due to higher cognitive processes rather than early visual processing. Sleep deprivation may differentially impair processing of more-detailed visual information. Features of the study design (eg, visual angle, duration of sleep deprivation) may influence whether peripheral visual-field neglect occurs.
To assess the feasibility and efficacy of sleep position modification in preventing supine sleep ... more To assess the feasibility and efficacy of sleep position modification in preventing supine sleep and improving sleep-disordered breathing and relevant clinical outcomes in positional Obstructive Sleep Apnea (OSA) patients. Eighty-six consecutive participants with moderate positional OSA on routine diagnostic polysomnography underwent a randomized controlled parallel group design trial of 4-weeks treatment using a sleep position modification device (active) or sleep hygiene advice (control). Outcomes were measured at baseline and following a 4-week treatment period. There was a significant reduction in the amount of supine sleep in the active group (mean ± SD change from baseline, active group 99.5 ± 85.2 minutes, control group 68.6 ± 103.2 minutes, p = 0.002), and an improvement in apnea-hypopnea index (AHI) (active group reduced by 9.9 ± 11.6, control group reduced by 5.3 ± 13.9, p = 0.013). Post-hoc analyses indicated that positional therapy was most effective for patients with baseline AHI cut-off above 20 (p = 0.02). Logistic regression showed that a treatment response (AHI &amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;lt; 10) was more likely in the active group (OR = 5.57), and those with higher baseline nadir oxygen desaturation (OR = 1.95) and non-supine AHI (OR = 0.55). There were no significant improvements in quality of life, daytime sleepiness, mood, symptoms, neuropsychological measures or blood pressure in the active group. The position device utilized in this study was effective in reducing supine sleep and AHI, which was significant in those with baseline AHI ≥20. Longer duration studies of physical treatments that modify sleep position are needed to explore further whether additional clinical benefits in are achievable.
Sleep-related breathing disorders encompass a range of disorders in which abnormal ventilation oc... more Sleep-related breathing disorders encompass a range of disorders in which abnormal ventilation occurs during sleep as a result of partial or complete obstruction of the upper airway, altered respiratory drive, abnormal chest wall movement, or respiratory muscle function. The most common of these is obstructive sleep apnea (OSA), occurring in both adults and children, and causing significant cognitive and daytime dysfunction and reduced quality of life. OSA patients experience repetitive brief cessation of breathing throughout the night, which causes intermittent hypoxemia (reductions in hemoglobin oxygen levels) and fragmented sleep patterns. These nocturnal events result in excessive daytime sleepiness, and changes in mood and cognition.Chronic excessive sleepiness during the day is a common symptom of sleep-related breathing disorders, which is assessed in sleep clinics both subjectively (questionnaire) and objectively (sleep latency tests). Mood changes are often reported by patients, including irritability, fatigue, depression, and anxiety. A wide range of cognitive deficits have been identified in untreated OSA patients, from attentional and vigilance, to memory and executive functions, and more complex tasks such as simulated driving. These changes are reflected in patient reports of difficulty in concentrating, increased forgetfulness, an inability to make decisions, and falling asleep at the wheel of a motor vehicle. These cognitive changes can also have significant downstream effects on daily functioning. Moderate to severe cases of the disorder are at a higher risk of having a motor vehicle accident, and may also have difficulties at work or school.A number of comorbidities may also influence the cognitive changes in OSA patients, including hypertension, diabetes, and stroke. These diseases can cause changes to neural vasculature and result in neural damage, leading to cognitive impairments. Examination of OSA patients using neuroimaging techniques such as structural magnetic resonance imaging and proton magnetic resonance spectroscopy has observed significant changes to brain structure and metabolism. The downstream effects of neural, cognitive, and daytime functional impairments can be significant if left untreated. A better understanding of the cognitive effects of these disorders, and development of more effective assessment tools for diagnosis, will aid early intervention and improve quality of life of the patient.
2012). A comparison of the effect of mobile phone use and alcohol consumption on driving simulati... more 2012). A comparison of the effect of mobile phone use and alcohol consumption on driving simulation performance.
There is some suggestion in the literature that professional drivers might self-select to be more... more There is some suggestion in the literature that professional drivers might self-select to be more resistant to the effects of sleep deprivation; however, this question has not been directly examined. The current laboratory study aimed to compare performance changes during acute sleep deprivation between professional and nonprofessional drivers. Twenty volunteer male professional drivers and 20 nonprofessional drivers performed a simulated driving task (AusEd) and the Psychomotor Vigilance Task (PVT) during 24 hours of continuous wakefulness. Ratings of subjective sleepiness were also examined. There was a progressive and significant increase in lateral lane position and speed variability on the simulated driving task and an increase in PVT reaction times and lapses after participants had been awake for 17 to 24 hours (Ps &amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;lt; .01). There was no difference in performance changes between the professional and nonprofessional drivers. Professional drivers in this study had the same susceptibility to sleep deprivation as nonprofessional drivers. This finding does not support the concept that professional drivers are resistant to sleep loss.
Drivers are not always aware that they are becoming impaired as a result of sleepiness. Using spe... more Drivers are not always aware that they are becoming impaired as a result of sleepiness. Using specific symptoms of sleepiness might assist with recognition of drowsiness related impairment and help drivers judge whether they are safe to drive a vehicle, however this has not been evaluated. In this study, 20 healthy volunteer professional drivers completed two randomized sessions in the laboratory - one under 24h of acute sleep deprivation, and one with alcohol. The Psychomotor Vigilance Task (PVT) and a 30min simulated driving task (AusEdTM) were performed every 3-4h in the sleep deprivation session, and at a BAC of 0.00% and 0.05% in the alcohol session, while electroencephalography (EEG) and eye movements were recorded. After each test session, drivers completed the Karolinska Sleepiness Scale (KSS) and the Sleepiness Symptoms Questionnaire (SSQ), which includes eight specific sleepiness and driving performance symptoms. A second baseline session was completed on a separate day by the professional drivers and in an additional 20 non-professional drivers for test-retest reliability. There was moderate test-retest agreement on the SSQ (r=0.59). Significant correlations were identified between individual sleepiness symptoms and the KSS score (r values 0.50-0.74, p&amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;lt;0.01 for all symptoms). The frequency of all SSQ items increased during sleep deprivation (χ(2) values of 28.4-80.2, p&amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;lt;0.01 for all symptoms) and symptoms were related to increased subjective sleepiness and performance deterioration. The symptoms &amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;quot;struggling to keep your eyes open&amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;quot;, &amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;quot;difficulty maintaining correct speed&amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;quot;, &amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;quot;reactions were slow&amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;quot; and &amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;quot;head dropping…
Objectives: Sleep deprivation and alcohol both impair driving performance. This study assessed th... more Objectives: Sleep deprivation and alcohol both impair driving performance. This study assessed the interactive effect of low-dose alcohol and extended wakefulness. Design: Repeated-measures, crossover design evaluating psychomotor and driving function in a non–sleep-deprived state and after extended wakefulness with and without low-dose alcohol. Participants: Nineteen volunteer professional drivers Intervention & Measurements: Driving simulation (AusEd™) and the Psychomotor Vigilance Task (PVT) were measured in a rested state (12-15 hours awake) and after extended wakefulness (18-21 hours awake) during two sessions. Alcohol was administered during one session, with performance measured at blood alcohol concentrations (BAC) of 0.00%, 0.03%, and 0.05% in a non–sleep-deprived state, and at 0.03% after extended wakefulness (at 01:00 and 03:00). During the second session, tests were performed at the same times without alcohol. Results: The combination of extended wakefulness and low-dose alcohol had significant deleterious effects on reaction time and lapses (PVT) and variation in lane position and speed (AusEd). Extended wakefulness (18-21 hours awake) combined with low-dose alcohol (0.03% BAC) resulted in more lapses (t = -2.75, P < 0.05) and greater variation in lane position (t = -3.94, P < 0.01) and speed (t = -2.79, P < 0.05) than did a BAC of 0.05% in a rested state. Conclusion: The combination of legal low-dose alcohol and extended wakefulness results in impairment worse than that at an alcohol level known to increase accident risk. Avoiding alcohol when driving after extended wakefulness may reduce accident risk. Keywords: Sleep deprivation, alcohol, driving,
Purpose A high prevalence of depressive symptomatology has been reported amongst sufferers of obs... more Purpose A high prevalence of depressive symptomatology has been reported amongst sufferers of obstructive sleep apnea (OSA), but it remains unclear as to whether this is due to their OSA or other factors associated with the disorder. The current study aimed to assess the incidence and aetiology of depression in a community sample of individuals presenting to the sleep laboratory for diagnostic assessment of OSA. Methods Forty-five consecutive individuals who presented to the sleep laboratory were recruited; of those, 34 were diagnosed with OSA, and 11 were primary snorers with no clinical or laboratory features of OSA. Nineteen control subjects were also recruited. Patients and controls completed the Beck Depression Inventory, the Profile of Mood States (POMS), and the Epworth Sleepiness Scale to assess their mood and sleepiness, prior to their polysomnography. Results All patients reported significantly more depressive symptoms compared with healthy controls, regardless of their degree of OSA. There were no significant differences between OSA patients and primary snorers on any of the mood and self-rated sleepiness measures. Depression scores were not significantly associated with any of the nocturnal variables. Regression analysis revealed that the POMS fatigue subscale explained the majority of the variance in subjects' depression scores. Conclusions Fatigue was the primary predictor of the level of depressive symptoms in patients who attended the sleep laboratory, regardless of the level of severity of sleepdisordered breathing. When considering treatment options, practitioners should be aware of the concomitant occurrence of depressive symptoms and fatigue in patients presenting with sleep complaints, which may not be due to a sleep disorder. Sleep Breath (2011) 15:439-445
Study Objectives: To determine whether cerebral metabolite changes may underlie abnormalities of ... more Study Objectives: To determine whether cerebral metabolite changes may underlie abnormalities of neurocognitive function and respiratory control in OSA. Design: Observational, before and after CPAP treatment. Participants: 30 untreated severe OSA patients, and 25 age-matched healthy controls, all males free of comorbidities, and all having had detailed structural brain analysis using voxel-based morphometry (VBM). Measurements and Results: Single voxel bilateral hippocampal and brainstem, and multivoxel frontal metabolite concentrations were measured using magnetic resonance spectroscopy (MRS) in a high resolution (3T) scanner. Subjects also completed a battery of neurocognitive tests. Patients had repeat testing after 6 months of CPAP. There were significant differences at baseline in frontal N-acetylaspartate/choline (NAA/Cho) ratios (patients [mean (SD)] 4.56 [0.41], controls 4.92 [0.44], P = 0.001), and in hippocampal choline/creatine (Cho/Cr) ratios (0.38 [0.04] vs 0.41 [0.04], P = 0.006), (both ANCOVA, with age and premorbid IQ as covariates). No longitudinal changes were seen with treatment (n = 27, paired t-tests), however the hippocampal differences were no longer significant at 6 months, and frontal NAA/Cr ratios were now also significantly different (patients 1.55 [0.13] vs control 1.65 [0.18] P = 0.01). No significant correlations were found between spectroscopy results and neurocognitive test results, but significant negative correlations were seen between arousal index and frontal NAA/Cho (r = −0.39, corrected P = 0.033) and between % total sleep time at SpO2 < 90% and hippocampal Cho/Cr (r = −0.40, corrected P = 0.01). Conclusions: OSA patients have brain metabolite changes detected by MRS, suggestive of decreased frontal lobe neuronal viability and integrity, and decreased hippocampal membrane turnover. These regions have previously been shown to have no gross structural lesions using VBM. Little change was seen with treatment with CPAP for 6 months. No correlation of metabolite concentrations was seen with results on neurocognitive tests, but there were significant negative correlations with OSA severity as measured by severity of nocturnal hypoxemia.
Drowsiness is a major risk factor for motor vehicle and occupational accidents. Real-time objecti... more Drowsiness is a major risk factor for motor vehicle and occupational accidents. Real-time objective indicators of drowsiness could potentially identify drowsy individuals with the goal of intervening before an accident occurs. Several ocular measures are promising objective indicators of drowsiness; however, there is a lack of studies evaluating their accuracy for detecting behavioral impairment due to drowsiness in real time. In this study, eye movement parameters were measured during vigilance tasks following restricted sleep and in a rested state (n = 33 participants) at three testing points (n = 71 data points) to compare ocular measures to a gold standard measure of drowsiness (OSLER). The utility of these parameters for detecting drowsiness-related errors was evaluated using receiver operating characteristic curves (ROC) (adjusted by clustering for participant) and identification of optimal cutoff levels for identifying frequent drowsiness-related errors (4 missed signals in a minute using OSLER). Their accuracy was tested for detecting increasing frequencies of behavioral lapses on a different task (psychomotor vigilance task [PVT]). Ocular variables which measured the average duration of eyelid closure (inter-event duration [IED]) and the ratio of the amplitude to velocity of eyelid closure were reliable indicators of frequent errors (area under the curve for ROC of 0.73 to 0.83, p &amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;lt; 0.05). IED produced a sensitivity and specificity of 71% and 88% for detecting ≥ 3 lapses (PVT) in a minute and 100% and 86% for ≥ 5 lapses. A composite measure of several eye movement characteristics (Johns Drowsiness Scale) provided sensitivities of 77% and 100% for detecting 3 and ≥ 5 lapses in a minute, with specificities of 85% and 83%, respectively. Ocular measures, particularly those measuring the average duration of episodes of eye closure are promising real-time indicators of drowsiness.
Mobile phone exposure-related effects on the human electroencephalogram (EEG) have been shown dur... more Mobile phone exposure-related effects on the human electroencephalogram (EEG) have been shown during both waking and sleep states, albeit with slight differences in the frequency affected. This discrepancy, combined with studies that failed to find effects, has led many to conclude that no consistent effects exist. We hypothesised that these differences might partly be due to individual variability in response, and that mobile phone emissions may in fact have large but differential effects on human brain activity. Twenty volunteers from our previous study underwent an adaptation night followed by two experimental nights in which they were randomly exposed to two conditions (Active and Sham), followed by a full-night sleep episode. The EEG spectral power was increased in the sleep spindle frequency range in the first 30 min of non-rapid eye movement (non-REM) sleep following Active exposure. This increase was more prominent in the participants that showed an increase in the original study. These results confirm previous findings of mobile phone-like emissions affecting the EEG during non-REM sleep. Importantly, this low-level effect was also shown to be sensitive to individual variability. Furthermore, this indicates that previous negative results are not strong evidence for a lack of an effect and, given the far-reaching implications of mobile phone research, we may need to rethink the interpretation of results and the manner in which research is conducted in this field.
Sleep loss, widespread in today's society and associated with a number of clinical conditions, ha... more Sleep loss, widespread in today's society and associated with a number of clinical conditions, has a detrimental effect on a variety of cognitive domains including attention. This study examined the sequelae of sleep deprivation upon BOLD fMRI activation during divided attention. Twelve healthy males completed two randomized sessions; one after 27 h of sleep deprivation and one after a normal night of sleep. During each session, BOLD fMRI was measured while subjects completed a cross-modal divided attention task (visual and auditory). After normal sleep, increased BOLD activation was observed bilaterally in the superior frontal gyrus and the inferior parietal lobe during divided attention performance. Subjects reported feeling significantly more sleepy in the sleep deprivation session, and there was a trend towards poorer divided attention task performance. Sleep deprivation led to a down regulation of activation in the left superior frontal gyrus, possibly reflecting an attenuation of top-down control mechanisms on the attentional system. These findings have implications for understanding the neural correlates of divided attention and the neurofunctional changes that occur in individuals who are sleep deprived.
Study Objectives: Previous studies have demonstrated that as little as 18 hours of sleep deprivat... more Study Objectives: Previous studies have demonstrated that as little as 18 hours of sleep deprivation can cause deleterious effects on performance. It has also been suggested that sleep deprivation can cause a “tunnel-vision” effect, in which attention is restricted to the center of the visual field. The current study aimed to replicate these behavioral effects and to examine the electrophysiological underpinnings of these changes. Design: Repeated-measures experimental study. Patients or Participants: Nineteen professional drivers (1 woman; mean age = 45.3 ± 9.1 years). Interventions: Two experimental sessions were performed; one following 27 hours of sleep deprivation and the other following a normal night of sleep, with control for circadian effects. Measurements & Results: A tunnel-vision task (central versus peripheral visual discrimination) and a standard checkerboard-viewing task were performed while 32-channel EEG was recorded. For the tunnelvision task, sleep deprivation resulted in an overall slowing of reaction times and increased errors of omission for both peripheral and foveal stimuli (P < 0.05). These changes were related to reduced P300 amplitude (indexing cognitive processing) but not measures of early visual processing. No evidence was found for an interaction effect between sleep deprivation and visual-field position, either in terms of behavior or electrophysiological responses. Slower processing of the sustained parvocellular visual pathway was demonstrated. Conclusions: These findings suggest that performance deficits on visual tasks during sleep deprivation are due to higher cognitive processes rather than early visual processing. Sleep deprivation may differentially impair processing of more-detailed visual information. Features of the study design (eg, visual angle, duration of sleep deprivation) may influence whether peripheral visual-field neglect occurs.
To assess the feasibility and efficacy of sleep position modification in preventing supine sleep ... more To assess the feasibility and efficacy of sleep position modification in preventing supine sleep and improving sleep-disordered breathing and relevant clinical outcomes in positional Obstructive Sleep Apnea (OSA) patients. Eighty-six consecutive participants with moderate positional OSA on routine diagnostic polysomnography underwent a randomized controlled parallel group design trial of 4-weeks treatment using a sleep position modification device (active) or sleep hygiene advice (control). Outcomes were measured at baseline and following a 4-week treatment period. There was a significant reduction in the amount of supine sleep in the active group (mean ± SD change from baseline, active group 99.5 ± 85.2 minutes, control group 68.6 ± 103.2 minutes, p = 0.002), and an improvement in apnea-hypopnea index (AHI) (active group reduced by 9.9 ± 11.6, control group reduced by 5.3 ± 13.9, p = 0.013). Post-hoc analyses indicated that positional therapy was most effective for patients with baseline AHI cut-off above 20 (p = 0.02). Logistic regression showed that a treatment response (AHI &amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;lt; 10) was more likely in the active group (OR = 5.57), and those with higher baseline nadir oxygen desaturation (OR = 1.95) and non-supine AHI (OR = 0.55). There were no significant improvements in quality of life, daytime sleepiness, mood, symptoms, neuropsychological measures or blood pressure in the active group. The position device utilized in this study was effective in reducing supine sleep and AHI, which was significant in those with baseline AHI ≥20. Longer duration studies of physical treatments that modify sleep position are needed to explore further whether additional clinical benefits in are achievable.
Sleep-related breathing disorders encompass a range of disorders in which abnormal ventilation oc... more Sleep-related breathing disorders encompass a range of disorders in which abnormal ventilation occurs during sleep as a result of partial or complete obstruction of the upper airway, altered respiratory drive, abnormal chest wall movement, or respiratory muscle function. The most common of these is obstructive sleep apnea (OSA), occurring in both adults and children, and causing significant cognitive and daytime dysfunction and reduced quality of life. OSA patients experience repetitive brief cessation of breathing throughout the night, which causes intermittent hypoxemia (reductions in hemoglobin oxygen levels) and fragmented sleep patterns. These nocturnal events result in excessive daytime sleepiness, and changes in mood and cognition.Chronic excessive sleepiness during the day is a common symptom of sleep-related breathing disorders, which is assessed in sleep clinics both subjectively (questionnaire) and objectively (sleep latency tests). Mood changes are often reported by patients, including irritability, fatigue, depression, and anxiety. A wide range of cognitive deficits have been identified in untreated OSA patients, from attentional and vigilance, to memory and executive functions, and more complex tasks such as simulated driving. These changes are reflected in patient reports of difficulty in concentrating, increased forgetfulness, an inability to make decisions, and falling asleep at the wheel of a motor vehicle. These cognitive changes can also have significant downstream effects on daily functioning. Moderate to severe cases of the disorder are at a higher risk of having a motor vehicle accident, and may also have difficulties at work or school.A number of comorbidities may also influence the cognitive changes in OSA patients, including hypertension, diabetes, and stroke. These diseases can cause changes to neural vasculature and result in neural damage, leading to cognitive impairments. Examination of OSA patients using neuroimaging techniques such as structural magnetic resonance imaging and proton magnetic resonance spectroscopy has observed significant changes to brain structure and metabolism. The downstream effects of neural, cognitive, and daytime functional impairments can be significant if left untreated. A better understanding of the cognitive effects of these disorders, and development of more effective assessment tools for diagnosis, will aid early intervention and improve quality of life of the patient.
2012). A comparison of the effect of mobile phone use and alcohol consumption on driving simulati... more 2012). A comparison of the effect of mobile phone use and alcohol consumption on driving simulation performance.
There is some suggestion in the literature that professional drivers might self-select to be more... more There is some suggestion in the literature that professional drivers might self-select to be more resistant to the effects of sleep deprivation; however, this question has not been directly examined. The current laboratory study aimed to compare performance changes during acute sleep deprivation between professional and nonprofessional drivers. Twenty volunteer male professional drivers and 20 nonprofessional drivers performed a simulated driving task (AusEd) and the Psychomotor Vigilance Task (PVT) during 24 hours of continuous wakefulness. Ratings of subjective sleepiness were also examined. There was a progressive and significant increase in lateral lane position and speed variability on the simulated driving task and an increase in PVT reaction times and lapses after participants had been awake for 17 to 24 hours (Ps &amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;lt; .01). There was no difference in performance changes between the professional and nonprofessional drivers. Professional drivers in this study had the same susceptibility to sleep deprivation as nonprofessional drivers. This finding does not support the concept that professional drivers are resistant to sleep loss.
Drivers are not always aware that they are becoming impaired as a result of sleepiness. Using spe... more Drivers are not always aware that they are becoming impaired as a result of sleepiness. Using specific symptoms of sleepiness might assist with recognition of drowsiness related impairment and help drivers judge whether they are safe to drive a vehicle, however this has not been evaluated. In this study, 20 healthy volunteer professional drivers completed two randomized sessions in the laboratory - one under 24h of acute sleep deprivation, and one with alcohol. The Psychomotor Vigilance Task (PVT) and a 30min simulated driving task (AusEdTM) were performed every 3-4h in the sleep deprivation session, and at a BAC of 0.00% and 0.05% in the alcohol session, while electroencephalography (EEG) and eye movements were recorded. After each test session, drivers completed the Karolinska Sleepiness Scale (KSS) and the Sleepiness Symptoms Questionnaire (SSQ), which includes eight specific sleepiness and driving performance symptoms. A second baseline session was completed on a separate day by the professional drivers and in an additional 20 non-professional drivers for test-retest reliability. There was moderate test-retest agreement on the SSQ (r=0.59). Significant correlations were identified between individual sleepiness symptoms and the KSS score (r values 0.50-0.74, p&amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;lt;0.01 for all symptoms). The frequency of all SSQ items increased during sleep deprivation (χ(2) values of 28.4-80.2, p&amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;lt;0.01 for all symptoms) and symptoms were related to increased subjective sleepiness and performance deterioration. The symptoms &amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;quot;struggling to keep your eyes open&amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;quot;, &amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;quot;difficulty maintaining correct speed&amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;quot;, &amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;quot;reactions were slow&amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;quot; and &amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;quot;head dropping…
Objectives: Sleep deprivation and alcohol both impair driving performance. This study assessed th... more Objectives: Sleep deprivation and alcohol both impair driving performance. This study assessed the interactive effect of low-dose alcohol and extended wakefulness. Design: Repeated-measures, crossover design evaluating psychomotor and driving function in a non–sleep-deprived state and after extended wakefulness with and without low-dose alcohol. Participants: Nineteen volunteer professional drivers Intervention & Measurements: Driving simulation (AusEd™) and the Psychomotor Vigilance Task (PVT) were measured in a rested state (12-15 hours awake) and after extended wakefulness (18-21 hours awake) during two sessions. Alcohol was administered during one session, with performance measured at blood alcohol concentrations (BAC) of 0.00%, 0.03%, and 0.05% in a non–sleep-deprived state, and at 0.03% after extended wakefulness (at 01:00 and 03:00). During the second session, tests were performed at the same times without alcohol. Results: The combination of extended wakefulness and low-dose alcohol had significant deleterious effects on reaction time and lapses (PVT) and variation in lane position and speed (AusEd). Extended wakefulness (18-21 hours awake) combined with low-dose alcohol (0.03% BAC) resulted in more lapses (t = -2.75, P < 0.05) and greater variation in lane position (t = -3.94, P < 0.01) and speed (t = -2.79, P < 0.05) than did a BAC of 0.05% in a rested state. Conclusion: The combination of legal low-dose alcohol and extended wakefulness results in impairment worse than that at an alcohol level known to increase accident risk. Avoiding alcohol when driving after extended wakefulness may reduce accident risk. Keywords: Sleep deprivation, alcohol, driving,
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Papers by Mark Howard
Design: Observational, before and after CPAP treatment.
Participants: 30 untreated severe OSA patients, and 25 age-matched healthy controls, all males free of comorbidities, and all having had detailed structural brain analysis using voxel-based morphometry (VBM).
Measurements and Results: Single voxel bilateral hippocampal and brainstem, and multivoxel frontal metabolite concentrations were measured using magnetic resonance spectroscopy (MRS) in a high resolution (3T) scanner. Subjects also completed a battery of neurocognitive tests. Patients had repeat testing after 6 months of CPAP. There were significant differences at baseline in frontal N-acetylaspartate/choline (NAA/Cho) ratios (patients [mean (SD)] 4.56 [0.41], controls 4.92 [0.44], P = 0.001), and in hippocampal choline/creatine (Cho/Cr) ratios (0.38 [0.04] vs 0.41
[0.04], P = 0.006), (both ANCOVA, with age and premorbid IQ as covariates). No longitudinal changes were seen with treatment (n = 27, paired t-tests), however the hippocampal differences were no longer significant at 6 months, and frontal NAA/Cr ratios were now also significantly different (patients 1.55 [0.13] vs control 1.65 [0.18] P = 0.01). No significant correlations were found between spectroscopy results and neurocognitive test results, but significant negative correlations were seen between arousal index and frontal NAA/Cho (r = −0.39, corrected P = 0.033) and between % total sleep time at SpO2 < 90% and hippocampal Cho/Cr (r = −0.40, corrected P = 0.01).
Conclusions: OSA patients have brain metabolite changes detected by MRS, suggestive of decreased frontal lobe neuronal viability and integrity, and decreased hippocampal membrane turnover. These regions have previously been shown to have no gross structural lesions using VBM. Little change was seen with treatment with CPAP for 6 months. No correlation of metabolite concentrations was seen with results on neurocognitive tests,
but there were significant negative correlations with OSA severity as measured by severity of nocturnal hypoxemia.
eye movement (non-REM) sleep following Active exposure. This increase was more prominent in the participants that showed an increase in the original study. These results confirm previous
findings of mobile phone-like emissions affecting the EEG during non-REM sleep. Importantly, this low-level effect was also shown to be sensitive to individual variability. Furthermore, this
indicates that previous negative results are not strong evidence for a lack of an effect and, given the far-reaching implications of mobile phone research, we may need to rethink the interpretation
of results and the manner in which research is conducted in this field.
Design: Repeated-measures experimental study.
Patients or Participants: Nineteen professional drivers (1 woman;
mean age = 45.3 ± 9.1 years).
Interventions: Two experimental sessions were performed; one following 27 hours of sleep deprivation and the other following a normal night of sleep, with control for circadian effects.
Measurements & Results: A tunnel-vision task (central versus peripheral visual discrimination) and a standard checkerboard-viewing task were performed while 32-channel EEG was recorded. For the tunnelvision task, sleep deprivation resulted in an overall slowing of reaction times and increased errors of omission for both peripheral and foveal stimuli (P < 0.05). These changes were related to reduced P300 amplitude (indexing cognitive processing) but not measures of early visual processing. No evidence was found for an interaction effect between sleep deprivation and visual-field position, either in terms of behavior or electrophysiological responses. Slower processing of the sustained parvocellular visual pathway was demonstrated.
Conclusions: These findings suggest that performance deficits on visual tasks during sleep deprivation are due to higher cognitive processes rather than early visual processing. Sleep deprivation may differentially impair processing of more-detailed visual information. Features of the study design (eg, visual angle, duration of sleep deprivation) may
influence whether peripheral visual-field neglect occurs.
Design: Repeated-measures, crossover design evaluating psychomotor and driving function in a non–sleep-deprived state and after extended wakefulness with and without low-dose alcohol.
Participants: Nineteen volunteer professional drivers
Intervention & Measurements: Driving simulation (AusEd™) and the Psychomotor Vigilance Task (PVT) were measured in a rested state (12-15 hours awake) and after extended wakefulness (18-21 hours awake) during two sessions. Alcohol was administered during one session, with performance measured at blood alcohol concentrations (BAC) of 0.00%, 0.03%, and 0.05% in a non–sleep-deprived state, and at 0.03% after extended wakefulness (at 01:00 and 03:00). During the second session, tests were performed at the same times without alcohol.
Results: The combination of extended wakefulness and low-dose alcohol had significant deleterious effects on reaction time and lapses (PVT) and variation in lane position and speed (AusEd). Extended wakefulness (18-21 hours awake) combined with low-dose alcohol (0.03% BAC) resulted in more lapses (t = -2.75, P < 0.05) and greater variation in lane position (t = -3.94, P < 0.01) and speed (t = -2.79, P < 0.05) than did a BAC of 0.05% in a rested state.
Conclusion: The combination of legal low-dose alcohol and extended wakefulness results in impairment worse than that at an alcohol level known to increase accident risk. Avoiding alcohol when driving after extended wakefulness may reduce accident risk.
Keywords: Sleep deprivation, alcohol, driving,
Design: Observational, before and after CPAP treatment.
Participants: 30 untreated severe OSA patients, and 25 age-matched healthy controls, all males free of comorbidities, and all having had detailed structural brain analysis using voxel-based morphometry (VBM).
Measurements and Results: Single voxel bilateral hippocampal and brainstem, and multivoxel frontal metabolite concentrations were measured using magnetic resonance spectroscopy (MRS) in a high resolution (3T) scanner. Subjects also completed a battery of neurocognitive tests. Patients had repeat testing after 6 months of CPAP. There were significant differences at baseline in frontal N-acetylaspartate/choline (NAA/Cho) ratios (patients [mean (SD)] 4.56 [0.41], controls 4.92 [0.44], P = 0.001), and in hippocampal choline/creatine (Cho/Cr) ratios (0.38 [0.04] vs 0.41
[0.04], P = 0.006), (both ANCOVA, with age and premorbid IQ as covariates). No longitudinal changes were seen with treatment (n = 27, paired t-tests), however the hippocampal differences were no longer significant at 6 months, and frontal NAA/Cr ratios were now also significantly different (patients 1.55 [0.13] vs control 1.65 [0.18] P = 0.01). No significant correlations were found between spectroscopy results and neurocognitive test results, but significant negative correlations were seen between arousal index and frontal NAA/Cho (r = −0.39, corrected P = 0.033) and between % total sleep time at SpO2 < 90% and hippocampal Cho/Cr (r = −0.40, corrected P = 0.01).
Conclusions: OSA patients have brain metabolite changes detected by MRS, suggestive of decreased frontal lobe neuronal viability and integrity, and decreased hippocampal membrane turnover. These regions have previously been shown to have no gross structural lesions using VBM. Little change was seen with treatment with CPAP for 6 months. No correlation of metabolite concentrations was seen with results on neurocognitive tests,
but there were significant negative correlations with OSA severity as measured by severity of nocturnal hypoxemia.
eye movement (non-REM) sleep following Active exposure. This increase was more prominent in the participants that showed an increase in the original study. These results confirm previous
findings of mobile phone-like emissions affecting the EEG during non-REM sleep. Importantly, this low-level effect was also shown to be sensitive to individual variability. Furthermore, this
indicates that previous negative results are not strong evidence for a lack of an effect and, given the far-reaching implications of mobile phone research, we may need to rethink the interpretation
of results and the manner in which research is conducted in this field.
Design: Repeated-measures experimental study.
Patients or Participants: Nineteen professional drivers (1 woman;
mean age = 45.3 ± 9.1 years).
Interventions: Two experimental sessions were performed; one following 27 hours of sleep deprivation and the other following a normal night of sleep, with control for circadian effects.
Measurements & Results: A tunnel-vision task (central versus peripheral visual discrimination) and a standard checkerboard-viewing task were performed while 32-channel EEG was recorded. For the tunnelvision task, sleep deprivation resulted in an overall slowing of reaction times and increased errors of omission for both peripheral and foveal stimuli (P < 0.05). These changes were related to reduced P300 amplitude (indexing cognitive processing) but not measures of early visual processing. No evidence was found for an interaction effect between sleep deprivation and visual-field position, either in terms of behavior or electrophysiological responses. Slower processing of the sustained parvocellular visual pathway was demonstrated.
Conclusions: These findings suggest that performance deficits on visual tasks during sleep deprivation are due to higher cognitive processes rather than early visual processing. Sleep deprivation may differentially impair processing of more-detailed visual information. Features of the study design (eg, visual angle, duration of sleep deprivation) may
influence whether peripheral visual-field neglect occurs.
Design: Repeated-measures, crossover design evaluating psychomotor and driving function in a non–sleep-deprived state and after extended wakefulness with and without low-dose alcohol.
Participants: Nineteen volunteer professional drivers
Intervention & Measurements: Driving simulation (AusEd™) and the Psychomotor Vigilance Task (PVT) were measured in a rested state (12-15 hours awake) and after extended wakefulness (18-21 hours awake) during two sessions. Alcohol was administered during one session, with performance measured at blood alcohol concentrations (BAC) of 0.00%, 0.03%, and 0.05% in a non–sleep-deprived state, and at 0.03% after extended wakefulness (at 01:00 and 03:00). During the second session, tests were performed at the same times without alcohol.
Results: The combination of extended wakefulness and low-dose alcohol had significant deleterious effects on reaction time and lapses (PVT) and variation in lane position and speed (AusEd). Extended wakefulness (18-21 hours awake) combined with low-dose alcohol (0.03% BAC) resulted in more lapses (t = -2.75, P < 0.05) and greater variation in lane position (t = -3.94, P < 0.01) and speed (t = -2.79, P < 0.05) than did a BAC of 0.05% in a rested state.
Conclusion: The combination of legal low-dose alcohol and extended wakefulness results in impairment worse than that at an alcohol level known to increase accident risk. Avoiding alcohol when driving after extended wakefulness may reduce accident risk.
Keywords: Sleep deprivation, alcohol, driving,