Acoustic Oddball during NREM Sleep: A Combined EEG/fMRI Study

Background: A condition vital for the consolidation and maintenance of sleep is generally reduced responsiveness to external stimuli. Despite this, the sleeper maintains a level of stimulus processing that allows to respond to potentially dangerous environmental signals. The mechanisms that subserve these contradictory functions are only incompletely understood. Methodology/Principal Findings: Using combined EEG/fMRI we investigated the neural substrate of sleep protection by applying an acoustic oddball paradigm during light NREM sleep. Further, we studied the role of evoked K-complexes (KCs), an electroencephalographic hallmark of NREM sleep with a still unknown role for sleep protection. Our main results were: (1) Other than in wakefulness, rare tones did not induce a blood oxygenation level dependent (BOLD) signal increase in the auditory pathway but a strong negative BOLD response in motor areas and the amygdala. (2) Stratification of rare tones by the presence of evoked KCs detected activation of the auditory cortex, hippocampus, superior and middle frontal gyri and posterior cingulate only for rare tones followed by a KC. (3) The typical high frontocentral EEG deflections of KCs were not paralleled by a BOLD equivalent. Conclusions/Significance: We observed that rare tones lead to transient disengagement of motor and amygdala responses during light NREM sleep. We interpret this as a sleep protective mechanism to delimit motor responses and to reduce the sensitivity of the amygdala towards further incoming stimuli. Evoked KCs are suggested to originate from a brain state wit

Electrophysiological evidence of enhanced performance monitoring in recently abstinent alcoholic men

RATIONALE: Chronic alcoholism is associated with mild to moderate cognitive impairment. Under certain conditions, impairment can be ameliorated by invoking compensatory processes. OBJECTIVE: To identify electrophysiological mechanisms of such compensation that would be required to resolve response conflict. METHODS: 14 abstinent alcoholic men and 14 similarly aged control men performed a variation of the Eriksen flanker task during an electroencephalography (EEG) recording to examine whether alcoholics could achieve and maintain control-level performance and whether EEG markers could identify evidence for the action of compensatory processes in the alcoholics. Monitoring processes engaged following a response were indexed by the correct related negativity (CRN) and error related negativity (ERN), two medial-frontal negative event-related potentials. RESULTS: The alcoholics were able to perform at control levels on accuracy and reaction time (RT). Alcoholics generated larger ERN amplitudes following incorrect responses and larger CRNs following correct responses than controls. Both groups showed evidence of post-error slowing. Larger CRN amplitudes in the alcoholics were related to longer RTs. Also observed in the alcoholics was an association between smaller CRN amplitudes and length of sobriety, suggesting a normalization of monitoring activity with extended abstinence. CONCLUSIONS: To the extent that greater amplitude of these electrophysiological markers of performance monitoring indexes greater resource allocation and performance compensation, the larger amplitudes observed in the alcoholic than control group support the view that elevated performance monitoring enables abstinent alcoholics to overcome response conflict, as was evident in their control-level performance

Characterization of K-Complexes and Slow Wave Activity in a Neural Mass Model

NREM sleep is characterized by two hallmarks, namely K-complexes (KCs) during sleep stage N2 and cortical slow oscillations (SOs) during sleep stage N3. While the underlying dynamics on the neuronal level is well known and can be easily measured, the resulting behavior on the macroscopic population level remains unclear. On the basis of an extended neural mass model of the cortex, we suggest a new interpretation of the mechanisms responsible for the generation of KCs and SOs. As the cortex transitions from wake to deep sleep, in our model it approaches an oscillatory regime via a Hopf bifurcation. Importantly, there is a canard phenomenon arising from a homoclinic bifurcation, whose orbit determines the shape of large amplitude SOs. A KC corresponds to a single excursion along the homoclinic orbit, while SOs are noise-driven oscillations around a stable focus. The model generates both time series and spectra that strikingly resemble real electroencephalogram data and points out possible differences between the different stages of natural sleep

Sleep problems during the menopausal transition: prevalence, impact, and management challenges

Fiona C Baker,1,2 Massimiliano de Zambotti,1 Ian M Colrain,1,3 Bei Bei4,5 1Center for Health Sciences, SRI International, Menlo Park, CA, USA; 2Brain Function Research Group, University of the Witwatersrand, Johannesburg, South Africa; 3Melbourne School of Psychological Sciences, University of Melbourne, 4Monash Institute of Cognitive and Clinical Neurosciences, School of Psychological Sciences, Faculty of Medicine, Nursing and Health Sciences, Monash University, 5Centre for Women’s Mental Health, Department of Psychiatry, University of Melbourne, Royal Women’s Hospital, Melbourne, VIC, Australia Abstract: A substantial number of women experience sleep difficulties in the approach to menopause and beyond, with 26% experiencing severe symptoms that impact daytime functioning, qualifying them for a diagnosis of insomnia. Here, we review both self-report and polysomnographic evidence for sleep difficulties in the context of the menopausal transition, considering severity of sleep complaints and links between hot flashes (HFs) and depression with poor sleep. Longitudinal population-based studies show that sleep difficulties are uniquely linked with menopausal stage and changes in follicle-stimulating hormone and estradiol, over and above the effects of age. A major contributor to sleep complaints in the context of the menopausal transition is HFs, and many, although not all, HFs are linked with polysomnographic-defined awakenings, with HF-associated wake time contributing significantly to overall wakefulness after sleep onset. Some sleep complaints may be comorbid with depressive disorders or attributed to sleep-related breathing or movement disorders, which increase in prevalence especially after menopause, and for some women, menopause, age, and environmental/behavioral factors may interact to disrupt sleep. Considering the unique and multifactorial basis for sleep difficulties in women transitioning menopause, we describe clinical assessment approaches and management options, including combination treatments, ranging from cognitive behavioral therapy for insomnia to hormonal and nonhormonal pharmacological options. Emerging studies suggest that the impact of severe insomnia symptoms could extend beyond immediate health care usage and quality of life issues to long-term mental and physical health, if left untreated in midlife women. Appropriate treatment, therefore, has immediate benefit as well as advantages for maintaining optimal health in the postmenopausal years. Keywords: insomnia, midlife women, hormone therapy, estradiol, hot flashes, vasomotor symptom

Disturbed Cerebellar Growth Trajectories in Adolescents Who Initiate Alcohol Drinking

BACKGROUND: The cerebellum is a target of alcoholism-related brain damage in adults, yet no study has prospectively tracked deviations from normal cerebellar growth trajectories in adolescents before and after initiating drinking. METHODS: Magnetic resonance imaging tracked developmental volume trajectories of 10 cerebellar lobule and vermis tissue constituents in 548 no/low drinking youths age 12 to 21 years at induction into this 5-site, NCANDA (National Consortium on Alcohol and NeuroDevelopment in Adolescence) study. Over the 3- to 4-year longitudinal examination yielding 2043 magnetic resonance imaging scans, 328 youths remained no/low drinkers, whereas 220 initiated substantial drinking after initial neuroimaging. RESULTS: Normal growth trajectories derived from no/low drinkers indicated that gray matter volumes of lobules V and VI, crus II, lobule VIIB, and lobule X declined faster with age in male youths than in female youths, whereas white matter volumes in crus I and crus II and lobules VIIIA and VIIIB expanded faster in female youths than in male youths; cerebrospinal fluid volume expanded faster in most cerebellar regions of male youths than female youths. Drinkers exhibited accelerated gray matter decline in anterior lobules and vermis, accelerated vermian white matter expansion, and accelerated cerebrospinal fluid volumes expansion of anterior lobules relative to youths who remained no/low drinkers. Analyses including both alcohol and marijuana did not support an independent role for marijuana in alcohol effects on cerebellar gray matter trajectories. CONCLUSIONS: Alcohol use-related cerebellar growth trajectory differences from normal involved anterior lobules and vermis of youths who initiated substantial drinking. These regions are commonly affected in alcohol-dependent adults, raising the possibility that cerebellar structures affected by youthful drinking may be vulnerable to age-alcohol interactions in later adulthood