http://download.neurosky.com/docs/papers/bcq/Klimesch_1999_EEG_alpha_and_theta_oscillations_reflect_cognitive_and_memory_performance.pdf

EEG alpha and theta oscillations reflect cognitive and memory performance: a review and analysis

The multidimensional Fatigue Inventory (MFI) psychometric qualities of an instrument to assess fatigue

1.0 BACKGROUND ACTIGRAPHY HAS BEEN USED TO STUDY SLEEP/WAKE PATTERNS FOR OVER 20 YEARS. The advantage of actigraphy over traditional polysomnography (PSG) is that actigraphy can conveniently record continuously for 24-hours a day for days, weeks or even longer. In 1995, Sadeh et al.,1 under the auspices of the American Sleep Disorders Association (now called the American Academy of Sleep Medicine, AASM), reviewed the current knowledge about the role of actigraphy in the evaluation of sleep disorders. They concluded that actigraphy does provide useful information and that it may be a “cost-effective method for assessing specific sleep disorders...[but that] methodological issues have not been systematically addressed in clinical research and practice.” Based on that task force’s report, the AASM Standards of Practice Committee concluded that actigraphy was not indicated for routine diagnosis or for assessment of severity or management of sleep disorders, but might be a useful adjunct for diagnosing insomnia, circadian rhythm disorders or excessive sleepiness.2 Since that time, actigraph technology has improved, and many more studies have been conducted. Several review papers have concluded that wrist actigraphy can usefully approximate sleep versus wake state during 24 hours and have noted that actigraphy has been used for monitoring insomnia, circadian sleep/wake disturbances, and periodic limb movement disorder.3,4 This paper begins where the 1995 paper left off. Under the auspices of the AASM, a new task force was established to review the current state of the art of this technology.

The Role of Actigraphy in the Study of Sleep and Circadian Rhythms AMERICAN ACADEMY OF SLEEP MEDICINE REVIEW PAPER

Deficits in daytime performance due to sleep loss are experienced universally and associated with a significant social, financial, and human cost. Microsleeps, sleep attacks, and lapses in cognition increase with sleep loss as a function of state instability. Sleep deprivation studies repeatedly show a variable (negative) impact on mood, cognitive performance, and motor function due to an increasing sleep propensity and destabilization of the wake state. Specific neurocognitive domains including executive attention, working memory, and divergent higher cognitive functions are particularly vulnerable to sleep loss. In humans, functional metabolic and neurophysiological studies demonstrate that neural systems involved in executive function (i.e., prefrontal cortex) are more susceptible to sleep deprivation in some individuals than others. Recent chronic partial sleep deprivation experiments, which more closely replicate sleep loss in society, demonstrate that profound neurocognitive deficits accumulate over time in the face of subjective adaptation to the sensation of sleepiness. Sleep deprivation associated with disease-related sleep fragmentation (i.e., sleep apnea and restless legs syndrome) also results in neurocognitive performance decrements similar to those seen in sleep restriction studies. Performance deficits associated with sleep disorders are often viewed as a simple function of disease severity; however, recent experiments suggest that individual vulnerability to sleep loss may play a more critical role than previously thought.

/pdf/neurocognitive-consequences-of-sleep-deprivation-hg8oxdvlng.pdf

Neurocognitive Consequences of Sleep Deprivation

A working model of depression implicating failure of the coordinated interactions of a distributed network of limbic-cortical pathways is proposed. Resting state patterns of regional glucose metabolism in idiopathic depressed patients, changes in metabolism with antidepressant treatment, and blood flow changes with induced sadness in healthy subjects were used to test and refine this hypothesis. Dorsal neocortical decreases and ventral paralimbic increases characterize both healthy sadness and depressive illness; concurrent inhibition of overactive paralimbic regions and normalization of hypofunctioning dorsal cortical sites characterize disease remission. Normal functioning of the rostral anterior cingulate, with its direct connections to these dorsal and ventral areas, is postulated to be additionally required for the observed reciprocal compensatory changes, since pretreatment metabolism in this region uniquely predicts antidepressant treatment response. This model is offered as an adaptable framework to facilitate continued integration of clinical imaging findings with complementary neuroanatomical, neurochemical, and electrophysiological studies in the investigation of the pathogenesis of affective disorders.

https://neuro.psychiatryonline.org/doi/pdfplus/10.1176/jnp.9.3.471

Limbic-cortical dysregulation: a proposed model of depression.

The purpose of this study was to develop and validate automatic scoring methods to distinguish sleep from wakefulness based on wrist activity. Forty-one subjects (18 normals and 23 with sleep or psychiatric disorders) wore a wrist actigraph during overnight polysomnography. In a randomly selected subsample of 20 subjects, candidate sleep/wake prediction algorithms were iteratively optimized against standard sleep/wake scores. The optimal algorithms obtained for various data collection epoch lengths were then prospectively tested on the remaining 21 subjects. The final algorithms correctly distinguished sleep from wakefulness approximately 88% of the time. Actigraphic sleep percentage and sleep latency estimates correlated 0.82 and 0.90, respectively, with corresponding parameters scored from the polysomnogram (p < 0.0001). Automatic scoring of wrist activity provides valuable information about sleep and wakefulness that could be useful in both clinical and research applications.

Automatic sleep/wake identification from wrist activity

OBJECTIVE: Sleep deprivation has been shown to have an antidepressant benefit in a subgroup of depressed patients. Functional imaging studies by the authors and others have suggested that patients with elevated metabolic rates in the anterior cingulate gyrus at baseline are more likely to respond to either sleep deprivation or antidepressant medications than patients with normal metabolic rates. The authors extend their earlier work in a larger group of patients and explore additional brain areas with statistical probability mapping. METHOD: Thirty-six patients with unipolar depression and 26 normal volunteers were studied with positron emission tomography before and after sleep deprivation. Response to sleep deprivation was defined as a 40% or larger decrease in total scores on the Hamilton Depression Rating Scale. RESULTS: One-third of the depressed patients had a significant response to sleep deprivation. Responders had higher relative metabolic rates in the medial prefrontal cortex, ventral anterior c...

https://ajp.psychiatryonline.org/doi/pdf/10.1176/ajp.156.8.1149

Prediction of Antidepressant Effects of Sleep Deprivation by Metabolic Rates in the Ventral Anterior Cingulate and Medial Prefrontal Cortex

Objective: Sleep deprivation is a rapid, nonpharmacologic antidepressant intervention that is effective for a subset of depressed patients The objective of this study was to identify which brαin structure's activitity differentiales responders from nonresponders and to study how metabolism in these brain regions changes with mood Method: Regional cerebral glucose metabolism was assesse by positron emission tomography (PET) with [ 18 F] deoxyglucose (FDG) before

Effect of sleep deprivation on brain metabolism of depressed patients.

Objective This study compared the severity of and the change in depressive symptoms among men with alcohol dependence, affective disorder, or both disorders during 4 weeks of inpatient treatment. Method After their primary and secondary psychiatric disorders were defined with the use of criteria based on chronology of symptoms, 54 unmedicated men entering treatment for alcohol dependence or affective disorder were assessed for 4 consecutive weeks with the Hamilton Depression Rating Scale. Results The findings indicate that the rate of remission of depressive symptoms was consistent with the primary diagnosis. Depressive symptoms remitted more rapidly among the men with primary alcoholism than among those with primary affective disorder. However, a minimum of 3 weeks of abstinence from alcohol appeared to be necessary to consistently differentiate the groups with dual diagnoses on the basis of their current depressive symptoms. Alcohol dependence occurring in conjunction with primary affective disorder did not intensify presenting depressive symptoms or retard the resolution of such symptoms. Conclusions Diagnoses of alcohol dependence and affective disorder based on symptom chronology appear to have prognostic significance with respect to remission of depressive symptoms in men with both diagnoses. Depressive symptoms of dysphoric mood, dysfunctional cognitions, vegetative symptoms, and anxiety/agitation showed different rates and levels of remission across the primary diagnostic groups.

Alcoholism and affective disorder: clinical course of depressive symptoms.

This study is the first report on the effects of total sleep deprivation (about 32 h) on regional cerebral glucose metabolism during wakefulness in man, using positron emission tomography (PET) with F-18 deoxyglucose (FDG). Sleep deprivation leads to a significant reorganization of regional cerebral metabolic activity, with relative decreases in the temporal lobes and increases in visual cortex. Absolute glucose metabolic measurements indicate a decrease in thalamus, basal ganglia, white matter, and cerebellum. No overall decrease in whole brain metabolism was noted after sleep deprivation. As expected, sleep deprivation significantly reduced visual vigilance as assessed by the continuous performance test and this decrease was correlated significantly with reduced metabolic rate in thalamic, basal ganglia, and limbic regions.

/pdf/the-effect-of-sleep-deprivation-on-cerebral-glucose-7yppwadssb.pdf

Gillin Jc

Papers

Automatic sleep/wake identification from wrist activity

Prediction of Antidepressant Effects of Sleep Deprivation by Metabolic Rates in the Ventral Anterior Cingulate and Medial Prefrontal Cortex

Effect of sleep deprivation on brain metabolism of depressed patients.

Alcoholism and affective disorder: clinical course of depressive symptoms.

The effect of sleep deprivation on cerebral glucose metabolic rate in normal humans assessed with positron emission tomography