Microsleep during Partial Sleep Deprivation in Depression

Hemmeter, Ulrich; Bischof, R.; Hatzinger, Martin; Seifritz, Erich; Holsboer‐Trachsler, Edith

doi:10.1016/s0006-3223(97)00297-7

Cited by 47 publications

(15 citation statements)

References 18 publications

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“…Individual frequency shifts in the EEG, as indicated by the lower traces in Figure 6, were assessed by PSD analyses in 4.0 s epochs across the entire session and showed marked elevations in the number of transient incidences in which power in the delta and beta bands increased in sleep-deprived animals. Such changes have been reported to reflect occurrences of “microsleep” episodes [30,31]. In the sleep deprivation + CX717 condition there was a distinct shift toward the normal vehicle profile of EEG and PSD traces (Figure 6, right) characterized by a marked reduction of power (F [2,61] = 6.17, p < 0.01) in the beta band and slower delta frequencies (Figure 6, right).…”

Section: Resultsmentioning

confidence: 68%

“…The performance levels of animals in the sleep deprivation condition were reduced significantly compared to normal vehicle sessions; however, a close examination of latencies (see Figures 4 and 5) shows that animals continued to respond in the match phase in a rapid manner (2.5–3.0 sec). The assessment of EEG parameters, although not designed to provide a thorough analysis of sleep architecture, suggests that animals were experiencing microsleep episodes during the sleep deprivation testing condition [30,31]. However, these instances did not significantly alter the mean number of trials completed during sessions that were the same duration as normal vehicle tests, nor was the latency to respond to events during the trial elevated more than 1–2 s above normal vehicle sessions (see Figures 4 and 9).…”

Section: Discussionmentioning

confidence: 99%

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Facilitation of Task Performance and Removal of the Effects of Sleep Deprivation by an Ampakine (CX717) in Nonhuman Primates

et al. 2005

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The deleterious effects of prolonged sleep deprivation on behavior and cognition are a concern in modern society. Persons at risk for impaired performance and health-related issues resulting from prolonged sleep loss would benefit from agents capable of reducing these detrimental effects at the time they are sleep deprived. Agents capable of improving cognition by enhancing brain activity under normal circumstances may also have the potential to reduce the harmful or unwanted effects of sleep deprivation. The significant prevalence of excitatory α-amino-3-hydroxy-5-methyl-4-isoxazolepropionic acid (AMPA) glutamatergic receptors in the brain provides a basis for implementing a class of drugs that could act to alter or remove the effects of sleep deprivation. The ampakine CX717 (Cortex Pharmaceuticals), a positive allosteric modulator of AMPA receptors, was tested for its ability to enhance performance of a cognitive, delayed match-to-sample task under normal circumstances in well-trained monkeys, as well as alleviate the detrimental effects of 30–36 h of sleep deprivation. CX717 produced a dose-dependent enhancement of task performance under normal alert testing conditions. Concomitant measures of regional cerebral metabolic rates for glucose (CMRglc) during the task, utilizing positron emission tomography, revealed increased activity in prefrontal cortex, dorsal striatum, and medial temporal lobe (including hippocampus) that was significantly enhanced over normal alert conditions following administration of CX717. A single night of sleep deprivation produced severe impairments in performance in the same monkeys, accompanied by significant alterations in task-related CMRglc in these same brain regions. However, CX717 administered to sleep-deprived monkeys produced a striking removal of the behavioral impairment and returned performance to above-normal levels even though animals were sleep deprived. Consistent with this recovery, CMRglc in all but one brain region affected by sleep deprivation was also returned to the normal alert pattern by the drug. The ampakine CX717, in addition to enhancing cognitive performance under normal alert conditions, also proved effective in alleviating impairment of performance due to sleep deprivation. Therefore, the ability to activate specific brain regions under normal alert conditions and alter the deleterious effects of sleep deprivation on activity in those same regions indicate a potential role for ampakines in sustaining performance under these types of adverse conditions.

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Section: Resultsmentioning

confidence: 68%

Section: Discussionmentioning

confidence: 99%

Facilitation of Task Performance and Removal of the Effects of Sleep Deprivation by an Ampakine (CX717) in Nonhuman Primates

et al. 2005

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“…One night of total sleep deprivation, known to augment adenosine signaling in the brain (Basheer et al, 2001; Benington et al, 1995; Mackiewicz et al, 2003), is one of the most effective treatments for the treatment of major depression (Hemmeter et al, 1998; Hemmeter et al, 2010). S-adenosylhomocysteine, a precursor of adenosine, is widely used for the treatment of major depression and several studies suggest therapeutic benefits (Carpenter, 2011; De Berardis et al, 2013).…”

Section: Adenosine-dependent Mechanisms and Therapeutic Applicationsmentioning

confidence: 99%

Comorbidities in Neurology: Is adenosine the common link?

Boison

Aronica

2015

Neuropharmacology

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Comorbidities in Neurology represent a major conceptual and therapeutic challenge. For example, temporal lobe epilepsy (TLE) is a syndrome comprised of epileptic seizures and comorbid symptoms including memory and psychiatric impairment, depression, and sleep dysfunction. Similarly, Alzheimer’s disease (AD), Parkinson’s disease (PD), and Amyotrophic Lateral Sclerosis (ALS) are accompanied by various degrees of memory dysfunction. Patients with AD have an increased likelihood for seizures, whereas all four conditions share certain aspects of psychosis, depression, and sleep dysfunction. This remarkable overlap suggests common pathophysiological mechanisms, which include synaptic dysfunction and synaptotoxicity, as well as glial activation and astrogliosis. Astrogliosis is linked to synapse function via the tripartite synapse, but astrocytes also control the availability of gliotransmitters and adenosine. Here we will specifically focus on the ‘adenosine hypothesis of comorbidities’ implying that astrocyte activation, via overexpression of adenosine kinase (ADK), induces a deficiency in the homeostatic tone of adenosine. We present evidence from patient-derived samples showing astrogliosis and overexpression of ADK as common pathological hallmark of epilepsy, AD, PD, and ALS. We discuss a transgenic ‘comorbidity model’, in which brain-wide overexpression of ADK and resulting adenosine deficiency produces a comorbid spectrum of seizures, altered dopaminergic function, attentional impairment, and deficits in cognitive domains and sleep regulation. We conclude that dysfunction of adenosine signaling is common in neurological conditions, that adenosine dysfunction can explain comorbid phenotypes, and that therapeutic adenosine augmentation might be effective for the treatment of comorbid symptoms in multiple neurological conditions.

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“…Further, the data are excellently evaluable using statistical approaches. Accordingly, there are many studies about qEEG changes in depression syndromes (Giles, Perlis, Reynolds, & Kupfer, 1998;Hemmeter, Bischof, Hatzinger, Seifritz, & Holsboer-Trachsler, 1998;Knott, Mahoney, Kennedy, & Evans, 2001;Schneider, Heimann, Mattes, Lutzenberger, & Birbaumer, 1992), Alzheimers disease (Dierks, Frölich, Ihl, & Maurer, 1995;Elmstahl, Rosen, & Gullberg, 1994;Ihl & Brinkmeyer, 1999), schizophrenia (Lund, Sponheim, Iacono, & Clementz, 1995;Murri, 1991;Sponheim, Clementz, Iacono, & Beiser, 1994;Stassen et al, 1999;Tauscher, Fischer, Neumeister, Rappelsberger, & Kasper, 1998;Wada, Nanbu, Jiang, Koshino, & Hashimoto, 1998a;Wada et al, 1998b). In comparison to these psychiatric applications, there are some studies utilizing qEEG in anorexia nervosa (AN) so far (Bradley et al, 1997;Bordallo, Diago, & Alberto, 1986;Crisp, Fenton, & Scotten, 1968;Delvenne, Kerkhofs, Appelboom-Fondu, Lucas, & Mendlewicz, 1992;Hughes, 1996;Lauer & Krieg, 1992;Neil, Merikangas JR, Foster, Merikangas KR, Spiker, & Kupfer, 1980;Rothenberger, Blanz, & Lehmkuhl, 1991;Struve 1986;Torigoe et al, 1999).…”

mentioning

confidence: 99%

Stable Asymmetric Interhemispheric Theta Power in Patients With Anorexia Nervosa During Haptic Perception Even After Weight Gain: A Longitudinal Study

Grünwald

Weiß

Assmann

et al. 2004

Journal of Clinical and Experimental Neuropsychology

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The aim of this study was to investigate the interhemispheric brain electrical asymmetries during a resting period and during haptic tasks in theta frequency band (4-8 Hz) between healthy controls (N = 10) and patients with anorexia nervosa (AN) (N = 10). Additionally, AN patients were investigated twice in a longitudinal design (T(0)-T(1)) to analyze treatment effects. At rest, a theta asymmetry was observed in the AN group during an acute stage of starvation (T(0)) but not after weight gain (T(1)). Importantly, theta asymmetry over central regions (C3-C4) was observed in the AN group during the acute stage of starvation (T(0) as well as after weight gain (T(1)) while performing haptic exploration task. In the control group, we found no significant theta asymmetry neither at rest nor during haptic explorations. Results are interpreted as an overarousal of the right hemisphere in AN patients during complex multisensory integration processing which is possibly a result of general functional deficits of the right hemisphere.

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Microsleep during Partial Sleep Deprivation in Depression

Cited by 47 publications

References 18 publications

Facilitation of Task Performance and Removal of the Effects of Sleep Deprivation by an Ampakine (CX717) in Nonhuman Primates

Facilitation of Task Performance and Removal of the Effects of Sleep Deprivation by an Ampakine (CX717) in Nonhuman Primates

Comorbidities in Neurology: Is adenosine the common link?

Stable Asymmetric Interhemispheric Theta Power in Patients With Anorexia Nervosa During Haptic Perception Even After Weight Gain: A Longitudinal Study

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