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Tóthfalusi László - One of the best experts on this subject based on the ideXlab platform.

  • Chronic escitalopram treatment attenuated the accelerated rapid eye movement sleep transitions after selective rapid eye movement sleep deprivation: a model-based analysis using Markov chains
    'Springer Science and Business Media LLC', 2014
    Co-Authors: Kostyalik Diána, Vas Szilvia, Kátai Zita, Kitka Tamás, Gyertyán István, Bagdy György, Tóthfalusi László
    Abstract:

    BackgroundShortened rapid eye movement (REM) sleep latency and increased REM sleep amount are presumed biological markers of depression. These sleep alterations are also observable in several animal models of depression as well as during the Rebound sleep after selective REM sleep deprivation (RD). Furthermore, REM sleep fragmentation is typically associated with stress procedures and anxiety. The selective serotonin reuptake inhibitor (SSRI) antidepressants reduce REM sleep time and increase REM latency after acute dosing in normal condition and even during REM Rebound following RD. However, their therapeutic outcome evolves only after weeks of treatment, and the effects of chronic treatment in REM-deprived animals have not been studied yet.ResultsChronic escitalopram- (10 mg/kg/day, osmotic minipump for 24 days) or vehicle-treated rats were subjected to a 3-day-long RD on day 21 using the flower pot procedure or kept in home cage. On day 24, fronto-parietal electroencephalogram, electromyogram and motility were recorded in the first 2 h of the passive phase. The observed sleep patterns were characterized applying standard sleep metrics, by modelling the transitions between sleep phases using Markov chains and by spectral analysis.Based on Markov chain analysis, chronic escitalopram treatment attenuated the REM sleep fragmentation [accelerated transition rates between REM and non-REM (NREM) stages, decreased REM sleep residence time between two transitions] during the Rebound sleep. Additionally, the antidepressant avoided the frequent awakenings during the first 30 min of recovery period. The spectral analysis showed that the SSRI prevented the RD-caused elevation in theta (5 inverted question mark9 Hz) power during slow-wave sleep. Conversely, based on the aggregate sleep metrics, escitalopram had only moderate effects and it did not significantly attenuate the REM Rebound after RD.ConclusionIn conclusion, chronic SSRI treatment is capable of reducing several effects on sleep which might be the consequence of the sub-chronic stress caused by the flower pot method. These data might support the antidepressant activity of SSRIs, and may allude that investigating the Rebound period following the flower pot protocol could be useful to detect antidepressant drug response. Markov analysis is a suitable method to study the sleep pattern

  • Chronic escitalopram treatment attenuated the accelerated rapid eye movement sleep transitions after selective rapid eye movement sleep deprivation: a model-based analysis using Markov chains
    'Springer Science and Business Media LLC', 2014
    Co-Authors: Kostyalik Diána, Vas Szilvia, Kátai Zita, Kitka Tamás, Gyertyán István, Bagdy György, Tóthfalusi László
    Abstract:

    BackgroundShortened rapid eye movement (REM) sleep latency and increased REM sleep amount are presumed biological markers of depression. These sleep alterations are also observable in several animal models of depression as well as during the Rebound sleep after selective REM sleep deprivation (RD). Furthermore, REM sleep fragmentation is typically associated with stress procedures and anxiety. The selective serotonin reuptake inhibitor (SSRI) antidepressants reduce REM sleep time and increase REM latency after acute dosing in normal condition and even during REM Rebound following RD. However, their therapeutic outcome evolves only after weeks of treatment, and the effects of chronic treatment in REM-deprived animals have not been studied yet.ResultsChronic escitalopram- (10 mg/kg/day, osmotic minipump for 24 days) or vehicle-treated rats were subjected to a 3-day-long RD on day 21 using the flower pot procedure or kept in home cage. On day 24, fronto-parietal electroencephalogram, electromyogram and motility were recorded in the first 2 h of the passive phase. The observed sleep patterns were characterized applying standard sleep metrics, by modelling the transitions between sleep phases using Markov chains and by spectral analysis.Based on Markov chain analysis, chronic escitalopram treatment attenuated the REM sleep fragmentation [accelerated transition rates between REM and non-REM (NREM) stages, decreased REM sleep residence time between two transitions] during the Rebound sleep. Additionally, the antidepressant avoided the frequent awakenings during the first 30 min of recovery period. The spectral analysis showed that the SSRI prevented the RD-caused elevation in theta (5¿9 Hz) power during slow-wave sleep. Conversely, based on the aggregate sleep metrics, escitalopram had only moderate effects and it did not significantly attenuate the REM Rebound after RD.ConclusionIn conclusion, chronic SSRI treatment is capable of reducing several effects on sleep which might be the consequence of the sub-chronic stress caused by the flower pot method. These data might support the antidepressant activity of SSRIs, and may allude that investigating the Rebound period following the flower pot protocol could be useful to detect antidepressant drug response. Markov analysis is a suitable method to study the sleep pattern

Max B Kelz - One of the best experts on this subject based on the ideXlab platform.

  • rapid eye movement sleep debt accrues in mice exposed to volatile anesthetics
    Anesthesiology, 2011
    Co-Authors: Jeremy Pick, Yihan Chen, Jason T Moore, Yi Sun, Abraham J Wyner, Eliot Friedman, Max B Kelz
    Abstract:

    BACKGROUND General anesthesia has been likened to a state in which anesthetized subjects are locked out of access to both rapid eye movement (REM) sleep and wakefulness. Were this true for all anesthetics, a significant REM Rebound after anesthetic exposure might be expected. However, for the intravenous anesthetic propofol, studies demonstrate that no sleep debt accrues. Moreover, preexisting sleep debts dissipate during propofol anesthesia. To determine whether these effects are specific to propofol or are typical of volatile anesthetics, the authors tested the hypothesis that REM sleep debt would accrue in rodents anesthetized with volatile anesthetics. METHODS Electroencephalographic and electromyographic electrodes were implanted in 10 mice. After 9-11 days of recovery and habituation to a 12 h:12 h light-dark cycle, baseline states of wakefulness, nonrapid eye movement sleep, and REM sleep were recorded in mice exposed to 6 h of an oxygen control and on separate days to 6 h of isoflurane, sevoflurane, or halothane in oxygen. All exposures were conducted at the onset of light. RESULTS Mice in all three anesthetized groups exhibited a significant doubling of REM sleep during the first 6 h of the dark phase of the circadian schedule, whereas only mice exposed to halothane displayed a significant increase in nonrapid eye movement sleep that peaked at 152% of baseline. CONCLUSION REM sleep Rebound after exposure to volatile anesthetics suggests that these volatile anesthetics do not fully substitute for natural sleep. This result contrasts with the published actions of propofol for which no REM sleep Rebound occurred.

Kostyalik Diána - One of the best experts on this subject based on the ideXlab platform.

  • Chronic escitalopram treatment attenuated the accelerated rapid eye movement sleep transitions after selective rapid eye movement sleep deprivation: a model-based analysis using Markov chains
    'Springer Science and Business Media LLC', 2014
    Co-Authors: Kostyalik Diána, Vas Szilvia, Kátai Zita, Kitka Tamás, Gyertyán István, Bagdy György, Tóthfalusi László
    Abstract:

    BackgroundShortened rapid eye movement (REM) sleep latency and increased REM sleep amount are presumed biological markers of depression. These sleep alterations are also observable in several animal models of depression as well as during the Rebound sleep after selective REM sleep deprivation (RD). Furthermore, REM sleep fragmentation is typically associated with stress procedures and anxiety. The selective serotonin reuptake inhibitor (SSRI) antidepressants reduce REM sleep time and increase REM latency after acute dosing in normal condition and even during REM Rebound following RD. However, their therapeutic outcome evolves only after weeks of treatment, and the effects of chronic treatment in REM-deprived animals have not been studied yet.ResultsChronic escitalopram- (10 mg/kg/day, osmotic minipump for 24 days) or vehicle-treated rats were subjected to a 3-day-long RD on day 21 using the flower pot procedure or kept in home cage. On day 24, fronto-parietal electroencephalogram, electromyogram and motility were recorded in the first 2 h of the passive phase. The observed sleep patterns were characterized applying standard sleep metrics, by modelling the transitions between sleep phases using Markov chains and by spectral analysis.Based on Markov chain analysis, chronic escitalopram treatment attenuated the REM sleep fragmentation [accelerated transition rates between REM and non-REM (NREM) stages, decreased REM sleep residence time between two transitions] during the Rebound sleep. Additionally, the antidepressant avoided the frequent awakenings during the first 30 min of recovery period. The spectral analysis showed that the SSRI prevented the RD-caused elevation in theta (5 inverted question mark9 Hz) power during slow-wave sleep. Conversely, based on the aggregate sleep metrics, escitalopram had only moderate effects and it did not significantly attenuate the REM Rebound after RD.ConclusionIn conclusion, chronic SSRI treatment is capable of reducing several effects on sleep which might be the consequence of the sub-chronic stress caused by the flower pot method. These data might support the antidepressant activity of SSRIs, and may allude that investigating the Rebound period following the flower pot protocol could be useful to detect antidepressant drug response. Markov analysis is a suitable method to study the sleep pattern

  • Chronic escitalopram treatment attenuated the accelerated rapid eye movement sleep transitions after selective rapid eye movement sleep deprivation: a model-based analysis using Markov chains
    'Springer Science and Business Media LLC', 2014
    Co-Authors: Kostyalik Diána, Vas Szilvia, Kátai Zita, Kitka Tamás, Gyertyán István, Bagdy György, Tóthfalusi László
    Abstract:

    BackgroundShortened rapid eye movement (REM) sleep latency and increased REM sleep amount are presumed biological markers of depression. These sleep alterations are also observable in several animal models of depression as well as during the Rebound sleep after selective REM sleep deprivation (RD). Furthermore, REM sleep fragmentation is typically associated with stress procedures and anxiety. The selective serotonin reuptake inhibitor (SSRI) antidepressants reduce REM sleep time and increase REM latency after acute dosing in normal condition and even during REM Rebound following RD. However, their therapeutic outcome evolves only after weeks of treatment, and the effects of chronic treatment in REM-deprived animals have not been studied yet.ResultsChronic escitalopram- (10 mg/kg/day, osmotic minipump for 24 days) or vehicle-treated rats were subjected to a 3-day-long RD on day 21 using the flower pot procedure or kept in home cage. On day 24, fronto-parietal electroencephalogram, electromyogram and motility were recorded in the first 2 h of the passive phase. The observed sleep patterns were characterized applying standard sleep metrics, by modelling the transitions between sleep phases using Markov chains and by spectral analysis.Based on Markov chain analysis, chronic escitalopram treatment attenuated the REM sleep fragmentation [accelerated transition rates between REM and non-REM (NREM) stages, decreased REM sleep residence time between two transitions] during the Rebound sleep. Additionally, the antidepressant avoided the frequent awakenings during the first 30 min of recovery period. The spectral analysis showed that the SSRI prevented the RD-caused elevation in theta (5¿9 Hz) power during slow-wave sleep. Conversely, based on the aggregate sleep metrics, escitalopram had only moderate effects and it did not significantly attenuate the REM Rebound after RD.ConclusionIn conclusion, chronic SSRI treatment is capable of reducing several effects on sleep which might be the consequence of the sub-chronic stress caused by the flower pot method. These data might support the antidepressant activity of SSRIs, and may allude that investigating the Rebound period following the flower pot protocol could be useful to detect antidepressant drug response. Markov analysis is a suitable method to study the sleep pattern

Jeremy Pick - One of the best experts on this subject based on the ideXlab platform.

  • rapid eye movement sleep debt accrues in mice exposed to volatile anesthetics
    Anesthesiology, 2011
    Co-Authors: Jeremy Pick, Yihan Chen, Jason T Moore, Yi Sun, Abraham J Wyner, Eliot Friedman, Max B Kelz
    Abstract:

    BACKGROUND General anesthesia has been likened to a state in which anesthetized subjects are locked out of access to both rapid eye movement (REM) sleep and wakefulness. Were this true for all anesthetics, a significant REM Rebound after anesthetic exposure might be expected. However, for the intravenous anesthetic propofol, studies demonstrate that no sleep debt accrues. Moreover, preexisting sleep debts dissipate during propofol anesthesia. To determine whether these effects are specific to propofol or are typical of volatile anesthetics, the authors tested the hypothesis that REM sleep debt would accrue in rodents anesthetized with volatile anesthetics. METHODS Electroencephalographic and electromyographic electrodes were implanted in 10 mice. After 9-11 days of recovery and habituation to a 12 h:12 h light-dark cycle, baseline states of wakefulness, nonrapid eye movement sleep, and REM sleep were recorded in mice exposed to 6 h of an oxygen control and on separate days to 6 h of isoflurane, sevoflurane, or halothane in oxygen. All exposures were conducted at the onset of light. RESULTS Mice in all three anesthetized groups exhibited a significant doubling of REM sleep during the first 6 h of the dark phase of the circadian schedule, whereas only mice exposed to halothane displayed a significant increase in nonrapid eye movement sleep that peaked at 152% of baseline. CONCLUSION REM sleep Rebound after exposure to volatile anesthetics suggests that these volatile anesthetics do not fully substitute for natural sleep. This result contrasts with the published actions of propofol for which no REM sleep Rebound occurred.

Oreste Marrone - One of the best experts on this subject based on the ideXlab platform.

  • Case Report ExtREMe REM Rebound during Continuous Positive Airway Pressure Titration for Obstructive Sleep Apnea in a Depressed Patient
    2020
    Co-Authors: Anna Lo Bue, Adriana Salvaggio, Giuseppe Insalaco, Oreste Marrone
    Abstract:

    A 20% increase in REM sleep duration has been proposed as a threshold to identify REM Rebound in patients with obstructive sleep apnea (OSA) who start continuous positive airway pressure (CPAP) treatment. We describe the case of one patient with OSA who showed an unexpectedly high degree of REM Rebound during titration of CPAP. A 34-year-old man was diagnosed with OSA. He REMained untreated for many years, during which he developed systemic hypertension, depression, and severe daytime somnolence. When he was reevaluated sixteen years later, his Epworth sleepiness score was 18, and his OSA had greatly worsened (apnea/hypopnea index: 47, lowest nocturnal saturation: 57%). He underwent a successful CPAP titration during nocturnal polysomnography. Electroencephalographic analysis of the sleep recording revealed a huge amount of REM sleep, accounting for 72% of the total sleep time. When asked, the patient referred that he had suddenly interrupted paroxetine assumption three days before the polysomnography. The very large REM Rebound observed in this patient could be due to additional effects of initiation of CPAP therapy and suspension of antidepressive treatment. This case does not report any dangerous consequence, but sudden antidepressive withdrawal could be dangerous for patients with OSA who develop hypoventilation during REM sleep with CPAP application

  • extREMe REM Rebound during continuous positive airway pressure titration for obstructive sleep apnea in a depressed patient
    Case Reports in Medicine, 2014
    Co-Authors: Anna Lo Bue, Adriana Salvaggio, Giuseppe Insalaco, Oreste Marrone
    Abstract:

    A 20% increase in REM sleep duration has been proposed as a threshold to identify REM Rebound in patients with obstructive sleep apnea (OSA) who start continuous positive airway pressure (CPAP) treatment. We describe the case of one patient with OSA who showed an unexpectedly high degree of REM Rebound during titration of CPAP. A 34-year-old man was diagnosed with OSA. He REMained untreated for many years, during which he developed systemic hypertension, depression, and severe daytime somnolence. When he was reevaluated sixteen years later, his Epworth sleepiness score was 18, and his OSA had greatly worsened (apnea/hypopnea index: 47, lowest nocturnal saturation: 57%). He underwent a successful CPAP titration during nocturnal polysomnography. Electroencephalographic analysis of the sleep recording revealed a huge amount of REM sleep, accounting for 72% of the total sleep time. When asked, the patient referred that he had suddenly interrupted paroxetine assumption three days before the polysomnography. The very large REM Rebound observed in this patient could be due to additional effects of initiation of CPAP therapy and suspension of antidepressive treatment. This case does not report any dangerous consequence, but sudden antidepressive withdrawal could be dangerous for patients with OSA who develop hypoventilation during REM sleep with CPAP application.

  • ExtREMe REM Rebound during Continuous Positive Airway Pressure Titration for Obstructive Sleep Apnea in a Depressed Patient
    2014
    Co-Authors: Anna Lo Bue, Adriana Salvaggio, Oreste Marrone
    Abstract:

    which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited. A 20 % increase in REM sleep duration has been proposed as a threshold to identify REM Rebound in patients with obstructive sleep apnea (OSA) who start continuous positive airway pressure (CPAP) treatment. We describe the case of one patient with OSA who showed an unexpectedly high degree of REM Rebound during titration of CPAP. A 34-year-old man was diagnosed with OSA. He REMained untreated for many years, during which he developed systemic hypertension, depression, and severe daytime somnolence. When he was reevaluated sixteen years later, his Epworth sleepiness score was 18, and his OSA had greatly worsened (apnea/hypopnea index: 47, lowest nocturnal saturation: 57%). He underwent a successful CPAP titration during nocturnal polysomnography. Electroencephalographic analysis of the sleep recording revealed a huge amount of REM sleep, accounting for 72 % of the total sleep time. When asked, the patient referred that he had suddenly interrupted paroxetine assumption three days before the polysomnography. The very large REM Rebound observed in this patient could be due to additional effects of initiation of CPAP therapy and suspension of antidepressive treatment. This case does not report any dangerous consequence, but sudden antidepressive withdrawal could be dangerous for patients with OSA who develop hypoventilation during REM sleep with CPAP application. 1