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Felsky D, Abdelhack M. Connecting mechanistic evidence for depression, anxiety, and insomnia with neuroimaging. Sleep Med Rev 2025; 81:102099. [PMID: 40359730 DOI: 10.1016/j.smrv.2025.102099] [Citation(s) in RCA: 0] [Impact Index Per Article: 0] [Reference Citation Analysis] [Track Full Text] [Journal Information] [Subscribe] [Scholar Register] [Indexed: 05/15/2025]
Affiliation(s)
- Daniel Felsky
- Krembil Centre for Neuroinformatics, Centre for Addiction and Mental Health, Toronto, ON, Canada; Department of Psychiatry and Institute of Medical Science, Temerty Faculty of Medicine, University of Toronto, Toronto, ON, Canada; Division of Biostatistics, Dalla Lana School of Public Health, University of Toronto, Toronto, ON, Canada; Departments of Anthropology, University of Toronto, Toronto, ON, Canada; Department of Public Health Sciences, University of Waterloo, Waterloo, ON, Canada; Rotman Research Institute, Baycrest Hospital, Toronto, ON, Canada.
| | - Mohamed Abdelhack
- Krembil Centre for Neuroinformatics, Centre for Addiction and Mental Health, Toronto, ON, Canada
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Le Bouthillier J, Ivers H, Morin CM. Intensive Sleep Retraining and Total Sleep Deprivation for Treating Chronic Insomnia: A Randomised Controlled Trial. J Sleep Res 2025:e70043. [PMID: 40295155 DOI: 10.1111/jsr.70043] [Citation(s) in RCA: 0] [Impact Index Per Article: 0] [Reference Citation Analysis] [Abstract] [Key Words] [Grants] [Track Full Text] [Journal Information] [Subscribe] [Scholar Register] [Received: 12/13/2024] [Revised: 02/19/2025] [Accepted: 03/06/2025] [Indexed: 04/30/2025]
Abstract
The aim of the study was to compare the efficacy of intensive sleep retraining (ISR) and total sleep deprivation (TSD) against a no-treatment control condition for treating chronic insomnia and examine two potential mechanisms: the resolution of conditioned insomnia and the increase in homeostatic sleep drive produced by sleep deprivation. Thirty-four adults with chronic sleep onset insomnia (with or without sleep maintenance difficulties) were randomised to ISR, TSD, or a control condition. The ISR condition consisted of a 38.5-h period of sleep deprivation, the last 21 h of which included 42 sleep onset trials; the TSD condition consisted of an equivalent 38.5-h sleep deprivation period without any sleep onset trials, and the control condition consisted of one night of habitual sleep in the laboratory. Significant decreases in insomnia severity were observed from pre- to post-treatment in both ISR and TSD, but not in the control condition. A significant reduction in sleep onset latency was observed during the same period for the ISR condition, but not for the TSD or control conditions, with no clinically meaningful change in anxiety or depressive symptoms. Significant decreases in fatigue were also observed for both ISR and TSD conditions during the same period. These results were generally significant at 3 months after treatment. Sleep improvements produced by ISR, and to a lesser extent by TSD, suggest that both the resolution of conditioned insomnia and the increase in homeostatic sleep drive represent important mechanisms responsible for the efficacy of ISR.
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Affiliation(s)
- J Le Bouthillier
- École de psychologie, Université Laval, Quebec City, Québec, Canada
- Centre d'étude des troubles du sommeil, Centre de recherche CERVO, Quebec City, Québec, Canada
| | - H Ivers
- École de psychologie, Université Laval, Quebec City, Québec, Canada
- Centre d'étude des troubles du sommeil, Centre de recherche CERVO, Quebec City, Québec, Canada
| | - C M Morin
- École de psychologie, Université Laval, Quebec City, Québec, Canada
- Centre d'étude des troubles du sommeil, Centre de recherche CERVO, Quebec City, Québec, Canada
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Li C, Lam YC, Hsiao JHW, Yee LTS, Zhang J, Lau EYY. Subclinically Depressed Individuals Showed Less Trust after a Night of Sleep Deprivation. THE SPANISH JOURNAL OF PSYCHOLOGY 2025; 28:e11. [PMID: 40260462 DOI: 10.1017/sjp.2025.11] [Citation(s) in RCA: 0] [Impact Index Per Article: 0] [Reference Citation Analysis] [Abstract] [Key Words] [MESH Headings] [Track Full Text] [Subscribe] [Scholar Register] [Indexed: 04/23/2025]
Abstract
Insufficient sleep's impact on cognitive and emotional function is well-documented, but its effects on social functioning remain understudied. This research investigates the influence of depressive symptoms on the relationship between sleep deprivation (SD) and social decision-making. Forty-two young adults were randomly assigned to either the SD or sleep control (SC) group. The SD group stayed awake in the laboratory, while the SC group had a normal night's sleep at home. During the subsequent morning, participants completed a Trust Game (TG) in which a higher monetary offer distributed by them indicated more trust toward their partners. They also completed an Ultimatum Game (UG) in which a higher acceptance rate indicated more rational decision-making. The results revealed that depressive symptoms significantly moderated the effect of SD on trust in the TG. However, there was no interaction between group and depressive symptoms found in predicting acceptance rates in the UG. This study demonstrates that individuals with higher levels of depressive symptoms display less trust after SD, highlighting the role of depressive symptoms in modulating the impact of SD on social decision-making. Future research should explore sleep-related interventions targeting the psychosocial dysfunctions of individuals with depression.
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Affiliation(s)
- Cheng Li
- The Education University of Hong Kong, China
| | | | | | | | | | - Esther Yuet Ying Lau
- The Education University of Hong Kong, China
- Hong Kong University of Science & Technology, China
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Boujelbane MA, Trabelsi K, Jahrami H, Ammar A, Salem A, Kerkeni M, Charfi A, Boukhris O, Clark CCT, Roufayel R, Bragazzi NL, Schöllhorn WI, Glenn JM, Chtourou H. The Effects of Time-Restricted Feeding on Handgrip Strength, Vigilance, and Perceived Anxiety and Depression in Older Adults: A Comparative Study Between Active and Sedentary Populations. Health Sci Rep 2025; 8:e70692. [PMID: 40260036 PMCID: PMC12010213 DOI: 10.1002/hsr2.70692] [Citation(s) in RCA: 0] [Impact Index Per Article: 0] [Reference Citation Analysis] [Abstract] [Key Words] [Track Full Text] [Figures] [Journal Information] [Subscribe] [Scholar Register] [Received: 11/10/2024] [Revised: 04/01/2025] [Accepted: 04/03/2025] [Indexed: 04/23/2025] Open
Abstract
Background and Aims Ramadan intermittent fasting (RIF), a form of time-restricted feeding, influences various physiological and psychological functions. However, its effects on older adults remain insufficiently understood. This study examined the impact of RIF on physical and mental health parameters, comparing active and sedentary older individuals. Specifically, we assessed handgrip strength (HGS), vigilance performance, anxiety, and depression levels to determine whether regular physical activity mitigates potential adverse effects of RIF. Methods Fifty-eight older adults (mean age 62.93 ± 3.99 years; 50% female) participated in this study. They were classified into an active group (n = 26) and sedentary group (n = 32) based on self-reported physical activity levels. Assessments were conducted before and during RIF and included HGS measurement using a handheld dynamometer, a digital psychomotor vigilance test, and validated questionnaires (General Anxiety Disorder-7, Geriatric Depression Scale, and Physical Activity Scale for the Elderly). Results During RIF, both groups showed significant improvements in vigilance, anxiety, and depression scores, with more pronounced benefits in the active group. However, sedentary participants experienced a decline in HGS, whereas active individuals maintained stable muscle strength. Conclusion Regular physical activity during RIF appears to enhance vigilance and mental health while preventing muscle strength decline in older adults. These findings highlight the importance of maintaining an active lifestyle during RIF to support both physical and mental health in aging populations.
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Affiliation(s)
- Mohamed Ali Boujelbane
- Department of Training and Movement Science, Institute of Sport ScienceJohannes Gutenberg‐University MainzMainzGermany
- High Institute of Sport and Physical EducationUniversity of SfaxSfaxTunisia
- Physical Activity, Sport, and Health, National Observatory of SportTunisTunisia
| | - Khaled Trabelsi
- High Institute of Sport and Physical EducationUniversity of SfaxSfaxTunisia
- Research Laboratory: Education, Motricité, Sport et Santé, EM2S, High Institute of Sport and Physical Education of SfaxUniversity of SfaxSfaxTunisia
- Department of Movement Sciences and Sports Training, School of Sport ScienceThe University of JordanAmmanJordan
| | - Haitham Jahrami
- College of Medicine and Medical SciencesArabian Gulf UniversityManamaKingdom of Bahrain
- Ministry of HealthManamaKingdom of Bahrain
| | - Achraf Ammar
- Department of Training and Movement Science, Institute of Sport ScienceJohannes Gutenberg‐University MainzMainzGermany
- High Institute of Sport and Physical EducationUniversity of SfaxSfaxTunisia
- Research Laboratory, Molecular Bases of Human Pathology Faculty of Medicine of SfaxUniversity of SfaxSfaxTunisia
| | - Atef Salem
- Department of Training and Movement Science, Institute of Sport ScienceJohannes Gutenberg‐University MainzMainzGermany
- High Institute of Sport and Physical EducationUniversity of SfaxSfaxTunisia
- Physical Activity, Sport, and Health, National Observatory of SportTunisTunisia
| | - Mohamed Kerkeni
- High Institute of Sport and Physical EducationUniversity of SfaxSfaxTunisia
- Research Laboratory: Education, Motricité, Sport et Santé, EM2S, High Institute of Sport and Physical Education of SfaxUniversity of SfaxSfaxTunisia
| | - Amir Charfi
- High Institute of Sport and Physical EducationUniversity of SfaxSfaxTunisia
| | - Omar Boukhris
- SIESTA Research Group, School of Allied Health, Human Services and SportLa Trobe UniversityMelbourneAustralia
- Sport, Performance, and Nutrition Research Group, School of Allied Health, Human Services and SportLa Trobe UniversityMelbourneAustralia
| | | | - Rabih Roufayel
- College of Engineering and TechnologyAmerican University of the Middle EastKuwait
| | - Nicola Luigi Bragazzi
- Laboratory for Industrial and Applied Mathematics, Department of Mathematics and StatisticsYork UniversityTorontoOntarioCanada
| | - Wolfgang I. Schöllhorn
- Department of Training and Movement Science, Institute of Sport ScienceJohannes Gutenberg‐University MainzMainzGermany
| | - Jordan M. Glenn
- Neurotrack TechnologiesRedwood CityCaliforniaUSA
- Department of Health, Human Performance and Recreation, Exercise Science Research CenterUniversity of ArkansasFayettevilleArkansasUSA
| | - Hamdi Chtourou
- High Institute of Sport and Physical EducationUniversity of SfaxSfaxTunisia
- Physical Activity, Sport, and Health, National Observatory of SportTunisTunisia
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Yasugaki S, Okamura H, Kaneko A, Hayashi Y. Bidirectional relationship between sleep and depression. Neurosci Res 2025; 211:57-64. [PMID: 37116584 DOI: 10.1016/j.neures.2023.04.006] [Citation(s) in RCA: 26] [Impact Index Per Article: 26.0] [Reference Citation Analysis] [Abstract] [Key Words] [MESH Headings] [Track Full Text] [Journal Information] [Subscribe] [Scholar Register] [Received: 10/13/2022] [Revised: 03/01/2023] [Accepted: 04/18/2023] [Indexed: 04/30/2023]
Abstract
Patients with depression almost inevitably exhibit abnormalities in sleep, such as shortened latency to enter rapid eye movement (REM) sleep and decrease in electroencephalogram delta power during non-REM sleep. Insufficient sleep can be stressful, and the accumulation of stress leads to the deterioration of mental health and contributes to the development of psychiatric disorders. Thus, it is likely that depression and sleep are bidirectionally related, i.e. development of depression contributes to sleep disturbances and vice versa. However, the relation between depression and sleep seems complicated. For example, acute sleep deprivation can paradoxically improve depressive symptoms. Thus, it is difficult to conclude whether sleep has beneficial or harmful effects in patients with depression. How antidepressants affect sleep in patients with depression might provide clues to understanding the effects of sleep, but caution is required considering that antidepressants have diverse effects other than sleep. Recent animal studies support the bidirectional relation between depression and sleep, and animal models of depression are expected to be beneficial for the identification of neuronal circuits that connect stress, sleep, and depression. This review provides a comprehensive overview regarding the current knowledge of the relationship between depression and sleep.
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Affiliation(s)
- Shinnosuke Yasugaki
- International Institute for Integrative Sleep Medicine (WPI-IIIS), University of Tsukuba, Tsukuba, Ibaraki 305-8575, Japan; Department of Biological Sciences, Graduate School of Science, The University of Tokyo, Bunkyo-ku, Tokyo 113-0033, Japan; Japan Society for the Promotion of Science (JSPS), Tokyo 102-0083, Japan
| | - Hibiki Okamura
- International Institute for Integrative Sleep Medicine (WPI-IIIS), University of Tsukuba, Tsukuba, Ibaraki 305-8575, Japan; Japan Society for the Promotion of Science (JSPS), Tokyo 102-0083, Japan; Program in Humanics, School of Integrative and Global Majors, University of Tsukuba, Tsukuba, Ibaraki 305-8575, Japan
| | - Ami Kaneko
- International Institute for Integrative Sleep Medicine (WPI-IIIS), University of Tsukuba, Tsukuba, Ibaraki 305-8575, Japan; Program in Humanics, School of Integrative and Global Majors, University of Tsukuba, Tsukuba, Ibaraki 305-8575, Japan
| | - Yu Hayashi
- International Institute for Integrative Sleep Medicine (WPI-IIIS), University of Tsukuba, Tsukuba, Ibaraki 305-8575, Japan; Department of Biological Sciences, Graduate School of Science, The University of Tokyo, Bunkyo-ku, Tokyo 113-0033, Japan.
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Long Z, Li J, Marino M. Brain structural changes underlying clinical symptom improvement following fast-acting treatments in treatment resistant depression. J Affect Disord 2025; 369:52-60. [PMID: 39326585 DOI: 10.1016/j.jad.2024.09.150] [Citation(s) in RCA: 0] [Impact Index Per Article: 0] [Reference Citation Analysis] [Abstract] [Key Words] [MESH Headings] [Track Full Text] [Journal Information] [Submit a Manuscript] [Subscribe] [Scholar Register] [Received: 06/19/2024] [Revised: 09/17/2024] [Accepted: 09/21/2024] [Indexed: 09/28/2024]
Abstract
BACKGROUND Electroconvulsive therapy (ECT), ketamine infusion (KI), and total sleep deprivation (TSD) are effective and fast in treating patients with treatment-resistant depression (TRD). However, it remains unclear whether the three treatments have the same effect on clinical symptom improvement and have common brain structural mechanisms. METHODS The current study included 127 TRD patients and 37 healthy controls, which were obtained from the Perturbation of the Treatment Resistant Depression Connectome Project. We aimed to investigate the shared and distinct brain structural changes underlying clinical symptom improvement among ECT, KI, and TSD treatments. RESULTS All of the three treatments significantly reduced the depressive symptoms in TRD patients, but they differently affected other clinical measurements. Neuroimaging results also revealed that all of ECT, KI, and TSD treatments significantly increased gray matter volume of left caudate after treatment in TRD patients. However, the gray matter volume of other brain regions including hippocampus, parahippocampus, amygdala, insula, fusiform gyrus, several occipital and temporal areas was increased only after ECT treatment. Still, the baseline or the change of gray matter volume did not correlate with the depressive symptom improvement for all of the three treatments. LIMITATIONS A higher sample size would be required to further validate our findings. CONCLUSIONS The results observed in the current study suggested that the ECT, KI, and TSD treatments differently affected clinical measurements and brain structures in TRD patients, though all of them were effective in depressive symptom improvement, which might facilitate the development of personalized treatment protocol for this disease.
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Affiliation(s)
- Zhiliang Long
- Sleep and NeuroImaging Center, Faculty of Psychology, Southwest University, Chongqing, PR China.
| | - Jiao Li
- Clinical Hospital of Chengdu Brain Science Institute, School of Life Science and Technology, University of Electronic Science and Technology of China, Chengdu, PR China; MOE Key Laboratory for Neuroinformation, High-Field Magnetic Resonance Brain Imaging Key Laboratory of Sichuan Province, University of Electronic Science and Technology of China, Chengdu, PR China
| | - Marco Marino
- Department of General Psychology, University of Padua, Italy; Movement Control and Neuroplasticity Research Group, KU Leuven, Leuven, Belgium
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Chai R, Bian WJ. Adolescent sleep and its disruption in depression and anxiety. Front Neurosci 2024; 18:1479420. [PMID: 39575099 PMCID: PMC11578994 DOI: 10.3389/fnins.2024.1479420] [Citation(s) in RCA: 0] [Impact Index Per Article: 0] [Reference Citation Analysis] [Abstract] [Key Words] [Track Full Text] [Journal Information] [Subscribe] [Scholar Register] [Received: 08/12/2024] [Accepted: 10/03/2024] [Indexed: 11/24/2024] Open
Abstract
Adolescence is a pivotal stage during development when one's personality, emotion, and behavioral traits are shaped to a great extent, and the underlying neural circuits undergo substantial developmental organizations. Dramatic and dynamic changes occur in sleep architecture throughout the postnatal developmental course. Insufficient sleep and disruption of sleep/wake coherence are prevalent among the adolescents worldwide, and even so in young patients with neuropsychiatric conditions. Although accumulating evidence has suggested a tight association between sleep disruption and depression/anxiety, the causal relationship remains largely unclear. More importantly, most of these studies focused on adult subjects, and little is known about the role of sleep during the development of mood and behavior. Here we review recent studies investigating the acute and chronic effects of adolescent sleep disruption on depression and anxiety both in humans and rodent models with focuses on the assessment methodology and age. By discussing the findings and unsolved problems, we hope to achieve a better understanding of the relationship between sleep and mental health in adolescents and provide insights for future research.
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Affiliation(s)
- Ruiming Chai
- Westlake Laboratory of Life Sciences and Biomedicine, Hangzhou, China
- School of Life Sciences, Westlake University, Hangzhou, China
- Institute of Biology, Westlake Institute for Advanced Study, Hangzhou, China
| | - Wen-Jie Bian
- Westlake Laboratory of Life Sciences and Biomedicine, Hangzhou, China
- School of Life Sciences, Westlake University, Hangzhou, China
- Institute of Biology, Westlake Institute for Advanced Study, Hangzhou, China
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Gonda X, Tarazi FI, Dome P. The emergence of antidepressant drugs targeting GABA A receptors: A concise review. Biochem Pharmacol 2024; 228:116481. [PMID: 39147329 DOI: 10.1016/j.bcp.2024.116481] [Citation(s) in RCA: 0] [Impact Index Per Article: 0] [Reference Citation Analysis] [Abstract] [Key Words] [MESH Headings] [Track Full Text] [Journal Information] [Subscribe] [Scholar Register] [Received: 05/21/2024] [Revised: 08/06/2024] [Accepted: 08/09/2024] [Indexed: 08/17/2024]
Abstract
Depression is among the most common psychiatric illnesses, which imposes a major socioeconomic burden on patients, caregivers, and the public health system. Treatment with classical antidepressants (e.g. tricyclic antidepressants and selective serotonine reuptake inhibitors), which primarily affect monoaminergic systems has several limitations, such as delayed onset of action and moderate efficacy in a relatively large proportion of depressed patients. Furthermore, depression is highly heterogeneus, and its different subtypes, including post-partum depression, involve distinct neurobiology, warranting a differential approach to pharmacotherapy. Given these shortcomings, the need for novel antidepressants that are superior in efficacy and faster in onset of action is fully justified. The development and market introduction of rapid-acting antidepressants has accelerated in recent years. Some of these new antidepressants act through the GABAergic system. In this review, we discuss the discovery, efficacy, and limitations of treatment with classic antidepressants. We provide a detailed discussion of GABAergic neurotransmission, with a special focus on GABAA receptors, and possible explanations for the mood-enhancing effects of GABAergic medications (in particular neurosteroids acting at GABAA receptors), and, ultimately, we present the most promising molecules belonging to this family which are currently used in clinical practice or are in late phases of clinical development.
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Affiliation(s)
- Xenia Gonda
- Department of Psychiatry and Psychotherapy, Semmelweis University, Budapest, Hungary; NAP3.0-SE Neuropsychopharmacology Research Group, Hungarian Brain Research Program, Semmelweis University, Budapest, Hungary.
| | - Frank I Tarazi
- Department of Psychiatry and Neurology, Harvard Medical School and McLean Hospital, Boston, MA, USA
| | - Peter Dome
- Department of Psychiatry and Psychotherapy, Semmelweis University, Budapest, Hungary; Nyiro Gyula National Institute of Psychiatry and Addictology, Budapest, Hungary
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Mauracher L, Serebriakova J, Niederstätter H, Parson W, Schurr T, Deisenhammer EA. Subclinical hypomanic experiences in young adults after sleep deprivation are independent of depressive disorders, chronotype or 5-HTTLPR polymorphism. World J Biol Psychiatry 2024; 25:384-392. [PMID: 39126213 DOI: 10.1080/15622975.2024.2382697] [Citation(s) in RCA: 0] [Impact Index Per Article: 0] [Reference Citation Analysis] [Abstract] [Key Words] [MESH Headings] [Track Full Text] [Journal Information] [Submit a Manuscript] [Subscribe] [Scholar Register] [Received: 04/29/2024] [Revised: 07/01/2024] [Accepted: 07/17/2024] [Indexed: 08/12/2024]
Abstract
INTRODUCTION The acute antidepressant effect of sleep deprivation (SD) in patients with depressive disorders has been studied for more than 60 years. However, hypomanic mood swings after partial or total SD have also been described in people without diagnosed mental disorders. Studying this phenomenon in the general population may yield insights about the mechanisms of therapeutic SD, mania and bipolar disorders. METHODS A cross-sectional sample of young adults was recruited and classified into those who described having regularly occurring subclinical hypomanic experiences (ROHE) after SD and those who did not. History of psychiatric and physical illness, with screening for depression and mania, as well as alcohol or drug consumption, family history of depressive disorders or suicide, 5-HTTLPR polymorphism, and MEQ-SA chronotype were collected. RESULTS A total of 251 participants were included; 39.0% indicated regularly having subclinical hypomanic experiences after SD. These experiences were not associated with depressive or mania screening, history of psychiatric illness, family history, 5-HTTLPR polymorphism, or MEQ-SA chronotype. CONCLUSIONS ROHE after non-therapeutic SD seem to be a relatively common phenomenon in young adults, independent of depressive mood state. Our results suggest that therapeutic SD may depend on a physiological phenomenon of subclinical affective disturbance after SD that affects a part of the general population, independent of psychiatric diagnosis. Further studies could elucidate associated factors and contribute to our understanding of (hypo-)manic mood states.
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Affiliation(s)
- Laurin Mauracher
- University Hospital for Psychiatry I, Medical University of Innsbruck, Innsbruck, Austria
| | - Jana Serebriakova
- University Hospital for Psychiatry I, Medical University of Innsbruck, Innsbruck, Austria
| | - Harald Niederstätter
- Institute of Forensic Medicine, Medical University of Innsbruck, Innsbruck, Austria
| | - Walther Parson
- Institute of Forensic Medicine, Medical University of Innsbruck, Innsbruck, Austria
| | - Timo Schurr
- University Hospital for Psychiatry I, Medical University of Innsbruck, Innsbruck, Austria
| | - Eberhard A Deisenhammer
- University Hospital for Psychiatry I, Medical University of Innsbruck, Innsbruck, Austria
- University Hospital for Psychiatry II, Medical University of Innsbruck, Innsbruck, Austria
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Palatine E, Phillips ML, Soehner AM. The effect of slow wave sleep deprivation on mood in adolescents with depressive symptoms: A pilot study. J Affect Disord 2024; 354:347-355. [PMID: 38479512 DOI: 10.1016/j.jad.2024.03.058] [Citation(s) in RCA: 0] [Impact Index Per Article: 0] [Reference Citation Analysis] [Abstract] [Key Words] [MESH Headings] [Track Full Text] [Journal Information] [Submit a Manuscript] [Subscribe] [Scholar Register] [Received: 11/17/2023] [Revised: 02/13/2024] [Accepted: 03/09/2024] [Indexed: 03/23/2024]
Abstract
BACKGROUND There is an urgent need for safe, rapid-acting treatment strategies for adolescent depression. In depressed adults, slow wave sleep deprivation (SWSD) improved next-day mood without disrupting sleep duration, but SWSD has not been tested in adolescents. In a pilot study, the aim was to assess the effect of SWSD on sleep physiology and mood outcomes (depression, rumination, anhedonia) among adolescents with depressive symptoms. METHODS Sixteen adolescents (17.44 ± 1.46 yr, 12 female) completed three nights of polysomnographic sleep recording: Baseline, SWSD, and Recovery nights. Acoustic stimulation (tones of random pitch, duration, and volume) suppressed slow wave sleep (SWS) in real-time during SWSD. After each night, depression, rumination, and anhedonia severity were assessed. RESULTS SWSD successfully suppressed SWS, increased N2, and had minimal impact on Rapid Eye Movement (REM), nocturnal awakenings, and total sleep time. While SWSD did not improve depression or anhedonia severity overall, lower baseline non-REM alpha activity and greater SWS rebound during recovery sleep correlated with SWSD-related reduction in clinician-rated depression severity. Next-day rumination severity decreased after SWSD, with sustained improvements following recovery sleep. However, rumination improvement was not associated with SWS suppression, but rather reduction in total sleep time and REM in exploratory correlation models. LIMITATIONS Small sample size and large proportion of females. CONCLUSION SWSD did not improve depression in adolescents overall but a subset with low non-REM alpha activity and intact homeostatic sleep regulation may benefit from this approach. Findings from this pilot study also suggest that partial sleep deprivation may be a beneficial therapeutic strategy for rumination in adolescents.
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Affiliation(s)
- Elise Palatine
- Department of Psychiatry, University of Pittsburgh School of Medicine, Pittsburgh, PA, USA
| | - Mary L Phillips
- Department of Psychiatry, University of Pittsburgh School of Medicine, Pittsburgh, PA, USA
| | - Adriane M Soehner
- Department of Psychiatry, University of Pittsburgh School of Medicine, Pittsburgh, PA, USA.
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11
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Cao Q, Wang Y, Ji Y, He Z, Lei X. Resting-State EEG Reveals Abnormal Microstate Characteristics of Depression with Insomnia. Brain Topogr 2024; 37:388-396. [PMID: 36892651 DOI: 10.1007/s10548-023-00949-w] [Citation(s) in RCA: 1] [Impact Index Per Article: 1.0] [Reference Citation Analysis] [Abstract] [Key Words] [MESH Headings] [Grants] [Track Full Text] [Journal Information] [Subscribe] [Scholar Register] [Received: 09/22/2022] [Accepted: 02/16/2023] [Indexed: 03/10/2023]
Abstract
Previous research revealed various aspects of resting-state EEG for depression and insomnia. However, the EEG characteristics of depressed subjects with insomnia are rarely studied, especially EEG microstates that capture the dynamic activities of the large-scale brain network. To fill these research gaps, the present study collected resting-state EEG data from 32 subclinical depression subjects with insomnia (SDI), 31 subclinical depression subjects without insomnia (SD), and 32 healthy controls (HCs). Four topographic maps were generated from clean EEG data after clustering and rearrangement. Temporal characteristics were obtained for statistical analysis, including cross-group variance analysis (ANOVA) and intra-group correlation analysis. In our study, the global clustering of all individuals in the EEG microstate analysis revealed the four previously discovered categories of microstates (A, B, C, and D). The occurrence of microstate B was lower in SDI than in SD and HC subjects. The correlation analysis showed that the total Pittsburgh Sleep Quality Index (PSQI) score negatively correlated with the occurrence of microstate C in SDI (r = - 0.415, p < 0.05). Conversely, there was a positive correlation between Self-rating Depression Scale (SDS) scores and the duration of microstate C in SD (r = 0.359, p < 0.05). These results indicate that microstates reflect altered large-scale brain network dynamics in subclinical populations. Abnormalities in the visual network corresponding to microstate B are an electrophysiological characteristic of subclinical individuals with symptoms of depressive insomnia. Further investigation is needed for microstate changes related to high arousal and emotional problems in people suffering from depression and insomnia.
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Affiliation(s)
- Qike Cao
- Sleep and NeuroImaging Center, Faculty of Psychology, Southwest University, Chongqing, 400715, China
- Key Laboratory of Cognition and Personality (Southwest University), Ministry of Education, Chongqing, 400715, China
| | - Yulin Wang
- Sleep and NeuroImaging Center, Faculty of Psychology, Southwest University, Chongqing, 400715, China
- Key Laboratory of Cognition and Personality (Southwest University), Ministry of Education, Chongqing, 400715, China
| | - Yufang Ji
- Sleep and NeuroImaging Center, Faculty of Psychology, Southwest University, Chongqing, 400715, China
- Key Laboratory of Cognition and Personality (Southwest University), Ministry of Education, Chongqing, 400715, China
| | - Zhihui He
- The Ninth People's Hospital of Chongqing, Chongqing, 400700, China
| | - Xu Lei
- Sleep and NeuroImaging Center, Faculty of Psychology, Southwest University, Chongqing, 400715, China.
- Key Laboratory of Cognition and Personality (Southwest University), Ministry of Education, Chongqing, 400715, China.
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12
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Sochal M, Ditmer M, Binienda A, Tarasiuk A, Białasiewicz P, Turkiewicz S, Karuga FF, Jakub F, Gabryelska A. Interactions between neurotrophins, mood, and physical activity under the conditions of sleep deprivation. Transl Psychiatry 2024; 14:158. [PMID: 38519465 PMCID: PMC10960007 DOI: 10.1038/s41398-024-02871-6] [Citation(s) in RCA: 0] [Impact Index Per Article: 0] [Reference Citation Analysis] [Abstract] [Key Words] [MESH Headings] [Track Full Text] [Journal Information] [Submit a Manuscript] [Subscribe] [Scholar Register] [Received: 12/24/2023] [Revised: 03/06/2024] [Accepted: 03/11/2024] [Indexed: 03/25/2024] Open
Abstract
Sleep deprivation (DS) is the forced elimination of sleep. While brain-derived neurotrophic factor (BDNF) has been extensively studied in the context of in mood changes following DS, the role of other neurotrophins remains elusive. This study explores the impact of DS on BDNF, glial cell line-derived neurotrophic factor (GDNF), neurotrophin-3 (NT3), and neurotrophin-4 (NT4) at mRNA and protein level, considering their potential links to mood disturbances. The study involved 81 participants subjected to polysomnography (PSG) and DS. Blood samples, mood assessments, and actigraphy data were collected twice, after PSG and DS. NT mRNA expression and serum protein concentrations of BDNF, GDNF, NT3, and NT4 were measured. Participants were divided into Responders and Non-Responders based on mood improvement after DS. DS reduced BDNF mRNA expression in all participants, with no change in serum BDNF protein. GDNF protein decreased in Non-Responders, while Responders exhibited reduced GDNF mRNA. NT3 protein increased in both groups, while NT3 mRNA decreased in Respondents. NT4 protein rose universally post-DS, but NT4 mRNA remained unchanged. Physical activity (PA) negatively correlated with mRNA expression of BDNF, GDNF, and NT3 post-DS. The study's short DS duration and exclusion of immature NT forms limit comprehensive insights. GDNF, together with NT3, might play an important role in mood response to DS. PA during DS seems to impair the mRNA expression of NTs in leukocytes. Future studies on the subject of sleep deprivation might consider investigating the relationship between BDNF and NT4 in the context of their apparent redundancy.
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Affiliation(s)
- Marcin Sochal
- Department of Sleep Medicine and Metabolic Disorders, Medical University of Lodz, Lodz, Poland.
| | - Marta Ditmer
- Department of Sleep Medicine and Metabolic Disorders, Medical University of Lodz, Lodz, Poland
| | - Agata Binienda
- Department of Biochemistry, Medical University of Lodz, Lodz, Poland
| | | | - Piotr Białasiewicz
- Department of Sleep Medicine and Metabolic Disorders, Medical University of Lodz, Lodz, Poland
| | - Szymon Turkiewicz
- Department of Sleep Medicine and Metabolic Disorders, Medical University of Lodz, Lodz, Poland
| | - Filip Franciszek Karuga
- Department of Sleep Medicine and Metabolic Disorders, Medical University of Lodz, Lodz, Poland
| | - Fichna Jakub
- Department of Biochemistry, Medical University of Lodz, Lodz, Poland
| | - Agata Gabryelska
- Department of Sleep Medicine and Metabolic Disorders, Medical University of Lodz, Lodz, Poland
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13
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Benasi G, Cheng B, Aggarwal B, St-Onge MP. The effects of sustained mild sleep restriction on stress and distress among healthy adults: Findings from two randomized crossover studies. Sleep Med 2024; 115:83-87. [PMID: 38342031 PMCID: PMC10932935 DOI: 10.1016/j.sleep.2024.02.001] [Citation(s) in RCA: 0] [Impact Index Per Article: 0] [Reference Citation Analysis] [Abstract] [Key Words] [MESH Headings] [Grants] [Track Full Text] [Journal Information] [Submit a Manuscript] [Subscribe] [Scholar Register] [Received: 09/14/2023] [Revised: 01/26/2024] [Accepted: 02/01/2024] [Indexed: 02/13/2024]
Abstract
OBJECTIVE/BACKGROUND Experimental studies suggest that sleep loss affects psychological outcomes. However, most studies focus on acute severe in-laboratory sleep restriction, with limited ecological validity. This study examines the impact of sustained mild sleep restriction (SR) on stress and distress among healthy adults in a naturalistic home environment. PATIENTS/METHODS We analyzed data from two randomized crossover studies. Individuals who regularly slept 7-9 h/night completed two 6-wk intervention phases separated by a 6-wk washout: habitual sleep (HS: maintenance of habitual bed and wake times) and SR (delayed bedtime by 1.5 h/night and maintenance of habitual wake time). Adherence to sleep duration requirements was verified with wrist actigraphy and daily sleep diaries during each intervention phase. Measures of perceived stress, subjective anxiety, subjective depression, rumination, and cortisol were collected at baseline and endpoint of each intervention phase. RESULTS Sixty-two participants (age 36.4 ± 14.0 y, 85.5 % women, 63.3 % racial/ethnic minority) were included in our analyses. Mean total sleep time was 7.4 ± 0.4 h/night during HS and 6.2 ± 0.4 h/night during SR (p < 0.001). Higher perceived stress (3.6 ± 1.0, p = 0.0007) and subjective anxiety (1.1 ± 0.5, p = 0.039) were observed after SR compared to HS. No effect of sleep condition was observed on subjective depression, rumination, and cortisol. CONCLUSIONS Our findings suggest that prolonged mildly insufficient sleep, similar to what commonly experienced in the real world, can lead to increased perceived stress and subjective anxiety in healthy adults. Addressing sleep loss, even if mild, should be a key component of interventions aimed at promoting mental health in the general population.
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Affiliation(s)
- Giada Benasi
- Division of General Medicine, Department of Medicine, Columbia University Irving Medical Center, New York, NY, USA.
| | - Bin Cheng
- Department of Biostatistics, Mailman School of Public Health, Columbia University Irving Medical Center, New York, NY, USA
| | - Brooke Aggarwal
- Division of Cardiology, Department of Medicine, Columbia University Irving Medical Center, New York, NY, USA; Center of Excellence for Sleep & Circadian Research, Department of Medicine, Columbia University Irving Medical Center, New York, NY, USA
| | - Marie-Pierre St-Onge
- Division of General Medicine, Department of Medicine, Columbia University Irving Medical Center, New York, NY, USA; Center of Excellence for Sleep & Circadian Research, Department of Medicine, Columbia University Irving Medical Center, New York, NY, USA
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14
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Meyer N, Lok R, Schmidt C, Kyle SD, McClung CA, Cajochen C, Scheer FAJL, Jones MW, Chellappa SL. The sleep-circadian interface: A window into mental disorders. Proc Natl Acad Sci U S A 2024; 121:e2214756121. [PMID: 38394243 PMCID: PMC10907245 DOI: 10.1073/pnas.2214756121] [Citation(s) in RCA: 21] [Impact Index Per Article: 21.0] [Reference Citation Analysis] [Abstract] [Key Words] [MESH Headings] [Grants] [Track Full Text] [Journal Information] [Subscribe] [Scholar Register] [Indexed: 02/25/2024] Open
Abstract
Sleep, circadian rhythms, and mental health are reciprocally interlinked. Disruption to the quality, continuity, and timing of sleep can precipitate or exacerbate psychiatric symptoms in susceptible individuals, while treatments that target sleep-circadian disturbances can alleviate psychopathology. Conversely, psychiatric symptoms can reciprocally exacerbate poor sleep and disrupt clock-controlled processes. Despite progress in elucidating underlying mechanisms, a cohesive approach that integrates the dynamic interactions between psychiatric disorder with both sleep and circadian processes is lacking. This review synthesizes recent evidence for sleep-circadian dysfunction as a transdiagnostic contributor to a range of psychiatric disorders, with an emphasis on biological mechanisms. We highlight observations from adolescent and young adults, who are at greatest risk of developing mental disorders, and for whom early detection and intervention promise the greatest benefit. In particular, we aim to a) integrate sleep and circadian factors implicated in the pathophysiology and treatment of mood, anxiety, and psychosis spectrum disorders, with a transdiagnostic perspective; b) highlight the need to reframe existing knowledge and adopt an integrated approach which recognizes the interaction between sleep and circadian factors; and c) identify important gaps and opportunities for further research.
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Affiliation(s)
- Nicholas Meyer
- Insomnia and Behavioural Sleep Medicine Clinic, University College London Hospitals NHS Foundation Trust, LondonWC1N 3HR, United Kingdom
- Department of Psychosis Studies, Institute of Psychology, Psychiatry, and Neuroscience, King’s College London, LondonSE5 8AF, United Kingdom
| | - Renske Lok
- Department of Psychiatry and Behavioral Sciences, Stanford University, Stanford, CA94305
| | - Christina Schmidt
- Sleep & Chronobiology Group, GIGA-Institute, CRC-In Vivo Imaging Unit, University of Liège, Liège, Belgium
- Psychology and Neuroscience of Cognition Research Unit, Faculty of Psychology, Speech and Language, University of Liège, Liège4000, Belgium
| | - Simon D. Kyle
- Sir Jules Thorn Sleep and Circadian Neuroscience Institute, Nuffield Department of Clinical Neurosciences, University of Oxford, OxfordOX1 3QU, United Kingdom
| | - Colleen A. McClung
- Translational Neuroscience Program, Department of Psychiatry, University of Pittsburgh School of Medicine, Pittsburgh, PA15219
| | - Christian Cajochen
- Centre for Chronobiology, Department for Adult Psychiatry, Psychiatric Hospital of the University of Basel, BaselCH-4002, Switzerland
- Research Cluster Molecular and Cognitive Neurosciences, Department of Biomedicine, University of Basel, BaselCH-4055, Switzerland
| | - Frank A. J. L. Scheer
- Medical Chronobiology Program, Division of Sleep and Circadian Disorders, Department of Medicine, Brigham and Women’s Hospital, Boston, MA02115
- Medical Chronobiology Program, Division of Sleep and Circadian Disorders, Department of Neurology, Brigham and Women’s Hospital, Boston, MA02115
- Division of Sleep Medicine, Harvard Medical School, Boston, MA02115
| | - Matthew W. Jones
- School of Physiology, Pharmacology and Neuroscience, Faculty of Health and Life Sciences, University of Bristol, BristolBS8 1TD, United Kingdom
| | - Sarah L. Chellappa
- School of Psychology, Faculty of Environmental and Life Sciences, University of Southampton, SouthamptonSO17 1BJ, United Kingdom
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15
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Sulaman BA, Kudlak T, Eban-Rothschild A. Dopamine's reach: Unlocked by sleep loss. Neuron 2024; 112:4-6. [PMID: 38176390 DOI: 10.1016/j.neuron.2023.11.015] [Citation(s) in RCA: 0] [Impact Index Per Article: 0] [Reference Citation Analysis] [Abstract] [MESH Headings] [Grants] [Track Full Text] [Journal Information] [Subscribe] [Scholar Register] [Received: 11/09/2023] [Revised: 11/14/2023] [Accepted: 11/15/2023] [Indexed: 01/06/2024]
Abstract
In this issue of Neuron, Wu et al.1 employ cutting-edge techniques to provide a mechanistic understanding of how sleep deprivation induces an altered affective state. They reveal a key function for dopaminergic signaling, and the formation of cortical spines, in this process.
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Affiliation(s)
- Bibi Alika Sulaman
- Department of Psychology, University of Michigan, Ann Arbor, MI 48109, USA; Neuroscience Graduate Program, University of Michigan, Ann Arbor, MI 48109, USA
| | - Tyler Kudlak
- Department of Psychology, University of Michigan, Ann Arbor, MI 48109, USA
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16
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Sochal M, Ditmer M, Białasiewicz P, Turkiewicz S, Karuga FF, Gabryelska A. Evaluation of cognitive and psychomotor faculties in relation to mood-related symptoms under the conditions of sleep deprivation. Front Psychiatry 2023; 14:1332831. [PMID: 38188046 PMCID: PMC10770828 DOI: 10.3389/fpsyt.2023.1332831] [Citation(s) in RCA: 0] [Impact Index Per Article: 0] [Reference Citation Analysis] [Abstract] [Key Words] [Track Full Text] [Figures] [Journal Information] [Submit a Manuscript] [Subscribe] [Scholar Register] [Received: 11/08/2023] [Accepted: 12/06/2023] [Indexed: 01/09/2024] Open
Abstract
Introduction Deprivation of sleep (DS) has been associated with changes in mood and cognitive function, rapidly but transiently improving the severity of depression symptoms. However, it remains unclear whether there are differences in performance between DS responders and non-responders. The relationship between DS, mood, cognitive, and psychomotor function is also poorly understood. Methods Participants (n = 77) underwent a baseline assessment of sleep under the control of polysomnography (PSG). Later they were subjected to DS with actigraphy monitoring. Evaluation of mood as well as completing a battery of tests assessing cognitive functions and eye-hand coordination was conducted four times, pre/post PSG and DS. Participants were further divided into respondents (RE, n = 48) and non-respondents (NR, n = 29) depending on alleviation of depression symptoms severity following DS. Results All participants exhibited increased response speed to visual triggers after DS compared to baseline (p = 0.024). Psychomotor vigilance test (PVT) results remained intact in the RE, whereas it was increased in the NR (p = 0.008). Exposure time in the eye-hand coordination test improved in both groups, but total error duration was reduced only in RE individuals (p < 0.001, p = 0.009 for RE and NR, respectively). All subjects were more proficient at trail-making test (p ≤ 0.001 for Part 1 and 2 in all, NR, RE). Stroop test also improved regardless of mood changes after DS (p = 0.007, p = 0.008 for Part 1 and 2, respectively); cognitive interference remained at a similar level within groups (p = 0.059, p = 0.057 for NR and RE, respectively). A positive correlation was observed between the difference in PSG morning/DS morning depression severity and vigilance (R = 0.37, p = 0.001, R = 0.33, p = 0.005, for error duration eye-hand coordination test and PVT total average score, respectively). Conclusion RE tend to maintain or improve cognitive function after DS, oppositely to NR. Vigilance in particular might be tightly associated with changes in depression symptoms after DS. Future studies should examine the biological basis behind the response to sleep loss.
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Affiliation(s)
- Marcin Sochal
- Department of Sleep Medicine and Metabolic Disorders, Medical University of Lodz, Lodz, Poland
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17
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Fernandez FX, Perlis ML. Animal models of human insomnia. J Sleep Res 2023; 32:e13845. [PMID: 36748845 PMCID: PMC10404637 DOI: 10.1111/jsr.13845] [Citation(s) in RCA: 6] [Impact Index Per Article: 3.0] [Reference Citation Analysis] [Abstract] [Key Words] [MESH Headings] [Grants] [Track Full Text] [Journal Information] [Subscribe] [Scholar Register] [Received: 12/16/2022] [Accepted: 01/20/2023] [Indexed: 02/08/2023]
Abstract
Insomnia disorder (chronic sleep continuity disturbance) is a debilitating condition affecting 5%-10% of the adult population worldwide. To date, researchers have attempted to model insomnia in animals through breeding strategies that create pathologically short-sleeping individuals or with drugs and environmental contexts that directly impose sleeplessness. While these approaches have been invaluable for identifying insomnia susceptibility genes and mapping the neural networks that underpin sleep-wake regulation, they fail to capture concurrently several of the core clinical diagnostic features of insomnia disorder in humans, where sleep continuity disturbance is self-perpetuating, occurs despite adequate sleep opportunity, and is often not accompanied by significant changes in sleep duration or architecture. In the present review, we discuss these issues and then outline ways animal models can be used to develop approaches that are more ecologically valid in their recapitulation of chronic insomnia's natural aetiology and pathophysiology. Conditioning of self-generated sleep loss with these methods promises to create a better understanding of the neuroadaptations that maintain insomnia, including potentially within the infralimbic cortex, a substrate at the crossroads of threat habituation and sleep.
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Affiliation(s)
| | - Michael L. Perlis
- Department of Psychiatry, University of Pennsylvania, Philadelphia, PA 19104, USA
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18
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Abdelhack M, Zhukovsky P, Milic M, Harita S, Wainberg M, Tripathy SJ, Griffiths JD, Hill SL, Felsky D. Opposing brain signatures of sleep in task-based and resting-state conditions. Nat Commun 2023; 14:7927. [PMID: 38040769 PMCID: PMC10692207 DOI: 10.1038/s41467-023-43737-7] [Citation(s) in RCA: 0] [Impact Index Per Article: 0] [Reference Citation Analysis] [Abstract] [Key Words] [MESH Headings] [Grants] [Track Full Text] [Journal Information] [Subscribe] [Scholar Register] [Received: 06/23/2023] [Accepted: 11/17/2023] [Indexed: 12/03/2023] Open
Abstract
Sleep and depression have a complex, bidirectional relationship, with sleep-associated alterations in brain dynamics and structure impacting a range of symptoms and cognitive abilities. Previous work describing these relationships has provided an incomplete picture by investigating only one or two types of sleep measures, depression, or neuroimaging modalities in parallel. We analyze the correlations between brainwide neural signatures of sleep, cognition, and depression in task and resting-state data from over 30,000 individuals from the UK Biobank and Human Connectome Project. Neural signatures of insomnia and depression are negatively correlated with those of sleep duration measured by accelerometer in the task condition but positively correlated in the resting-state condition. Our results show that resting-state neural signatures of insomnia and depression resemble that of rested wakefulness. This is further supported by our finding of hypoconnectivity in task but hyperconnectivity in resting-state data in association with insomnia and depression. These observations dispute conventional assumptions about the neurofunctional manifestations of hyper- and hypo-somnia, and may explain inconsistent findings in the literature.
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Affiliation(s)
- Mohamed Abdelhack
- Krembil Centre for Neuroinformatics, Centre for Addiction and Mental Health, Toronto, ON, Canada
| | - Peter Zhukovsky
- Campbell Family Mental Health Research Institute, Centre for Addiction and Mental Health, Toronto, ON, Canada
- Center for Depression, Anxiety and Stress Research, McLean Hospital, Boston, MA, USA
| | - Milos Milic
- Krembil Centre for Neuroinformatics, Centre for Addiction and Mental Health, Toronto, ON, Canada
| | - Shreyas Harita
- Krembil Centre for Neuroinformatics, Centre for Addiction and Mental Health, Toronto, ON, Canada
- Department of Physiology, Temerty Faculty of Medicine, University of Toronto, Toronto, ON, Canada
| | - Michael Wainberg
- Krembil Centre for Neuroinformatics, Centre for Addiction and Mental Health, Toronto, ON, Canada
- Department of Psychiatry, Temerty Faculty of Medicine, University of Toronto, Toronto, ON, Canada
- Institute of Medical Science, University of Toronto, Toronto, ON, Canada
- Prosserman Centre for Population Health Research, Lunenfeld-Tanenbaum Research Institute, Sinai Health, Toronto, ON, Canada
| | - Shreejoy J Tripathy
- Krembil Centre for Neuroinformatics, Centre for Addiction and Mental Health, Toronto, ON, Canada
- Campbell Family Mental Health Research Institute, Centre for Addiction and Mental Health, Toronto, ON, Canada
- Department of Physiology, Temerty Faculty of Medicine, University of Toronto, Toronto, ON, Canada
- Department of Psychiatry, Temerty Faculty of Medicine, University of Toronto, Toronto, ON, Canada
- Institute of Medical Science, University of Toronto, Toronto, ON, Canada
| | - John D Griffiths
- Krembil Centre for Neuroinformatics, Centre for Addiction and Mental Health, Toronto, ON, Canada
- Campbell Family Mental Health Research Institute, Centre for Addiction and Mental Health, Toronto, ON, Canada
- Department of Physiology, Temerty Faculty of Medicine, University of Toronto, Toronto, ON, Canada
- Institute of Medical Science, University of Toronto, Toronto, ON, Canada
| | - Sean L Hill
- Krembil Centre for Neuroinformatics, Centre for Addiction and Mental Health, Toronto, ON, Canada
- Campbell Family Mental Health Research Institute, Centre for Addiction and Mental Health, Toronto, ON, Canada
- Department of Physiology, Temerty Faculty of Medicine, University of Toronto, Toronto, ON, Canada
- Department of Psychiatry, Temerty Faculty of Medicine, University of Toronto, Toronto, ON, Canada
- Institute of Medical Science, University of Toronto, Toronto, ON, Canada
- Vector Institute for Artificial Intelligence, Toronto, ON, Canada
| | - Daniel Felsky
- Krembil Centre for Neuroinformatics, Centre for Addiction and Mental Health, Toronto, ON, Canada.
- Department of Physiology, Temerty Faculty of Medicine, University of Toronto, Toronto, ON, Canada.
- Institute of Medical Science, University of Toronto, Toronto, ON, Canada.
- Department of Biostatistics, Dalla Lana School of Public Health, University of Toronto, Toronto, ON, Canada.
- Rotman Research Institute, Baycrest Hospital, Toronto, ON, Canada.
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Goldschmied JR, Boland E, Palermo E, Barilla H, Dinges DF, Detre JA, Basner M, Sheline YI, Rao H, Gehrman P. Antidepressant effects of acute sleep deprivation are reduced in highly controlled environments. J Affect Disord 2023; 340:412-419. [PMID: 37553017 PMCID: PMC10528033 DOI: 10.1016/j.jad.2023.07.116] [Citation(s) in RCA: 0] [Impact Index Per Article: 0] [Reference Citation Analysis] [Abstract] [Key Words] [MESH Headings] [Grants] [Track Full Text] [Journal Information] [Submit a Manuscript] [Subscribe] [Scholar Register] [Received: 04/18/2023] [Revised: 07/23/2023] [Accepted: 07/31/2023] [Indexed: 08/10/2023]
Abstract
BACKGROUND Numerous studies summarized in a recent meta-analysis have shown sleep deprivation rapidly improves depressive symptoms in approximately 50 % of individuals with major depressive disorder (MDD), however those studies were typically conducted in clinical settings. Here we investigated the effects of sleep deprivation utilizing a highly controlled experimental approach. METHODS 36 antidepressant-free individuals with MDD and 10 healthy controls (HC) completed a 5 day/4-night protocol consisting of adaptation, baseline, total sleep deprivation (TSD), and recovery phases. Light was kept consistently dim (≤50 lx), meals were regulated, and activity was restricted. In-the-moment mood was assessed using a modified Hamilton Rating Scale for Depression (HRSD) at screening and each morning following the experimental nights. RESULTS Day of study had a significant effect on mood in both groups. Post-hoc analyses revealed that significant effects were attributed to mood improvement in the MDD group following study initiation prior to beginning TSD, and in the HC group following recovery sleep, but were not due to mood improvement in the MDD group during TSD. No further improvement in mood occurred during 36 h of TSD. LIMITATIONS Strict eligibility requirements may limit generalizability. The requirement to be medication free may have biased toward a less severely depressed sample. CONCLUSIONS Results revealed that individuals with moderate MDD can experience a significant reduction in depressive symptoms upon entering a highly controlled laboratory environment. Environmental effects on mood can be substantial and need to be considered.
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Affiliation(s)
- Jennifer R Goldschmied
- Department of Psychiatry, University of Pennsylvania, 3535 Market St., Philadelphia, PA 19104, United States.
| | - Elaine Boland
- Department of Psychiatry, University of Pennsylvania, 3535 Market St., Philadelphia, PA 19104, United States; Behavioral Health Service, Cpl. Michael J. Crescenz VA Medical Center, 3900 Woodland Ave., Philadelphia, PA 19104, United States.
| | - Emma Palermo
- Department of Psychiatry, Massachusetts General Hospital, 55 Fruit St., Boston, MA 02114, United States.
| | - Holly Barilla
- Department of Psychiatry, University of Pennsylvania, 3535 Market St., Philadelphia, PA 19104, United States.
| | - David F Dinges
- Department of Psychiatry, University of Pennsylvania, 3535 Market St., Philadelphia, PA 19104, United States.
| | - John A Detre
- Department of Neurology, University of Pennsylvania, 3400 Spruce St., Philadelphia, PA 19104, United States.
| | - Mathias Basner
- Department of Psychiatry, University of Pennsylvania, 3535 Market St., Philadelphia, PA 19104, United States.
| | - Yvette I Sheline
- Department of Psychiatry, University of Pennsylvania, 3535 Market St., Philadelphia, PA 19104, United States.
| | - Hengyi Rao
- Department of Neurology, University of Pennsylvania, 3400 Spruce St., Philadelphia, PA 19104, United States.
| | - Philip Gehrman
- Department of Psychiatry, University of Pennsylvania, 3535 Market St., Philadelphia, PA 19104, United States; Behavioral Health Service, Cpl. Michael J. Crescenz VA Medical Center, 3900 Woodland Ave., Philadelphia, PA 19104, United States.
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20
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Shi S, Zhang M, Xie W, Ju P, Chen N, Wang F, Lyu D, Wang M, Hong W. Sleep deprivation alleviates depression-like behaviors in mice via inhibiting immune and inflammatory pathways and improving neuroplasticity. J Affect Disord 2023; 340:100-112. [PMID: 37543111 DOI: 10.1016/j.jad.2023.07.119] [Citation(s) in RCA: 7] [Impact Index Per Article: 3.5] [Reference Citation Analysis] [Abstract] [Key Words] [MESH Headings] [Track Full Text] [Journal Information] [Submit a Manuscript] [Subscribe] [Scholar Register] [Received: 04/21/2023] [Revised: 07/27/2023] [Accepted: 07/31/2023] [Indexed: 08/07/2023]
Abstract
BACKGROUND Sleep deprivation (SD) has been suggested to have a rapid antidepressant effect. There is substantial evidence that neuroinflammation and neuroplasticity play critical roles in the pathophysiology and treatment of depression. Here, we investigated the mechanisms of SD to alleviate depression-like behaviors of mice, and the role of neuroinflammation and neuroplasticity in it. METHODS Adult male C57BL/6 J mice were subjected to chronic restraint stress (CRS) for 6 weeks, and 6 h of SD were administrated. Behavioral tests were performed to measure depression-like behaviors. RNA-sequencing and bioinformatic analysis were performed in the anterior cingulate cortex (ACC). The differentially expressed genes were confirmed by quantitative real-time polymerase chain reaction (RT-qPCR). Neuroinflammation and neuroplasticity were measured by western blotting and immunofluorescence staining. RESULTS Behavioral tests demonstrated that SD swiftly attenuated the depression-like behaviors induced by CRS. RNA-sequencing identified the upregulated immune and inflammatory pathways after CRS exposure were downregulated by SD. Furthermore, SD reversed the levels of immune and inflammation-related mRNA, pro-inflammatory factors and microglia activation in ACC. Additionally, the impaired neuroplasticity elicited by CRS in the prefrontal cortex (PFC) and ACC were improved by SD. LIMITATIONS More in-depth studies are required to determine the role of different SD protocols in depressive symptoms and their underlying mechanisms. CONCLUSIONS Our study revealed the rapid antidepressant effect of SD on CRS mice through the reduction of the neuroinflammatory response in ACC and the improvement of neuroplasticity in PFC and ACC, providing a theoretical basis for the clinical application of SD as a rapid antidepressant treatment.
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Affiliation(s)
- Shuxiang Shi
- Shanghai Mental Health Center, Shanghai Jiao Tong University School of Medicine, Shanghai 200030, China; Shanghai Key Laboratory of Psychotic Disorders, Shanghai 201108, China
| | - Mengke Zhang
- Shanghai Mental Health Center, Shanghai Jiao Tong University School of Medicine, Shanghai 200030, China; Shanghai Key Laboratory of Psychotic Disorders, Shanghai 201108, China
| | - Weijie Xie
- Shanghai Mental Health Center, Shanghai Jiao Tong University School of Medicine, Shanghai 200030, China; Shanghai Key Laboratory of Psychotic Disorders, Shanghai 201108, China
| | - Peijun Ju
- Shanghai Mental Health Center, Shanghai Jiao Tong University School of Medicine, Shanghai 200030, China; Shanghai Key Laboratory of Psychotic Disorders, Shanghai 201108, China
| | - Ningning Chen
- Shanghai Mental Health Center, Shanghai Jiao Tong University School of Medicine, Shanghai 200030, China; Shanghai Key Laboratory of Psychotic Disorders, Shanghai 201108, China
| | - Fan Wang
- Shanghai Mental Health Center, Shanghai Jiao Tong University School of Medicine, Shanghai 200030, China; Shanghai Key Laboratory of Psychotic Disorders, Shanghai 201108, China
| | - Dongbin Lyu
- Shanghai Mental Health Center, Shanghai Jiao Tong University School of Medicine, Shanghai 200030, China; Shanghai Key Laboratory of Psychotic Disorders, Shanghai 201108, China
| | - Meiti Wang
- Shanghai Mental Health Center, Shanghai Jiao Tong University School of Medicine, Shanghai 200030, China; Shanghai Key Laboratory of Psychotic Disorders, Shanghai 201108, China.
| | - Wu Hong
- Shanghai Mental Health Center, Shanghai Jiao Tong University School of Medicine, Shanghai 200030, China; Shanghai Key Laboratory of Psychotic Disorders, Shanghai 201108, China; Mental Health Branch, China Hospital Development Institute, Shanghai Jiao Tong University, Shanghai 200030, China.
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21
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Chai Y, Sheline YI, Oathes DJ, Balderston NL, Rao H, Yu M. Functional connectomics in depression: insights into therapies. Trends Cogn Sci 2023; 27:814-832. [PMID: 37286432 PMCID: PMC10476530 DOI: 10.1016/j.tics.2023.05.006] [Citation(s) in RCA: 29] [Impact Index Per Article: 14.5] [Reference Citation Analysis] [Abstract] [Key Words] [MESH Headings] [Grants] [Track Full Text] [Journal Information] [Subscribe] [Scholar Register] [Received: 11/29/2022] [Revised: 05/09/2023] [Accepted: 05/09/2023] [Indexed: 06/09/2023]
Abstract
Depression is a common mental disorder characterized by heterogeneous cognitive and behavioral symptoms. The emerging research paradigm of functional connectomics has provided a quantitative theoretical framework and analytic tools for parsing variations in the organization and function of brain networks in depression. In this review, we first discuss recent progress in depression-associated functional connectome variations. We then discuss treatment-specific brain network outcomes in depression and propose a hypothetical model highlighting the advantages and uniqueness of each treatment in relation to the modulation of specific brain network connectivity and symptoms of depression. Finally, we look to the future promise of combining multiple treatment types in clinical practice, using multisite datasets and multimodal neuroimaging approaches, and identifying biological depression subtypes.
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Affiliation(s)
- Ya Chai
- Key Laboratory of Brain-Machine Intelligence for Information Behavior (Ministry of Education and Shanghai), School of Business and Management, Shanghai International Studies University, Shanghai, China; Center for Functional Neuroimaging, Perelman School of Medicine, University of Pennsylvania, Philadelphia, PA, USA
| | - Yvette I Sheline
- Center for Neuromodulation in Depression and Stress (CNDS), Perelman School of Medicine, University of Pennsylvania, Philadelphia, PA, USA; Department of Psychiatry, Perelman School of Medicine, University of Pennsylvania, Philadelphia, PA, USA; Department of Radiology, Perelman School of Medicine, University of Pennsylvania, Philadelphia, PA, USA; Department of Neurology, Perelman School of Medicine, University of Pennsylvania, Philadelphia, PA, USA.
| | - Desmond J Oathes
- Center for Neuromodulation in Depression and Stress (CNDS), Perelman School of Medicine, University of Pennsylvania, Philadelphia, PA, USA; Penn Brain Science, Translation, Innovation and Modulation Center (brainSTIM), Perelman School of Medicine, University of Pennsylvania, Philadelphia, PA, USA.
| | - Nicholas L Balderston
- Center for Neuromodulation in Depression and Stress (CNDS), Perelman School of Medicine, University of Pennsylvania, Philadelphia, PA, USA
| | - Hengyi Rao
- Key Laboratory of Brain-Machine Intelligence for Information Behavior (Ministry of Education and Shanghai), School of Business and Management, Shanghai International Studies University, Shanghai, China; Center for Functional Neuroimaging, Perelman School of Medicine, University of Pennsylvania, Philadelphia, PA, USA.
| | - Meichen Yu
- Indiana Alzheimer's Disease Research Center, Indiana University School of Medicine, Indianapolis, IN, USA; Department of Radiology and Imaging Sciences, Indiana University School of Medicine, Indianapolis, IN, USA; Indiana University Network Science Institute, Bloomington, IN, USA.
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Chakrabarti S, Jolly AJ, Singh P, Yadhav N. Role of adjunctive nonpharmacological strategies for treatment of rapid-cycling bipolar disorder. World J Psychiatry 2023; 13:495-510. [PMID: 37701540 PMCID: PMC10494771 DOI: 10.5498/wjp.v13.i8.495] [Citation(s) in RCA: 1] [Impact Index Per Article: 0.5] [Reference Citation Analysis] [Abstract] [Key Words] [Track Full Text] [Download PDF] [Journal Information] [Submit a Manuscript] [Subscribe] [Scholar Register] [Received: 04/26/2023] [Revised: 06/23/2023] [Accepted: 07/11/2023] [Indexed: 08/17/2023] Open
Abstract
Rapid-cycling bipolar disorder (RCBD) is a phase of bipolar disorder defined by the presence of ≥ 4 mood episodes in a year. It is a common phenomenon characterized by greater severity, a predominance of depression, higher levels of disability, and poorer overall outcomes. It is resistant to treatment by conventional pharmacotherapy. The existing literature underlines the scarcity of evi-dence and the gaps in knowledge about the optimal treatment strategies for RCBD. However, most reviews have considered only pharmacological treatment options for RCBD. Given the treatment-refractory nature of RCBD, nonpharmacological interventions could augment medications but have not been adequately examined. This review carried out an updated and comprehensive search for evidence regarding the role of nonpharmacological therapies as adjuncts to medications in RCBD. We identified 83 reviews and meta-analyses concerning the treatment of RCBD. Additionally, we found 42 reports on adjunctive nonpharmacological treatments in RCBD. Most of the evidence favoured concomitant electroconvulsive therapy as an acute and maintenance treatment. There was pre-liminary evidence to suggest that chronotherapeutic treatments can provide better outcomes when combined with medications. The research on adjunctive psychotherapy was particularly scarce but suggested that psychoeducation, cognitive behavioural therapy, family interventions, and supportive psychotherapy may be helpful. The overall quality of evidence was poor and suffered from several methodological shortcomings. There is a need for more methodologically sound research in this area, although clinicians can use the existing evidence to select and individualize nonpharmacological treatment options for better management of RCBD. Patient summaries are included to highlight some of the issues concerning the implementation of adjunctive nonpharmacological treatments.
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Affiliation(s)
- Subho Chakrabarti
- Department of Psychiatry, Postgraduate Institute of Medical Education and Research, Chandigarh 160012, Chandigarh UT, India
| | - Amal J Jolly
- Department of Psychiatry, Black Country Healthcare NHS Foundation Trust, Dudley DY2 8PS, West Midlands, United Kingdom
| | - Pranshu Singh
- Department of Psychiatry, All India Institute of Medical Sciences, Jodhpur 342005, Rajasthan, India
| | - Nidhi Yadhav
- Department of Psychiatry, Postgraduate Institute of Medical Education and Research, Chandigarh 160012, Chandigarh UT, India
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23
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Chernyshev OY. Sleep Deprivation and Its Consequences. Continuum (Minneap Minn) 2023; 29:1234-1252. [PMID: 37590831 DOI: 10.1212/con.0000000000001323] [Citation(s) in RCA: 0] [Impact Index Per Article: 0] [Reference Citation Analysis] [Abstract] [MESH Headings] [Track Full Text] [Journal Information] [Subscribe] [Scholar Register] [Indexed: 08/19/2023]
Abstract
OBJECTIVE This article reviews the clinical, cognitive, behavioral, and physiologic consequences of sleep deprivation in relation to general neurology practice. LATEST DEVELOPMENTS Despite being one of the most common sleep problems in modern society, the role of sleep deprivation is underrecognized and underestimated in clinical medicine and general neurology practice. The recognition, diagnosis, and management of sleep deprivation in neurologic practice have only recently received close attention. The consequences of sleep deprivation involve all aspects of general neurology practice, including individuals with neurologic disease, neurologists, communities, and health care systems. The identification and timely management of sleep deprivation symptoms may help to improve symptoms of underlying primary neurologic disorders. ESSENTIAL POINTS This article emphasizes complexities related to the identification and evaluation of sleep deprivation in general neurology practice and describes the consequences of sleep deprivation. By recognizing sleep deprivation in patients with neurologic conditions, the neurologist can provide comprehensive care and contribute to improved clinical and neurologic outcomes.
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Taraku B, Zavaliangos-Petropulu A, Loureiro JR, Al-Sharif NB, Kubicki A, Joshi SH, Woods RP, Espinoza R, Narr KL, Sahib AK. White matter microstructural perturbations after total sleep deprivation in depression. Front Psychiatry 2023; 14:1195763. [PMID: 37457774 PMCID: PMC10345348 DOI: 10.3389/fpsyt.2023.1195763] [Citation(s) in RCA: 1] [Impact Index Per Article: 0.5] [Reference Citation Analysis] [Abstract] [Key Words] [Grants] [Track Full Text] [Figures] [Journal Information] [Submit a Manuscript] [Subscribe] [Scholar Register] [Received: 03/28/2023] [Accepted: 06/06/2023] [Indexed: 07/18/2023] Open
Abstract
Background Total sleep deprivation (TSD) transiently reverses depressive symptoms in a majority of patients with depression. How TSD modulates diffusion tensor imaging (DTI) measures of white matter (WM) microstructure, which may be linked with TSD's rapid antidepressant effects, remains uncharacterized. Methods Patients with depression (N = 48, mean age = 33, 26 women) completed diffusion-weighted imaging and Hamilton Depression Rating (HDRS) and rumination scales before and after >24 h of TSD. Healthy controls (HC) (N = 53, 23 women) completed the same assessments at baseline, and after receiving TSD in a subset of HCs (N = 15). Tract based spatial statistics (TBSS) investigated voxelwise changes in fractional anisotropy (FA) across major WM pathways pre-to-post TSD in patients and HCs and between patients and HCs at baseline. Post hoc analyses tested for TSD effects for other diffusion metrics, and the relationships between change in diffusion measures with change in mood and rumination symptoms. Results Significant improvements in mood and rumination occurred in patients with depression (both p < 0.001), but not in HCs following TSD. Patients showed significant (p < 0.05, corrected) decreases in FA values in multiple WM tracts, including the body of the corpus callosum and anterior corona radiata post-TSD. Significant voxel-level changes in FA were not observed in HCs who received TSD (p > 0.05). However, differential effects of TSD between HCs and patients were found in the superior corona radiata, frontal WM and the posterior thalamic radiation (p < 0.05, corrected). A significant (p < 0.05) association between change in FA and axial diffusivity within the right superior corona radiata and improvement in rumination was found post-TSD in patients. Conclusion Total sleep deprivation leads to rapid microstructural changes in WM pathways in patients with depression that are distinct from WM changes associated with TSD observed in HCs. WM tracts including the superior corona radiata and posterior thalamic radiation could be potential biomarkers of the rapid therapeutic effects of TSD. Changes in superior corona radiata FA, in particular, may relate to improvements in maladaptive rumination.
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Affiliation(s)
- Brandon Taraku
- Department of Neurology, Ahmanson-Lovelace Brain Mapping Center, University of California, Los Angeles, Los Angeles, CA, United States
| | - Artemis Zavaliangos-Petropulu
- Department of Neurology, Ahmanson-Lovelace Brain Mapping Center, University of California, Los Angeles, Los Angeles, CA, United States
| | - Joana R. Loureiro
- Department of Neurology, Ahmanson-Lovelace Brain Mapping Center, University of California, Los Angeles, Los Angeles, CA, United States
| | - Noor B. Al-Sharif
- Department of Neurology, Ahmanson-Lovelace Brain Mapping Center, University of California, Los Angeles, Los Angeles, CA, United States
| | - Antoni Kubicki
- Department of Neurology, Ahmanson-Lovelace Brain Mapping Center, University of California, Los Angeles, Los Angeles, CA, United States
| | - Shantanu H. Joshi
- Department of Neurology, Ahmanson-Lovelace Brain Mapping Center, University of California, Los Angeles, Los Angeles, CA, United States
| | - Roger P. Woods
- Department of Neurology, Ahmanson-Lovelace Brain Mapping Center, University of California, Los Angeles, Los Angeles, CA, United States
- Department of Psychiatry and Biobehavioral Sciences, University of California, Los Angeles, Los Angeles, CA, United States
| | - Randall Espinoza
- Department of Psychiatry and Biobehavioral Sciences, University of California, Los Angeles, Los Angeles, CA, United States
| | - Katherine L. Narr
- Department of Neurology, Ahmanson-Lovelace Brain Mapping Center, University of California, Los Angeles, Los Angeles, CA, United States
- Department of Psychiatry and Biobehavioral Sciences, University of California, Los Angeles, Los Angeles, CA, United States
| | - Ashish K. Sahib
- Department of Neurology, Ahmanson-Lovelace Brain Mapping Center, University of California, Los Angeles, Los Angeles, CA, United States
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25
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Chai Y, Gehrman P, Yu M, Mao T, Deng Y, Rao J, Shi H, Quan P, Xu J, Zhang X, Lei H, Fang Z, Xu S, Boland E, Goldschmied JR, Barilla H, Goel N, Basner M, Thase ME, Sheline YI, Dinges DF, Detre JA, Zhang X, Rao H. Enhanced amygdala-cingulate connectivity associates with better mood in both healthy and depressive individuals after sleep deprivation. Proc Natl Acad Sci U S A 2023; 120:e2214505120. [PMID: 37339227 PMCID: PMC10293819 DOI: 10.1073/pnas.2214505120] [Citation(s) in RCA: 3] [Impact Index Per Article: 1.5] [Reference Citation Analysis] [Abstract] [Key Words] [MESH Headings] [Grants] [Track Full Text] [Journal Information] [Subscribe] [Scholar Register] [Received: 09/02/2022] [Accepted: 05/08/2023] [Indexed: 06/22/2023] Open
Abstract
Sleep loss robustly disrupts mood and emotion regulation in healthy individuals but can have a transient antidepressant effect in a subset of patients with depression. The neural mechanisms underlying this paradoxical effect remain unclear. Previous studies suggest that the amygdala and dorsal nexus (DN) play key roles in depressive mood regulation. Here, we used functional MRI to examine associations between amygdala- and DN-related resting-state connectivity alterations and mood changes after one night of total sleep deprivation (TSD) in both healthy adults and patients with major depressive disorder using strictly controlled in-laboratory studies. Behavioral data showed that TSD increased negative mood in healthy participants but reduced depressive symptoms in 43% of patients. Imaging data showed that TSD enhanced both amygdala- and DN-related connectivity in healthy participants. Moreover, enhanced amygdala connectivity to the anterior cingulate cortex (ACC) after TSD associated with better mood in healthy participants and antidepressant effects in depressed patients. These findings support the key role of the amygdala-cingulate circuit in mood regulation in both healthy and depressed populations and suggest that rapid antidepressant treatment may target the enhancement of amygdala-ACC connectivity.
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Affiliation(s)
- Ya Chai
- Key Laboratory of Brain-Machine Intelligence for Information Behavior (Ministry of Education and Shanghai), School of Business and Management, Shanghai International Studies University, Shanghai201620, China
- Center for Functional Neuroimaging and Department of Neurology, Perelman School of Medicine, University of Pennsylvania, Philadelphia, PA19104
| | - Philip Gehrman
- Department of Psychiatry, Perelman School of Medicine, University of Pennsylvania, Philadelphia, PA19104
| | - Meichen Yu
- Indiana Alzheimer’s Disease Research Center, School of Medicine, Indiana University, Indianapolis, IN46202
- Indiana University Network Science Institute, Bloomington, IN47408
| | - Tianxin Mao
- Key Laboratory of Brain-Machine Intelligence for Information Behavior (Ministry of Education and Shanghai), School of Business and Management, Shanghai International Studies University, Shanghai201620, China
- Center for Functional Neuroimaging and Department of Neurology, Perelman School of Medicine, University of Pennsylvania, Philadelphia, PA19104
| | - Yao Deng
- Key Laboratory of Brain-Machine Intelligence for Information Behavior (Ministry of Education and Shanghai), School of Business and Management, Shanghai International Studies University, Shanghai201620, China
- Center for Functional Neuroimaging and Department of Neurology, Perelman School of Medicine, University of Pennsylvania, Philadelphia, PA19104
| | - Joy Rao
- Center for Functional Neuroimaging and Department of Neurology, Perelman School of Medicine, University of Pennsylvania, Philadelphia, PA19104
| | - Hui Shi
- Center for Functional Neuroimaging and Department of Neurology, Perelman School of Medicine, University of Pennsylvania, Philadelphia, PA19104
- Beijing An Zhen Hospital, Capital Medical University, Beijing100029, China
| | - Peng Quan
- Center for Functional Neuroimaging and Department of Neurology, Perelman School of Medicine, University of Pennsylvania, Philadelphia, PA19104
- Research Center for Quality of Life and Applied Psychology, Guangdong Medical University, Dongguan, Guangdong524023, China
| | - Jing Xu
- Key Laboratory of Brain-Machine Intelligence for Information Behavior (Ministry of Education and Shanghai), School of Business and Management, Shanghai International Studies University, Shanghai201620, China
- Center for Functional Neuroimaging and Department of Neurology, Perelman School of Medicine, University of Pennsylvania, Philadelphia, PA19104
| | - Xiaocui Zhang
- Center for Functional Neuroimaging and Department of Neurology, Perelman School of Medicine, University of Pennsylvania, Philadelphia, PA19104
- Medical Psychological Center, The Second Xiangya Hospital, Central South University, Changsha, Hunan410017, China
| | - Hui Lei
- Center for Functional Neuroimaging and Department of Neurology, Perelman School of Medicine, University of Pennsylvania, Philadelphia, PA19104
- College of Education, Hunan Agricultural University, Changsha, Hunan410127, China
| | - Zhuo Fang
- Center for Functional Neuroimaging and Department of Neurology, Perelman School of Medicine, University of Pennsylvania, Philadelphia, PA19104
- Brain and Mind Research Institute, University of Ottawa, Ottawa, ON K1H 8M5, Canada
| | - Sihua Xu
- Key Laboratory of Brain-Machine Intelligence for Information Behavior (Ministry of Education and Shanghai), School of Business and Management, Shanghai International Studies University, Shanghai201620, China
- Center for Functional Neuroimaging and Department of Neurology, Perelman School of Medicine, University of Pennsylvania, Philadelphia, PA19104
| | - Elaine Boland
- Department of Psychiatry, Perelman School of Medicine, University of Pennsylvania, Philadelphia, PA19104
- Mental Illness Research Education and Clinical Center, Corporal Michael J. Crescenz Veterans Affairs Medical Center, Philadelphia, PA19104
| | - Jennifer R. Goldschmied
- Department of Psychiatry, Perelman School of Medicine, University of Pennsylvania, Philadelphia, PA19104
| | - Holly Barilla
- Department of Psychiatry, Perelman School of Medicine, University of Pennsylvania, Philadelphia, PA19104
| | - Namni Goel
- Biological Rhythms Research Laboratory, Department of Psychiatry and Behavioral Sciences, Rush University Medical Center, Chicago, IL60612
| | - Mathias Basner
- Division of Sleep and Chronobiology, Department of Psychiatry, Perelman School of Medicine, University of Pennsylvania, Philadelphia, PA19104
| | - Michael E. Thase
- Department of Psychiatry, Perelman School of Medicine, University of Pennsylvania, Philadelphia, PA19104
- Mental Illness Research Education and Clinical Center, Corporal Michael J. Crescenz Veterans Affairs Medical Center, Philadelphia, PA19104
| | - Yvette I. Sheline
- Department of Psychiatry, Perelman School of Medicine, University of Pennsylvania, Philadelphia, PA19104
- Center for Neuromodulation in Depression and Stress, Perelman School of Medicine, University of Pennsylvania, Philadelphia, PA19104
| | - David F. Dinges
- Division of Sleep and Chronobiology, Department of Psychiatry, Perelman School of Medicine, University of Pennsylvania, Philadelphia, PA19104
| | - John A. Detre
- Center for Functional Neuroimaging and Department of Neurology, Perelman School of Medicine, University of Pennsylvania, Philadelphia, PA19104
| | - Xiaochu Zhang
- Key Laboratory of Brain-Machine Intelligence for Information Behavior (Ministry of Education and Shanghai), School of Business and Management, Shanghai International Studies University, Shanghai201620, China
- Department of Radiology, the First Affiliated Hospital of University of Science and Technology of China, School of Life Science, Division of Life Science and Medicine, University of Science and Technology of China, Hefei, Anhui230026, China
- Department of Psychology, School of Humanities and Social Science, University of Science and Technology of China, Anhui230026, China
| | - Hengyi Rao
- Key Laboratory of Brain-Machine Intelligence for Information Behavior (Ministry of Education and Shanghai), School of Business and Management, Shanghai International Studies University, Shanghai201620, China
- Center for Functional Neuroimaging and Department of Neurology, Perelman School of Medicine, University of Pennsylvania, Philadelphia, PA19104
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26
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He C, Xiao L, Xu J, Cui Y, Huang Y, Li Y, Tang Y, Xu S, Wang H, Cai Y, Guo X, Su T. Effect of sleep deprivation plus existing therapies on depression: A systematic review and meta-analysis of randomized controlled trials. Int J Psychophysiol 2023; 184:1-11. [PMID: 36481460 DOI: 10.1016/j.ijpsycho.2022.11.016] [Citation(s) in RCA: 4] [Impact Index Per Article: 2.0] [Reference Citation Analysis] [Abstract] [Key Words] [Track Full Text] [Journal Information] [Subscribe] [Scholar Register] [Received: 03/02/2022] [Revised: 09/06/2022] [Accepted: 11/29/2022] [Indexed: 12/12/2022]
Abstract
BACKGROUNDS Depression is the most common mental disorder in the world. Sleep deprivation (SD) is a well-known antidepressant. Several recombination protocols (including medications, bright light treatment [BLT], cognitive-behavioral therapy, sleep phrase advance/sleep phrase delay [SPA/SPD], and repetitive transcranial magnetic stimulation [rTMS]) have been developed to improve and maintain the effect of SD. However, relapse after recovery sleep has been reported, and different recombination protocols result in different outcomes. METHODS The Embase, Cochrane, PubMed, CBM, Web of Science, and CINAHL databases were searched for clinical trials assessing depression and SD. Three independent reviewers classified forty-three abstracts. The Hamilton Depression Rating Scale was used to assess the outcomes. RESULTS Compared with existing therapy, patients receiving SD displayed a significant improvement in clinician-rated depressive symptoms (MD -1.48 [95 % CI -2.60, -0.37], p < 0.05). A significant decrease was found in the subgroups of SD plus SPA/SPD (odds ratio 3.90 [95 % CI 1.66, 9.17], p < 0.05), total sleep deprivation[TSD] plus BLT (MD -3.28 [95 % CI -5.06, -1.50], p < 0.05), and partial sleep deprivation[PSD] plus rTMS (MD -7.94 [95 % CI -11.44, -4.45], p < 0.05). No significant differences were observed in the other subgroups. CONCLUSIONS Adding SD to existing therapies showed a positive outcome in improving depression treatment, which provides evidence for the use of SD in treating depression. Further studies are needed to determine the precise effects of SD plus other interventions.
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Affiliation(s)
- Chen He
- Department of Psychology, Naval Medical University, Shanghai, China
| | - Lei Xiao
- Department of Psychology, Naval Medical University, Shanghai, China
| | - Jingzhou Xu
- Department of Psychology, Naval Medical University, Shanghai, China
| | - Yi Cui
- Department of Psychology, Naval Medical University, Shanghai, China
| | - Yujia Huang
- Department of Psychology, Naval Medical University, Shanghai, China
| | - Yinan Li
- Department of Psychology, Naval Medical University, Shanghai, China
| | - Yunxiang Tang
- Department of Psychology, Naval Medical University, Shanghai, China
| | - Shuyu Xu
- Department of Psychology, Naval Medical University, Shanghai, China
| | - Hao Wang
- Department of Psychology, Naval Medical University, Shanghai, China
| | - Yili Cai
- Department of Psychology, Naval Medical University, Shanghai, China
| | - Xin Guo
- Department of Psychology, Naval Medical University, Shanghai, China
| | - Tong Su
- Department of Psychology, Naval Medical University, Shanghai, China.
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27
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Reichert CF, Deboer T, Landolt HP. Adenosine, caffeine, and sleep-wake regulation: state of the science and perspectives. J Sleep Res 2022; 31:e13597. [PMID: 35575450 PMCID: PMC9541543 DOI: 10.1111/jsr.13597] [Citation(s) in RCA: 67] [Impact Index Per Article: 22.3] [Reference Citation Analysis] [Abstract] [Key Words] [Track Full Text] [Download PDF] [Figures] [Journal Information] [Subscribe] [Scholar Register] [Received: 03/17/2022] [Accepted: 03/18/2022] [Indexed: 01/11/2023]
Abstract
For hundreds of years, mankind has been influencing its sleep and waking state through the adenosinergic system. For ~100 years now, systematic research has been performed, first started by testing the effects of different dosages of caffeine on sleep and waking behaviour. About 70 years ago, adenosine itself entered the picture as a possible ligand of the receptors where caffeine hooks on as an antagonist to reduce sleepiness. Since the scientific demonstration that this is indeed the case, progress has been fast. Today, adenosine is widely accepted as an endogenous sleep‐regulatory substance. In this review, we discuss the current state of the science in model organisms and humans on the working mechanisms of adenosine and caffeine on sleep. We critically investigate the evidence for a direct involvement in sleep homeostatic mechanisms and whether the effects of caffeine on sleep differ between acute intake and chronic consumption. In addition, we review the more recent evidence that adenosine levels may also influence the functioning of the circadian clock and address the question of whether sleep homeostasis and the circadian clock may interact through adenosinergic signalling. In the final section, we discuss the perspectives of possible clinical applications of the accumulated knowledge over the last century that may improve sleep‐related disorders. We conclude our review by highlighting some open questions that need to be answered, to better understand how adenosine and caffeine exactly regulate and influence sleep.
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Affiliation(s)
- Carolin Franziska Reichert
- Centre for Chronobiology, University Psychiatric Clinics Basel, Basel, Switzerland.,Transfaculty Research Platform Molecular and Cognitive Neurosciences, University of Basel, Basel, Switzerland.,Center for Affective, Stress, and Sleep Disorders, University Psychiatric Clinics Basel, Basel, Switzerland
| | - Tom Deboer
- Laboratory for Neurophysiology, Department of Cell and Chemical Biology, Leiden University Medical Center, Leiden, the Netherlands
| | - Hans-Peter Landolt
- Institute of Pharmacology and Toxicology, University of Zürich, Zürich, Switzerland.,Sleep & Health Zürich, University Center of Competence, University of Zürich, Zürich, Switzerland
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28
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Mitter P, De Crescenzo F, Loo Yong Kee K, Xia J, Roberts S, Kurtulumus A, Kyle SD, Geddes JR, Cipriani A. Sleep deprivation as a treatment for major depressive episodes: a systematic review and meta-analysis. Sleep Med Rev 2022; 64:101647. [DOI: 10.1016/j.smrv.2022.101647] [Citation(s) in RCA: 0] [Impact Index Per Article: 0] [Reference Citation Analysis] [Track Full Text] [Journal Information] [Subscribe] [Scholar Register] [Received: 11/30/2021] [Accepted: 05/19/2022] [Indexed: 10/18/2022]
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29
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Voldsbekk I, Bjørnerud A, Groote I, Zak N, Roelfs D, Maximov II, Geier O, Due-Tønnessen P, Bøen E, Kuiper YS, Løkken LL, Strømstad M, Blakstvedt TY, Bjorvatn B, Malt UF, Westlye LT, Elvsåshagen T, Grydeland H. Evidence for widespread alterations in cortical microstructure after 32 h of sleep deprivation. Transl Psychiatry 2022; 12:161. [PMID: 35422097 PMCID: PMC9010475 DOI: 10.1038/s41398-022-01909-x] [Citation(s) in RCA: 5] [Impact Index Per Article: 1.7] [Reference Citation Analysis] [Abstract] [Key Words] [Track Full Text] [Download PDF] [Figures] [Journal Information] [Submit a Manuscript] [Subscribe] [Scholar Register] [Received: 10/18/2021] [Revised: 03/17/2022] [Accepted: 03/21/2022] [Indexed: 12/03/2022] Open
Abstract
Cortical microstructure is influenced by circadian rhythm and sleep deprivation, yet the precise underpinnings of these effects remain unclear. The ratio between T1-weighted and T2-weighted magnetic resonance images (T1w/T2w ratio) has been linked to myelin levels and dendrite density and may offer novel insight into the intracortical microstructure of the sleep deprived brain. Here, we examined intracortical T1w/T2w ratio in 41 healthy young adults (26 women) before and after 32 h of either sleep deprivation (n = 18) or a normal sleep-wake cycle (n = 23). Linear models revealed significant group differences in T1w/T2w ratio change after 32 h in four clusters, including bilateral effects in the insular, cingulate, and superior temporal cortices, comprising regions involved in attentional, auditory and pain processing. Across clusters, the sleep deprived group showed an increased T1w/T2w ratio, while the normal sleep-wake group exhibited a reduced ratio. These changes were not explained by in-scanner head movement, and 95% of the effects across clusters remained significant after adjusting for cortical thickness and hydration. Compared with a normal sleep-wake cycle, 32 h of sleep deprivation yields intracortical T1w/T2w ratio increases. While the intracortical changes detected by this study could reflect alterations in myelin or dendritic density, or both, histological analyses are needed to clarify the precise underlying cortical processes.
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Affiliation(s)
- Irene Voldsbekk
- Department of Psychology, University of Oslo, Oslo, Norway. .,Norwegian Centre for Mental Disorders Research (NORMENT), Institute of Clinical Medicine, University of Oslo & Division of Mental Health and Addiction, Oslo University Hospital, Oslo, Norway. .,Computational Radiology and Artificial Intelligence (CRAI), Division of Radiology and Nuclear Medicine, Oslo University Hospital, Oslo, Norway.
| | - Atle Bjørnerud
- grid.5510.10000 0004 1936 8921Department of Psychology, University of Oslo, Oslo, Norway ,grid.55325.340000 0004 0389 8485Computational Radiology and Artificial Intelligence (CRAI), Division of Radiology and Nuclear Medicine, Oslo University Hospital, Oslo, Norway ,grid.5510.10000 0004 1936 8921Department of Physics, University of Oslo, Oslo, Norway
| | - Inge Groote
- grid.55325.340000 0004 0389 8485Computational Radiology and Artificial Intelligence (CRAI), Division of Radiology and Nuclear Medicine, Oslo University Hospital, Oslo, Norway ,grid.417292.b0000 0004 0627 3659Department of Radiology, Vestfold Hospital Trust, Tønsberg, Norway
| | - Nathalia Zak
- grid.55325.340000 0004 0389 8485Norwegian Centre for Mental Disorders Research (NORMENT), Institute of Clinical Medicine, University of Oslo & Division of Mental Health and Addiction, Oslo University Hospital, Oslo, Norway ,grid.55325.340000 0004 0389 8485Department of Diagnostic Physics, Division of Radiology and Nuclear Medicine, Oslo University Hospital, Oslo, Norway
| | - Daniel Roelfs
- grid.55325.340000 0004 0389 8485Norwegian Centre for Mental Disorders Research (NORMENT), Institute of Clinical Medicine, University of Oslo & Division of Mental Health and Addiction, Oslo University Hospital, Oslo, Norway ,grid.5510.10000 0004 1936 8921Institute of Clinical Medicine, University of Oslo, Oslo, Norway
| | - Ivan I. Maximov
- grid.5510.10000 0004 1936 8921Department of Psychology, University of Oslo, Oslo, Norway ,grid.55325.340000 0004 0389 8485Norwegian Centre for Mental Disorders Research (NORMENT), Institute of Clinical Medicine, University of Oslo & Division of Mental Health and Addiction, Oslo University Hospital, Oslo, Norway ,grid.477239.c0000 0004 1754 9964Department of Health and Functioning, Western Norway University of Applied Sciences, Bergen, Norway
| | - Oliver Geier
- grid.55325.340000 0004 0389 8485Department of Diagnostic Physics, Division of Radiology and Nuclear Medicine, Oslo University Hospital, Oslo, Norway
| | - Paulina Due-Tønnessen
- grid.55325.340000 0004 0389 8485Division of Radiology and Nuclear Medicine, Oslo University Hospital, Oslo, Norway
| | - Erlend Bøen
- grid.55325.340000 0004 0389 8485Psychosomatic and CL Psychiatry, Division of Mental Health and Addiction, Oslo University Hospital, Oslo, Norway
| | - Yvonne S. Kuiper
- grid.55325.340000 0004 0389 8485Department of Diagnostic Physics, Division of Radiology and Nuclear Medicine, Oslo University Hospital, Oslo, Norway
| | - Lise-Linn Løkken
- grid.55325.340000 0004 0389 8485Department of Diagnostic Physics, Division of Radiology and Nuclear Medicine, Oslo University Hospital, Oslo, Norway
| | - Marie Strømstad
- grid.5510.10000 0004 1936 8921Department of Psychology, University of Oslo, Oslo, Norway
| | - Taran Y. Blakstvedt
- grid.5510.10000 0004 1936 8921Department of Psychology, University of Oslo, Oslo, Norway
| | - Bjørn Bjorvatn
- grid.7914.b0000 0004 1936 7443Department of Global Public Health and Primary Care, University of Bergen, Bergen, Norway ,grid.412008.f0000 0000 9753 1393Norwegian Competence Centre for Sleep Disorders, Haukeland University Hospital, Bergen, Norway
| | - Ulrik F. Malt
- grid.55325.340000 0004 0389 8485Psychosomatic and CL Psychiatry, Division of Mental Health and Addiction, Oslo University Hospital, Oslo, Norway
| | - Lars T. Westlye
- grid.5510.10000 0004 1936 8921Department of Psychology, University of Oslo, Oslo, Norway ,grid.55325.340000 0004 0389 8485Norwegian Centre for Mental Disorders Research (NORMENT), Institute of Clinical Medicine, University of Oslo & Division of Mental Health and Addiction, Oslo University Hospital, Oslo, Norway ,grid.5510.10000 0004 1936 8921KG Jebsen Centre for Neurodevelopmental Disorders, University of Oslo, Oslo, Norway
| | - Torbjørn Elvsåshagen
- grid.55325.340000 0004 0389 8485Norwegian Centre for Mental Disorders Research (NORMENT), Institute of Clinical Medicine, University of Oslo & Division of Mental Health and Addiction, Oslo University Hospital, Oslo, Norway ,grid.5510.10000 0004 1936 8921Institute of Clinical Medicine, University of Oslo, Oslo, Norway ,grid.55325.340000 0004 0389 8485Department of Neurology, Oslo University Hospital, Oslo, Norway
| | - Håkon Grydeland
- Department of Psychology, University of Oslo, Oslo, Norway. .,Centre for Lifespan Changes in Brain and Cognition, Department of Psychology, University of Oslo, Oslo, Norway.
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30
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Saksvik-Lehouillier I, Langvik E, Saksvik SB, Kallestad H, Follesø HS, Austad SB, Dahlberg J, Ringen H, Tanum T, Sørengaard TA, Karlsen HR, Smedbøl T, Olsen A. High neuroticism is associated with reduced negative affect following sleep deprivation. PERSONALITY AND INDIVIDUAL DIFFERENCES 2022. [DOI: 10.1016/j.paid.2021.111291] [Citation(s) in RCA: 0] [Impact Index Per Article: 0] [Reference Citation Analysis] [Track Full Text] [Journal Information] [Submit a Manuscript] [Subscribe] [Scholar Register] [Indexed: 10/20/2022]
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Gorgulu Y, Caliyurt O, Kose Cinar R, Sonmez MB. Acute sleep deprivation immediately increases serum GDNF, BDNF and VEGF levels in healthy subjects. Sleep Biol Rhythms 2022; 20:73-79. [PMID: 38469072 PMCID: PMC10897642 DOI: 10.1007/s41105-021-00341-w] [Citation(s) in RCA: 7] [Impact Index Per Article: 2.3] [Reference Citation Analysis] [Abstract] [Key Words] [Grants] [Track Full Text] [Journal Information] [Subscribe] [Scholar Register] [Received: 01/04/2021] [Accepted: 07/08/2021] [Indexed: 12/17/2022]
Abstract
Acute sleep deprivation upregulates hippocampal neurogenesis. Neurotrophic factors such as glial cell line-derived neurotrophic factor (GDNF), brain-derived neurotrophic factor (BDNF), and vascular endothelial growth factor (VEGF) are mediators of neuronal plasticity and neurogenesis. These neurotrophins are involved in sleep and sleep disorders and are associated with sleep deprivation. In this study, it is aimed to investigate the changes of neurotrophin levels with total sleep deprivation in healthy individuals. Seventeen healthy young adults with a mean age of 19.8 (SD = 1.0) years underwent an experimental protocol consisting of 36 h of total sleep deprivation. Venous blood samples were obtained on Day1 at 09.00, on Day2 at 09.00, and at 21.00. Serum levels of neurotrophins were detected using the ELISA method. The participants were asked to mark the scores corresponding to their subjective energy, happiness, depression, tension levels on the visual analog scale; and sleepiness level on the Epworth Sleepiness Scale; during the course of the study. As a result of 36 h of sleep deprivation, serum GDNF, BDNF, and VEGF levels showed a statistically significant increase compared to the baseline values in the participants included in the study (P < 0.0001). While this increase was evident in 24 h, it continued after 36 h. In parallel, sleepiness levels, subjective depression, and tension levels increased, on the other hand, subjective energy and happiness scores decreased at a statistically significant level at the end of the study compared to basal values (P < 0.0001). The results show that acute sleep deprivation significantly affects and increases serum levels of neurotrophic factors, and it seems that these effects are likely to occur as an immediate response to the stress and disruption caused by sleep deprivation.
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Affiliation(s)
- Yasemin Gorgulu
- Department of Psychiatry, Faculty of Medicine, Trakya University, Balkan Campus, 22030 Edirne, Turkey
| | - Okan Caliyurt
- Department of Psychiatry, Faculty of Medicine, Trakya University, Balkan Campus, 22030 Edirne, Turkey
| | - Rugul Kose Cinar
- Department of Psychiatry, Faculty of Medicine, Trakya University, Balkan Campus, 22030 Edirne, Turkey
| | - Mehmet Bulent Sonmez
- Department of Psychiatry, Faculty of Medicine, Trakya University, Balkan Campus, 22030 Edirne, Turkey
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32
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Bisdounis L, Saunders KEA, Farley HJ, Lee CK, McGowan NM, Espie CA, Kyle SD. Psychological and behavioural interventions in bipolar disorder that target sleep and circadian rhythms: A systematic review of randomised controlled trials. Neurosci Biobehav Rev 2022; 132:378-390. [PMID: 34871635 DOI: 10.1016/j.neubiorev.2021.12.002] [Citation(s) in RCA: 12] [Impact Index Per Article: 4.0] [Reference Citation Analysis] [Abstract] [Key Words] [MESH Headings] [Grants] [Track Full Text] [Journal Information] [Subscribe] [Scholar Register] [Received: 07/02/2021] [Revised: 11/18/2021] [Accepted: 12/01/2021] [Indexed: 01/10/2023]
Abstract
Sleep and circadian disruptions are prominent symptoms of bipolar disorder (BD) and potential targets for adjunctive interventions. The aim of this review was to appraise the effectiveness of psychological and behavioural interventions in BD that target sleep and circadian rhythms, as reported by randomised controlled trials. Nineteen studies met the inclusion/exclusion criteria. They were summarised via narrative synthesis and meta-analysis wherever appropriate. Six studies delivered bright light therapy, five interpersonal and social rhythm therapy, two blue-light blocking glasses, one cognitive behavioural therapy for insomnia, one total sleep deprivation, and four combination treatments. More than half of the studies (N = 10, 52 %) did not measure sleep or circadian rhythms despite being the principal target of the intervention. Overall, the evidence base for the effectiveness of these interventions was limited. There was a small number of studies for each intervention, and a lack of consistency in protocols and outcomes. Meta-analysis was possible for the effect of bright light therapy on depression, revealing a medium-to-large post-treatment effect (Nc = 6; g=-0.74 [95 % CI=-1.05 to -0.42], p < 0.001).
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Affiliation(s)
- Lampros Bisdounis
- Sleep and Circadian Neuroscience Institute, Nuffield Department of Clinical Neurosciences, University of Oxford, United Kingdom; Department of Psychiatry, Warneford Hospital, University of Oxford, United Kingdom.
| | - Kate E A Saunders
- Department of Psychiatry, Warneford Hospital, University of Oxford, United Kingdom; Oxford Health NHS Foundation Trust, Warneford Hospital, Oxford, United Kingdom
| | - Hannah J Farley
- Clinical Medical School, Medical Sciences Division, Academic Centre, John Radcliffe Hospital, University of Oxford, United Kingdom
| | - Charlotte K Lee
- Clinical Medical School, Medical Sciences Division, Academic Centre, John Radcliffe Hospital, University of Oxford, United Kingdom
| | - Niall M McGowan
- Department of Psychiatry, Warneford Hospital, University of Oxford, United Kingdom; Oxford Health NHS Foundation Trust, Warneford Hospital, Oxford, United Kingdom
| | - Colin A Espie
- Sleep and Circadian Neuroscience Institute, Nuffield Department of Clinical Neurosciences, University of Oxford, United Kingdom
| | - Simon D Kyle
- Sleep and Circadian Neuroscience Institute, Nuffield Department of Clinical Neurosciences, University of Oxford, United Kingdom
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Out-patient triple chronotherapy for the rapid treatment and maintenance of response in depression: feasibility and pilot randomised controlled trial. BJPsych Open 2021. [PMCID: PMC8693902 DOI: 10.1192/bjo.2021.1044] [Citation(s) in RCA: 1] [Impact Index Per Article: 0.3] [Reference Citation Analysis] [Abstract] [Track Full Text] [Download PDF] [Figures] [Journal Information] [Submit a Manuscript] [Subscribe] [Scholar Register] [Indexed: 11/23/2022] Open
Abstract
Background Triple chronotherapy (sleep deprivation for 36 h, followed by 4 days of advancing the time of sleep and daily morning bright-light therapy for 6 months) has demonstrated benefits for the rapid treatment of depressive symptoms in four small controlled trials of in-patients. Aims To test the feasibility of recruitment and delivery of triple chronotherapy for out-patients with depression (ISRCTN17706836; NCT03405493). Method In a single-blind trial, 82 participants were randomised to triple chronotherapy or a control intervention. The primary outcome was the number of participants recruited per month and adherence to the protocol. Secondary outcomes included the 6-item Hamilton Rating Scale for Depression (HRSD-6) at 1 week. Timings of observer ratings were baseline and 1, 2, 4, 8 and 26 weeks after randomisation. Results The triple chronotherapy group stayed awake for the planned 36 h and 89.9% adhered to the plan of phase advance of their sleep over the following 4 days. We achieved our recruitment target (60 participants completed the trial within 13 months). There were no reported adverse side-effects. We found a significant difference between the groups by intention-to-treat analysis for the HRSD-6 at weeks 1, 8 and 26. There was a large effect size of Cohen's d = 0.8 on HRSD-6 score at week 1, increasing to d = 1.30 at week 26. A response (≥50% reduction in symptoms) was achieved by 33.3% in the triple chronotherapy group and 16.2% in the control group. This stayed relatively steady until week 26 (35.9 v. 13.9%). Conclusions Triple chronotherapy produced a significant and rapid benefit after 1 week in out-patients with depression that was sustained at 26 weeks. Cost-effectiveness trials with a larger clinical sample are required.
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Guinjoan SM, Bär KJ, Camprodon JA. Cognitive effects of rapid-acting treatments for resistant depression: Just adverse, or contributing to clinical efficacy? J Psychiatr Res 2021; 140:512-521. [PMID: 34157590 PMCID: PMC8319118 DOI: 10.1016/j.jpsychires.2021.06.026] [Citation(s) in RCA: 3] [Impact Index Per Article: 0.8] [Reference Citation Analysis] [Abstract] [Key Words] [Track Full Text] [Journal Information] [Submit a Manuscript] [Subscribe] [Scholar Register] [Received: 03/17/2021] [Revised: 06/07/2021] [Accepted: 06/13/2021] [Indexed: 12/28/2022]
Abstract
Major Depressive Disorder is a major public health problem and has a high rate of treatment resistance. Fear conditioning has been proposed as a potential mechanism sustaining negative affect in mood disorders. With the aim of exploring cognitive effects of rapid-acting antidepressant treatments as a potential mechanism of action that can be targeted by neuromodulation, we performed a narrative review of the extant literature on effects of electroconvulsive therapy, ketamine or esketamine, and sleep deprivation on emotional/fear memory retrieval-reconsolidation. We explore interference with reconsolidation as a potential common pathway that explains in part the efficacy of rapid-acting antidepressant treatments with disparate mechanisms of action. We propose the testable hypothesis that fear learning circuits can be specifically targeted by neuromodulation to attempt rapid amelioration of depressive symptoms (especially repetitive negative thinking) while limiting unspecific, untoward cognitive side effects.
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Affiliation(s)
- Salvador M. Guinjoan
- Principal Investigator, Laureate Institute for Brain Research, Tulsa, Oklahoma, United States of America,Schools of Medicine and Psychology, University of Buenos Aires, CONICET, Argentina,Mailing Address: Salvador M. Guinjoan, Laureate Institute for Brain Research, 6655 South Yale Avenue, Tulsa, Oklahoma 74136-3326, United States of America,
| | - Karl-Jürgen Bär
- Chief, Departments of Psychosomatic Medicine and Gerontopsychiatry and Psychotherapy, University Hospital Jena, Jena, Germany
| | - Joan A. Camprodon
- Director, Division of Neuropsychiatry, Massachusetts General Hospital and Harvard Medical School
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35
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Huang T, Balasubramanian R, Yao Y, Clis CB, Shadyab AH, Liu B, Tworoger SS, Rexrode KM, Manson JE, Kubzansky LD, Hankinson SE. Associations of depression status with plasma levels of candidate lipid and amino acid metabolites: a meta-analysis of individual data from three independent samples of US postmenopausal women. Mol Psychiatry 2021; 26:3315-3327. [PMID: 32859999 PMCID: PMC7914294 DOI: 10.1038/s41380-020-00870-9] [Citation(s) in RCA: 28] [Impact Index Per Article: 7.0] [Reference Citation Analysis] [Abstract] [Key Words] [Track Full Text] [Download PDF] [Figures] [Journal Information] [Submit a Manuscript] [Subscribe] [Scholar Register] [Received: 09/04/2019] [Revised: 08/04/2020] [Accepted: 08/14/2020] [Indexed: 01/05/2023]
Abstract
Recent animal and small clinical studies have suggested depression is related to altered lipid and amino acid profiles. However, this has not been examined in a population-based sample, particularly in women. We identified multiple metabolites associated with depression as potential candidates from prior studies. Cross-sectional data from three independent samples of postmenopausal women were analyzed, including women from the Women's Health Initiative-Observational Study (WHI-OS, n = 926), the WHI-Hormone Trials (WHI-HT; n = 1,325), and the Nurses' Health Study II Mind-Body Study (NHSII-MBS; n = 218). Positive depression status was defined as having any of the following: elevated depressive symptoms, antidepressant use, or depression history. Plasma metabolites were measured using liquid chromatography-tandem mass spectrometry (21 phosphatidylcholines (PCs), 7 lysophosphatidylethanolamines, 5 ceramides, 3 branched chain amino acids, and 9 neurotransmitters). Associations between depression status and metabolites were evaluated using multivariable linear regression; results were pooled by random-effects meta-analysis with multiple testing adjustment using the false discovery rate (FDR). Prevalence rates of positive depression status were 24.4% (WHI-OS), 25.7% (WHI-HT), and 44.7% (NHSII-MBS). After multivariable adjustment, positive depression status was associated with higher levels of glutamate and PC 36 : 1/38 : 3, and lower levels of tryptophan and GABA-to-glutamate and GABA-to-glutamine ratio (FDR-p < 0.05). Positive associations with LPE 18 : 0/18 : 1 and inverse associations with valine and serotonin were also observed, although these associations did not survive FDR adjustment. Associations of positive depression status with several candidate metabolites including PC 36 : 1/38 : 3 and amino acids involved in neurotransmission suggest potential depression-related metabolic alterations in postmenopausal women, with possible implications for later chronic disease.
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Affiliation(s)
- Tianyi Huang
- Channing Division of Network Medicine, Department of Medicine, Brigham and Women's Hospital, and Harvard Medical School, Boston, MA, USA.
| | - Raji Balasubramanian
- Department of Biostatistics and Epidemiology, University of Massachusetts Amherst, Amherst, MA
| | - Yubing Yao
- Department of Biostatistics and Epidemiology, University of Massachusetts Amherst, Amherst, MA
| | | | - Aladdin H. Shadyab
- Department of Family Medicine and Public Health, University of California San Diego School of Medicine, La Jolla, CA
| | - Buyun Liu
- Department of Epidemiology, College of Public Health, University of Iowa, Iowa City, IA
| | - Shelley S. Tworoger
- Department of Cancer Epidemiology, H. Lee Moffitt Cancer Center and Research Institute, Tampa, FL,Department of Epidemiology, Harvard T.H. Chan School of Public Health, Boston, MA
| | - Kathryn M. Rexrode
- Division of Women’s Health, Department of Medicine, Brigham and Women’s Hospital, Boston, MA,Division of Preventive Medicine, Department of Medicine, Brigham and Women's Hospital and Harvard Medical School, Boston, MA
| | - JoAnn E. Manson
- Channing Division of Network Medicine, Department of Medicine, Brigham and Women’s Hospital and Harvard Medical School, Boston, MA,Department of Epidemiology, Harvard T.H. Chan School of Public Health, Boston, MA,Division of Preventive Medicine, Department of Medicine, Brigham and Women's Hospital and Harvard Medical School, Boston, MA
| | - Laura D. Kubzansky
- Department of Social and Behavioral Sciences, Harvard T.H. Chan School of Public Health, Boston, MA
| | - Susan E. Hankinson
- Channing Division of Network Medicine, Department of Medicine, Brigham and Women’s Hospital and Harvard Medical School, Boston, MA,Department of Biostatistics and Epidemiology, University of Massachusetts Amherst, Amherst, MA
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36
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Bean CAL, Ciesla JA. Naturalistic Partial Sleep Deprivation Leads to Greater Next-Day Anxiety: The Moderating Role of Baseline Anxiety and Depression. Behav Ther 2021; 52:861-873. [PMID: 34134826 DOI: 10.1016/j.beth.2020.10.008] [Citation(s) in RCA: 2] [Impact Index Per Article: 0.5] [Reference Citation Analysis] [Abstract] [Key Words] [Track Full Text] [Journal Information] [Submit a Manuscript] [Subscribe] [Scholar Register] [Received: 05/28/2020] [Revised: 10/24/2020] [Accepted: 10/27/2020] [Indexed: 11/27/2022]
Abstract
The detrimental effects of insufficient sleep on emotional functioning have been well established. Total sleep deprivation usually leads to increased anxiety and depressive symptoms the following day. However, no study has yet examined the relationships between unmanipulated partial sleep deprivation and next-day symptoms of anxiety and depression in everyday life, which this study sought to characterize. Participants (N = 94) completed daily diary surveys twice per day for 2 weeks without instructions to alter their sleep in any way. Nights of spontaneous, naturally occurring partial sleep deprivation were followed by increased levels of self-reported symptoms of anxious arousal the next day, but were unrelated to next-day symptoms of anhedonic depression or general distress. The relationship between partial sleep deprivation and next-day anxious arousal was found to be moderated by both baseline depressive symptoms and anxiety such that individuals reporting higher levels of depression or anxiety at baseline showed relatively greater increases in symptoms of anxiety following partial sleep deprivation. These results suggest that partial sleep deprivation occurring in everyday life can lead to higher next-day levels of anxious arousal, a relationship that is particularly deleterious for individuals with higher overall levels of anxiety or depressive symptoms.
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37
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Pavlova MK, Ng M, Allen RM, Boly M, Kothare S, Zaveri H, Zee PC, Adler G, Buchanan GF, Quigg MS, on behalf of the Sleep and Epilepsy Workgroup. Proceedings of the Sleep and Epilepsy Workgroup: Section 2 Comorbidities: Sleep Related Comorbidities of Epilepsy. Epilepsy Curr 2021; 21:15357597211004549. [PMID: 33843327 PMCID: PMC8609600 DOI: 10.1177/15357597211004549] [Citation(s) in RCA: 6] [Impact Index Per Article: 1.5] [Reference Citation Analysis] [Abstract] [Key Words] [Grants] [Track Full Text] [Download PDF] [Figures] [Journal Information] [Subscribe] [Scholar Register] [Indexed: 11/16/2022] Open
Abstract
Epilepsy is a chronic disease with multiple, complex comorbidities. Bidirectional relationships exist among seizures, sleep, circadian rhythms, and diseases within and outside of the central nervous system. Seizures fragment sleep and can contribute to development of sleep disorders, which in turn leads to worse overall health and more seizures. Moreover, treatment options are often limited by interactions with anti-seizure medications. Advances in the fields of epilepsy and in sleep medicine have been made separately, and therefore treating patients with these comorbidities necessitates interdisciplinary approach. The focus of this section of the Sleep and Epilepsy Workgroup was to identify methods of collaboration and outline investigational, educational, and treatment priorities to mutually advance what we consider a combined field.
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Affiliation(s)
- Milena K. Pavlova
- Department of Neurology, Brigham and Women’s Hospital and Harvard Medical School, Boston, MA, USA
| | - Marcus Ng
- Department of Internal Medicine, University of Manitoba, Winnipeg, Canada
- Department of Biomedical Engineering, University of Manitoba, Winnipeg, Canada
| | | | - Melanie Boly
- Department of Neurology, School of Medicine and Public Health, University of Wisconsin, Madison, WI, USA
| | - Sanjeev Kothare
- Northwell Health and Donald, Barbara Zucker School of Medicine, Hofstra/Northwell, NY, USA
| | - Hiten Zaveri
- Department of Neurology, Yale School of Medicine, New Haven, CT, USA
| | - Phyllis C. Zee
- Department of Neurology, Feinberg School of Medicine, Northwestern University, Chicago, IL, USA
| | - Gail Adler
- Department of Medicine, Brigham and Women’s Hospital, Boston, MA, USA
| | - Gordon F. Buchanan
- Department of Neurology, Iowa Neuroscience Institute, University of Iowa Carver College of Medicine, IA, USA
| | - Mark S. Quigg
- Department of Neurology, University of Virginia School of Medicine, Charlottesville, VA, USA
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38
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Gottlieb JF, Goel N, Chen S, Young MA. Meta-analysis of sleep deprivation in the acute treatment of bipolar depression. Acta Psychiatr Scand 2021; 143:319-327. [PMID: 33190220 PMCID: PMC8283955 DOI: 10.1111/acps.13255] [Citation(s) in RCA: 6] [Impact Index Per Article: 1.5] [Reference Citation Analysis] [Abstract] [Key Words] [MESH Headings] [Grants] [Track Full Text] [Journal Information] [Submit a Manuscript] [Subscribe] [Scholar Register] [Received: 08/19/2020] [Revised: 11/04/2020] [Accepted: 11/08/2020] [Indexed: 12/14/2022]
Abstract
BACKGROUND Sleep deprivation (SD) is an antidepressant intervention with multiple administration formats that has been investigated primarily with uncontrolled clinical trials and qualitative reviews of the literature. The validity and applicability of these findings to the treatment of bipolar depression (BPD) is uncertain. METHODS A PRISMA-based systematic review of the literature and meta-analysis were conducted to determine the efficacy of SD in the treatment of BPD and to identify moderator variables that influence response rate. RESULTS From a sample of 15 studies covering 384 patients, the overall, mean response rate to SD was 47.6% (CI 36.0%, 59.5%). This response rate compared post-SD to pre-SD depression scores, and not to a placebo control condition. Of several potential moderating variables examined, the use of adjunctive pharmacotherapy achieved statistical significance with response rates of 59.4% [CI 48.5, 69.5] for patients using adjunctive medication vs 27.4% [CI 17.8, 39.8] for patients not using adjunctive medication. CONCLUSIONS This meta-analysis of SD in the treatment of BPD found an overall, response rate of almost 50%, reinforcing earlier estimates of efficacy. The use of adjunctive pharmacotherapy had a statistically significant moderating effect on SD response suggesting that clinical practice should routinely pair these interventions. These findings provide a higher level of evidence supporting the use of SD, especially when used with medication, and should inform future management guidelines for the treatment of BPD.
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Affiliation(s)
- John F. Gottlieb
- Department of Psychiatry and Behavioral Sciences, Feinberg School of Medicine, Northwestern University, Chicago, IL 60610 USA
- Chicago Psychiatry Associates, 25 E Washington St., Suite 1805, Chicago, IL 60602 USA
| | - Namni Goel
- Biological Rhythms Research Laboratory, Department of Psychiatry and Behavioral Sciences, Rush University Medical Center, Chicago, IL 60612 USA
| | - Shenghao Chen
- Department of Psychology, Florida State University, Tallahassee, FL 32303 USA
| | - Michael A. Young
- Department of Psychology, Illinois Institute of Technology, Chicago, IL 60616 USA
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39
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Circadian depression: A mood disorder phenotype. Neurosci Biobehav Rev 2021; 126:79-101. [PMID: 33689801 DOI: 10.1016/j.neubiorev.2021.02.045] [Citation(s) in RCA: 60] [Impact Index Per Article: 15.0] [Reference Citation Analysis] [Abstract] [Key Words] [Journal Information] [Subscribe] [Scholar Register] [Received: 08/06/2020] [Revised: 02/18/2021] [Accepted: 02/28/2021] [Indexed: 12/15/2022]
Abstract
Major mood syndromes are among the most common and disabling mental disorders. However, a lack of clear delineation of their underlying pathophysiological mechanisms is a major barrier to prevention and optimised treatments. Dysfunction of the 24-h circadian system is a candidate mechanism that has genetic, behavioural, and neurobiological links to mood syndromes. Here, we outline evidence for a new clinical phenotype, which we have called 'circadian depression'. We propose that key clinical characteristics of circadian depression include disrupted 24-h sleep-wake cycles, reduced motor activity, low subjective energy, and weight gain. The illness course includes early age-of-onset, phenomena suggestive of bipolarity (defined by bidirectional associations between objective motor and subjective energy/mood states), poor response to conventional antidepressant medications, and concurrent cardiometabolic and inflammatory disturbances. Identifying this phenotype could be clinically valuable, as circadian-targeted strategies show promise for reducing depressive symptoms and stabilising illness course. Further investigation of underlying circadian disturbances in mood syndromes is needed to evaluate the clinical utility of this phenotype and guide the optimal use of circadian-targeted interventions.
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40
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Geoffroy PA, Palagini L. Biological rhythms and chronotherapeutics in depression. Prog Neuropsychopharmacol Biol Psychiatry 2021; 106:110158. [PMID: 33152388 DOI: 10.1016/j.pnpbp.2020.110158] [Citation(s) in RCA: 41] [Impact Index Per Article: 10.3] [Reference Citation Analysis] [Abstract] [Key Words] [MESH Headings] [Track Full Text] [Journal Information] [Submit a Manuscript] [Subscribe] [Scholar Register] [Received: 09/02/2020] [Revised: 10/14/2020] [Accepted: 10/27/2020] [Indexed: 12/28/2022]
Abstract
Depressive syndromes are frequent and heterogeneous brain conditions with more than 90% of patients suffering from sleep complaints. Better characterizing this "sleep" domain may allow to both better treat acute episodes with existing chronotherapeutics, but also to prevent the manifestation or recurrences of mood disorders. This work aims to i) review theoretical and fundamental data of chronotherapeutics, and ii) provide practical recommendations. Light therapy (LT) can be used as a first-line monotherapy of moderate to severe depression of all subtypes. LT can be also used as a combination with antidepressant to maximize patients' response rates, which has a clear superiority to antidepressant alone. Sleep deprivation (SD) is a rapid and powerful chronotherapeutic with antidepressant responses within hours in 45-60% of patients with unipolar or bipolar depression. Different strategies should be combined to stabilize the SD antidepressant effect, including concomitant medications, repeated SD, combination with sleep phase advance and/or LT (triple chronotherapy). Melatonin treatment is of interest in remitted patients with mood disorder to prevent relapses or recurrences, if a complaint of insomnia, poor sleep quality or phase delay syndrome is associated. During the acute phase, melatonin could be used as an adjuvant treatment for symptoms of insomnia associated with depression. The cognitive behavioral therapy for insomnia (CBT-I) can be recommend to treat insomnia during euthymic phases. The Interpersonal and social rhythm therapy (IPSRT) is indicated for the acute treatment of bipolar depression and for the prevention of mood episodes. Chronotherapeutics should always be associated with behavioral measures for healthy sleep.
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Affiliation(s)
- Pierre A Geoffroy
- Département de psychiatrie et d'addictologie, AP-HP, GHU Paris Nord, DMU Neurosciences, Hopital Bichat - Claude Bernard, F-75018 Paris, France; GHU Paris - Psychiatry & Neurosciences, 1 rue Cabanis, 75014 Paris, France; Université de Paris, NeuroDiderot, Inserm, F-75019 Paris, France.
| | - Laura Palagini
- Department of Clinical and Experimental Medicine, Psychiatric Section, University of Pisa; Azienda Ospedaliera Universitaria Pisana (AUOP), Pisa, Italy
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41
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Li BZ, Cao Y, Zhang Y, Chen Y, Gao YH, Peng JX, Shao YC, Zhang X. Relation of Decreased Functional Connectivity Between Left Thalamus and Left Inferior Frontal Gyrus to Emotion Changes Following Acute Sleep Deprivation. Front Neurol 2021; 12:642411. [PMID: 33716944 PMCID: PMC7952868 DOI: 10.3389/fneur.2021.642411] [Citation(s) in RCA: 15] [Impact Index Per Article: 3.8] [Reference Citation Analysis] [Abstract] [Key Words] [Track Full Text] [Download PDF] [Figures] [Journal Information] [Subscribe] [Scholar Register] [Received: 12/16/2020] [Accepted: 02/01/2021] [Indexed: 12/14/2022] Open
Abstract
Objective: The thalamus is a key node for sleep-wake pathway gate switching during acute sleep deprivation (ASD), and studies have shown that it plays a certain role in emotion changes. However, there are no studies on the association between the thalamus and emotion changes in ASD. In this study, we used resting-state functional magnetic resonance imaging (R-fMRI) to explore whether changes in the functional connections between the thalamus and other brain regions are related to emotion changes and further explored the function of the thalamus under total ASD conditions. Method: Thirty healthy, right-handed adult men underwent emotional assessment according to the Profile of Mood States Scale and R-fMRI scans before and after ASD. The correlations between changes in functional connectivity between the thalamus and other brain regions and emotion changes were then studied. Results: Positive emotions and psychomotor performance were reduced, and negative emotions were increased following ASD. The functional connections between the left thalamus and left middle temporal gyrus, left inferior frontal gyrus, right thalamus, right inferior temporal gyrus, left middle temporal pole gyrus, right calcarine, left cuneus, left rectus and left medial superior frontal gyrus were significantly altered. Decreased functional connectivity between left thalamus and left inferior frontal gyrus related to emotion changes following ASD. Conclusion: This study finds that functional changes in the thalamus are associated with emotion changes during ASD, suggesting that the left thalamus probably plays an essential role in emotion changes under ASD conditions.
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Affiliation(s)
- Bo-zhi Li
- Department of Neurology, Secondary Medical Center, National Clinical Research Center for Geriatric Disease, Chinese PLA General Hospital, Beijing, China
| | - Ya Cao
- Department of Neurology, First Medical Center, Chinese PLA General Hospital, Beijing, China
| | - Ying Zhang
- Department of Medical Psychology, Eighth Medical Center, Chinese PLA General Hospital, Beijing, China
| | - Yang Chen
- School of Biological Science and Medical Engineering, Beihang University, Beijing, China
| | - Yu-hong Gao
- Department of Neurology, Secondary Medical Center, National Clinical Research Center for Geriatric Disease, Chinese PLA General Hospital, Beijing, China
| | - Jia-xi Peng
- Department of Psychology, Beijing Sport University, Beijing, China
| | - Yong-cong Shao
- Department of Psychology, Beijing Sport University, Beijing, China
| | - Xi Zhang
- Department of Neurology, Secondary Medical Center, National Clinical Research Center for Geriatric Disease, Chinese PLA General Hospital, Beijing, China
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42
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Sleep and chronotype in relation to work-related stress and negative affect: The moderating role of a flexible start of work. SOMNOLOGIE 2021. [DOI: 10.1007/s11818-021-00294-9] [Citation(s) in RCA: 6] [Impact Index Per Article: 1.5] [Reference Citation Analysis] [Abstract] [Track Full Text] [Journal Information] [Subscribe] [Scholar Register] [Indexed: 12/18/2022]
Abstract
Abstract
Objectives
The present study investigated the relationships between sleep (sleep duration and need for additional sleep time in the morning), chronotype, work-related stress, and negative affect in daytime workers. Furthermore, it was examined whether a flexible start of work moderates these relationships.
Methods
A cross-sectional online study was conducted. Participants were 438 (247 female) daytime workers between 18 and 73 years (mean = 37.68, standard deviation = 12.39). The questionnaire included the “sleep duration” subscale of the Pittsburgh Sleep Quality Index (PSQI), the Morningness–Eveningness Questionnaire (MEQ), two subscales of the Trier Inventory for the Assessment of Chronic Stress (TICS), the negative affect scale of the Positive and Negative Affect Schedule (PANAS), questions regarding how many minutes participants would like to sleep longer in the morning, and how flexible their start of work is.
Results
Short sleep duration and a greater need for additional sleep in the morning were significantly associated with late chronotype. Shorter sleep duration, a greater need for additional sleep, and a late chronotype were associated with higher work-related stress and negative affect. A flexible start of work moderated these relationships: People with longer sleep duration, less need for additional sleep time, and an early chronotype showed lower stress and negative affect levels when having a flexible start of work. A flexible start of work showed no or negative effects on workers with shorter sleep duration, a greater need for additional sleep time, or a late chronotype.
Conclusions
The effect of a flexible start of work for daytime worker’s well-being depends on a person’s individual sleep timing and chronotype.
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Fehér KD, Wunderlin M, Maier JG, Hertenstein E, Schneider CL, Mikutta C, Züst MA, Klöppel S, Nissen C. Shaping the slow waves of sleep: A systematic and integrative review of sleep slow wave modulation in humans using non-invasive brain stimulation. Sleep Med Rev 2021; 58:101438. [PMID: 33582581 DOI: 10.1016/j.smrv.2021.101438] [Citation(s) in RCA: 35] [Impact Index Per Article: 8.8] [Reference Citation Analysis] [Abstract] [Key Words] [Track Full Text] [Journal Information] [Subscribe] [Scholar Register] [Received: 02/01/2020] [Revised: 10/14/2020] [Accepted: 11/10/2020] [Indexed: 01/19/2023]
Abstract
The experimental study of electroencephalographic slow wave sleep (SWS) stretches over more than half a century and has corroborated its importance for basic physiological processes, such as brain plasticity, metabolism and immune system functioning. Alterations of SWS in aging or pathological conditions suggest that modulating SWS might constitute a window for clinically relevant interventions. This work provides a systematic and integrative review of SWS modulation through non-invasive brain stimulation in humans. A literature search using PubMed, conducted in May 2020, identified 3220 studies, of which 82 fulfilled inclusion criteria. Three approaches have been adopted to modulate the macro- and microstructure of SWS, namely auditory, transcranial electrical and transcranial magnetic stimulation. Our current knowledge about the modulatory mechanisms, the space of stimulation parameters and the physiological and behavioral effects are reported and evaluated. The integration of findings suggests that sleep slow wave modulation bears the potential to promote our understanding of the functions of SWS and to develop new treatments for conditions of disrupted SWS.
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Affiliation(s)
- Kristoffer D Fehér
- University Hospital of Psychiatry and Psychotherapy, University of Bern, Switzerland
| | - Marina Wunderlin
- University Hospital of Old Age Psychiatry and Psychotherapy, University of Bern, Switzerland
| | - Jonathan G Maier
- University Hospital of Psychiatry and Psychotherapy, University of Bern, Switzerland
| | - Elisabeth Hertenstein
- University Hospital of Psychiatry and Psychotherapy, University of Bern, Switzerland
| | - Carlotta L Schneider
- University Hospital of Psychiatry and Psychotherapy, University of Bern, Switzerland
| | - Christian Mikutta
- University Hospital of Psychiatry and Psychotherapy, University of Bern, Switzerland; Privatklinik Meiringen, Meiringen, Switzerland
| | - Marc A Züst
- University Hospital of Old Age Psychiatry and Psychotherapy, University of Bern, Switzerland
| | - Stefan Klöppel
- University Hospital of Old Age Psychiatry and Psychotherapy, University of Bern, Switzerland
| | - Christoph Nissen
- University Hospital of Psychiatry and Psychotherapy, University of Bern, Switzerland.
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Rojas M, Chávez-Castillo M, Pírela D, Ortega Á, Salazar J, Cano C, Chacín M, Riaño M, Batista MJ, Díaz EA, Rojas-Quintero J, Bermúdez V. Chronobiology and Chronotherapy in Depression: Current Knowledge and Chronotherapeutic Promises. CURRENT PSYCHIATRY RESEARCH AND REVIEWS 2021. [DOI: 10.2174/2666082216999201124152432] [Citation(s) in RCA: 1] [Impact Index Per Article: 0.3] [Reference Citation Analysis] [Abstract] [Track Full Text] [Journal Information] [Subscribe] [Scholar Register] [Indexed: 11/22/2022]
Abstract
Background:
Depression is a heavily prevalent mental disorder. Symptoms of depression
extend beyond mood, cognition, and behavior to include a spectrum of somatic manifestations in all
organic systems. Changes in sleep and neuroendocrine rhythms are especially prominent, and disruptions
of circadian rhythms have been closely related to the neurobiology of depression. With the
advent of increased research in chronobiology, various pathophysiologic mechanisms have been
proposed, including anomalies of sleep architecture, the effects of clock gene polymorphisms in
monoamine metabolism, and the deleterious impact of social zeitgebers. The identification of these
chronodisruptions has propelled the emergence of several chronotherapeutic strategies, both pharmacological
and non-pharmacological, with varying degrees of clinical evidence.
Methods:
The fundamental objective of this review is to integrate current knowledge about the role
of chronobiology and depression and to summarize the interventions developed to resynchronize
biorhythms both within an individual and with geophysical time.
Results:
We have found that among the non-pharmacological alternatives, triple chronotherapywhich
encompasses bright light therapy, sleep deprivation therapy, and consecutive sleep phase
advance therapy-has garnered the most considerable scientific interest. On the other hand,
agomelatine appears to be the most promising pharmacological option, given its unique melatonergic
pharmacodynamics.
Conclusions:
Research in chronotherapy as a treatment for depression is currently booming. Novel
interventions could play a significant role in adopting new options for the treatment of depression,
with Tripe Cronotherapy standing out as the most promising treatment.
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Affiliation(s)
- Milagros Rojas
- Endocrine and Metabolic Diseases Research Center, School of Medicine, University of Zulia, Maracaibo, Venezuela
| | - Mervin Chávez-Castillo
- Endocrine and Metabolic Diseases Research Center, School of Medicine, University of Zulia, Maracaibo, Venezuela
| | - Daniela Pírela
- Endocrine and Metabolic Diseases Research Center, School of Medicine, University of Zulia, Maracaibo, Venezuela
| | - Ángel Ortega
- Endocrine and Metabolic Diseases Research Center, School of Medicine, University of Zulia, Maracaibo, Venezuela
| | - Juan Salazar
- Endocrine and Metabolic Diseases Research Center, School of Medicine, University of Zulia, Maracaibo, Venezuela
| | - Clímaco Cano
- Endocrine and Metabolic Diseases Research Center, School of Medicine, University of Zulia, Maracaibo, Venezuela
| | - Maricarmen Chacín
- Universidad Simon Bolivar, Facultad de Ciencias de la Salud, Barranquilla, Colombia
| | - Manuel Riaño
- Universidad Simon Bolívar, Facultad de Ciencias Juridicas y Sociales, Cucuta, Colombia
| | - María Judith Batista
- Universidad Simon Bolívar, Facultad de Ciencias Juridicas y Sociales, Cucuta, Colombia
| | - Edgar Alexis Díaz
- Universidad Simon Bolívar, Facultad de Ciencias Juridicas y Sociales, Cucuta, Colombia
| | - Joselyn Rojas-Quintero
- Pulmonary and Critical Care Medicine Department, Brigham and Women’s Hospital, Harvard Medical School, Boston, MA 02115, United States
| | - Valmore Bermúdez
- Universidad Simon Bolivar, Facultad de Ciencias de la Salud, Barranquilla, Colombia
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Ioannou M, Wartenberg C, Greenbrook JTV, Larson T, Magnusson K, Schmitz L, Sjögren P, Stadig I, Szabó Z, Steingrimsson S. Sleep deprivation as treatment for depression: Systematic review and meta-analysis. Acta Psychiatr Scand 2021; 143:22-35. [PMID: 33145770 PMCID: PMC7839702 DOI: 10.1111/acps.13253] [Citation(s) in RCA: 45] [Impact Index Per Article: 11.3] [Reference Citation Analysis] [Abstract] [Key Words] [MESH Headings] [Track Full Text] [Download PDF] [Figures] [Journal Information] [Submit a Manuscript] [Subscribe] [Scholar Register] [Received: 03/25/2020] [Revised: 10/19/2020] [Accepted: 10/22/2020] [Indexed: 12/13/2022]
Abstract
OBJECTIVE To systematically review evidence on the efficacy and safety of sleep deprivation (SD) as a treatment option for patients with unipolar or bipolar depression. METHODS A systematic review according to PRISMA guidelines was conducted. The certainty of evidence was assessed using the GRADE approach. Controlled trials were included in efficacy analysis, case series for evaluating complications and qualitative studies for patients' experiences. RESULTS Eight controlled studies (368 patients), one qualitative study and seven case series (825 patients) were included. One week after treatment start, SD combined with standard treatment did not reduce depressive symptoms compared with standard treatment (standardized mean difference, SMD = -0.29, [95% confidence interval, CI: -0.84 to 0.25], p = 0.29). When excluding a study in elderly patients in a post hoc analysis, the difference was statistically significant (SMD = -0.54 ([95% CI: -0.86 to -0.22], p < 0.001)) but it diminished two weeks after treatment start. No superiority of SD was found compared with antidepressants, but SD may be superior to exercise in certain settings. It is uncertain whether SD affects quality of sleep, quality of life, everyday functioning or length of stay. Apart from switch to mania (ranging between 2.7% and 10.7%), no other serious complications were reported. CONCLUSION Sleep deprivation has been studied in a wide range of settings resulting in divergent results for the short-term efficacy on depressive symptoms. Post hoc analyses indicated that there may be a significant but transient effect in certain populations. Further studies should focus on identifying subgroups of responders as well as examining feasibility in routine clinical care.
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Affiliation(s)
- Michael Ioannou
- Region Västra GötalandPsykiatri AffektivaDepartment of PsychiatrySahlgrenska University HospitalGothenburgSweden
- Institute of Neuroscience and PhysiologySahlgrenska AcademyUniversity of GothenburgGothenburgSweden
| | | | - Josephine T. V. Greenbrook
- School of LawMason Institute for Medicine, Life Science and the LawUniversity of EdinburghEdinburghScotland
- Department of the Life Context and Health PromotionInstitute of Health and Care SciencesSahlgrenska AcademyUniversity of GothenburgGothenburgSweden
| | - Tomas Larson
- Region Västra GötalandPsykiatri AffektivaDepartment of PsychiatrySahlgrenska University HospitalGothenburgSweden
- Institute of Neuroscience and PhysiologySahlgrenska AcademyUniversity of GothenburgGothenburgSweden
| | - Kajsa Magnusson
- Region Västra GötalandMedical LibrarySahlgrenska University HospitalGothenburgSweden
| | - Linnea Schmitz
- Region Västra GötalandPsykiatri AffektivaDepartment of PsychiatrySahlgrenska University HospitalGothenburgSweden
| | | | - Ida Stadig
- Region Västra GötalandMedical LibrarySahlgrenska University HospitalGothenburgSweden
| | - Zoltán Szabó
- Region Västra GötalandPsykiatri AffektivaDepartment of PsychiatrySahlgrenska University HospitalGothenburgSweden
| | - Steinn Steingrimsson
- Region Västra GötalandPsykiatri AffektivaDepartment of PsychiatrySahlgrenska University HospitalGothenburgSweden
- Institute of Neuroscience and PhysiologySahlgrenska AcademyUniversity of GothenburgGothenburgSweden
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46
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Kurczewska E, Ferensztajn-Rochowiak E, Rybakowski F, Michalak M, Rybakowski J. Treatment-resistant depression: Neurobiological correlates and the effect of sleep deprivation with sleep phase advance for the augmentation of pharmacotherapy. World J Biol Psychiatry 2021; 22:58-69. [PMID: 32295463 DOI: 10.1080/15622975.2020.1755449] [Citation(s) in RCA: 5] [Impact Index Per Article: 1.3] [Reference Citation Analysis] [Abstract] [Key Words] [Track Full Text] [Journal Information] [Submit a Manuscript] [Subscribe] [Scholar Register] [Indexed: 12/17/2022]
Abstract
OBJECTIVES To assess the neurobiology of treatment-resistant depression (TRD), and factors connected with improvement after total sleep deprivation (TSD) with sleep phase advance (SPA), for the augmentation of pharmacotherapy. METHODS The study comprised 43 patients with TRD, (15 male, 28 female), aged 48 ± 13 years, with the illness duration 12 ± 9 years, and the depressive episode 8 ± 7 months. TRD was defined as a lack of significant improvement despite at least two antidepressant treatments and the augmentation with mood-stabilisers. Clinical improvement (response) was a reduction of ≥50% of points in the Hamilton Depression Rating Scale (HDRS), and the remission criterion was ≤7 points in HDRS, lasting until the 14th day after TSD + SPA. RESULTS TRD severity was associated with greater activity of the hypothalamic-pituitary-adrenal axis, the pro-inflammatory status of the immune system and lower reactivity of the hypothalamic-pituitary-thyroid axis. The response was achieved by 18 of 42 subjects, and connected with the later onset and shorter duration of the disease. In responders, there was a decrease in cortisol and interferon-gamma. In all subjects, a decrease in thyroid hormones was observed. CONCLUSIONS TRD can improve after augmentation of pharmacotherapy by TSD + SPA and some biological changes may be compatible with a decrease in allostatic load.
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Affiliation(s)
- Ewa Kurczewska
- Department of Adult Psychiatry, Poznan University of Medical Sciences, Poznan, Poland
| | | | - Filip Rybakowski
- Department of Adult Psychiatry, Poznan University of Medical Sciences, Poznan, Poland
| | - Michał Michalak
- Department of Computer Science and Statistics, Poznan University of Medical Sciences, Poznan, Poland
| | - Janusz Rybakowski
- Department of Adult Psychiatry, Poznan University of Medical Sciences, Poznan, Poland.,Department of Psychiatric Nursing, Poznan University of Medical Sciences, Poznan, Poland
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47
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Haarsma J, Harmer CJ, Tamm S. A continuum hypothesis of psychotomimetic rapid antidepressants. Brain Neurosci Adv 2021; 5:23982128211007772. [PMID: 34017922 PMCID: PMC8114748 DOI: 10.1177/23982128211007772] [Citation(s) in RCA: 1] [Impact Index Per Article: 0.3] [Reference Citation Analysis] [Abstract] [Key Words] [Track Full Text] [Download PDF] [Figures] [Journal Information] [Subscribe] [Scholar Register] [Received: 09/30/2020] [Accepted: 03/08/2021] [Indexed: 01/10/2023] Open
Abstract
Ketamine, classical psychedelics and sleep deprivation are associated with rapid effects on depression. Interestingly, these interventions also have common psychotomimetic actions, mirroring aspects of psychosis such as an altered sense of self, perceptual distortions and distorted thinking. This raises the question whether these interventions might be acute antidepressants through the same mechanisms that underlie some of their psychotomimetic effects. That is, perhaps some symptoms of depression can be understood as occupying the opposite end of a spectrum where elements of psychosis can be found on the other side. This review aims at reviewing the evidence underlying a proposed continuum hypothesis of psychotomimetic rapid antidepressants, suggesting that a range of psychotomimetic interventions are also acute antidepressants as well as trying to explain these common features in a hierarchical predictive coding framework, where we hypothesise that these interventions share a common mechanism by increasing the flexibility of prior expectations. Neurobiological mechanisms at play and the role of different neuromodulatory systems affected by these interventions and their role in controlling the precision of prior expectations and new sensory evidence will be reviewed. The proposed hypothesis will also be discussed in relation to other existing theories of antidepressants. We also suggest a number of novel experiments to test the hypothesis and highlight research areas that could provide further insights, in the hope to better understand the acute antidepressant properties of these interventions.
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Affiliation(s)
- Joost Haarsma
- Wellcome Centre for Human Neuroimaging, University College London, London, UK
| | - Catherine J Harmer
- Department of Psychiatry and Oxford Health NHS Foundation Trust, Warneford Hospital, University of Oxford, Oxford, UK
| | - Sandra Tamm
- Department of Psychiatry and Oxford Health NHS Foundation Trust, Warneford Hospital, University of Oxford, Oxford, UK
- Stress Research Institute, Department of Psychology, Stockholm University, Stockholm, Sweden
- Department of Clinical Neuroscience, Karolinska Institute, Stockholm, Sweden
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48
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Ioannou M, Szabó Z, Widmark-Jensen M, Vyrinis G, Karlsson C, Steingrimsson S. Total Sleep Deprivation Followed by Bright Light Therapy as Rapid Relief for Depression: A Pragmatic Randomized Controlled Trial. Front Psychiatry 2021; 12:705090. [PMID: 34526921 PMCID: PMC8435586 DOI: 10.3389/fpsyt.2021.705090] [Citation(s) in RCA: 1] [Impact Index Per Article: 0.3] [Reference Citation Analysis] [Abstract] [Key Words] [Track Full Text] [Download PDF] [Figures] [Journal Information] [Submit a Manuscript] [Subscribe] [Scholar Register] [Received: 05/04/2021] [Accepted: 08/11/2021] [Indexed: 11/17/2022] Open
Abstract
Background: Total sleep deprivation (TSD) combined with bright light therapy (BLT) has been suggested as a valuable add-on to standard treatment for rapid relief of depression. However, there is a lack of randomized controlled trials in real-life clinical settings. The aim of this pragmatic randomized clinical trial was to investigate the effectiveness, acceptance, and feasibility of TSD combined with BLT as add-on to standard treatment for depression in a real-life clinical setting. Methods: Thirty-three inpatients were randomly assigned to either: a) an intervention group receiving a single-night TSD followed by 6 days BLT (10.000 lux, 30 min/day) as add-on to standard treatment; or b) a control group receiving a short sleep-hygiene consultation in addition to standard treatment. The follow-up period was 1 week. Results: No statistical differences were found in response rates, reduction of depressive and insomnia symptoms, length of stay, readmission rate, and clinical improvement. Both groups reported positive experiences toward the received treatment with low drop-out rates. Conclusions: One-night TSD followed by BLT was not effective as a rapid relief for depression at 1-week follow-up; however, the treatment was feasible and well-tolerated.
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Affiliation(s)
- Michael Ioannou
- University of Gothenburg, Sahlgrenska Academy, Institute of Neuroscience and Physiology, Gothenburg, Sweden.,Region Västra Götaland, Psykiatri Affektiva, Department of Psychiatry, Sahlgrenska University Hospital, Gothenburg, Sweden
| | - Zoltán Szabó
- Region Västra Götaland, Psykiatri Affektiva, Department of Psychiatry, Sahlgrenska University Hospital, Gothenburg, Sweden
| | - Mats Widmark-Jensen
- Region Halland, Varberg's Hospital, Anaesthesia and Intensive Care, Varberg, Sweden
| | - Georgios Vyrinis
- Region Västra Götaland, Psykiatri Affektiva, Department of Psychiatry, Sahlgrenska University Hospital, Gothenburg, Sweden
| | - Christopher Karlsson
- Region Västra Götaland, Psykiatri Affektiva, Department of Psychiatry, Sahlgrenska University Hospital, Gothenburg, Sweden
| | - Steinn Steingrimsson
- University of Gothenburg, Sahlgrenska Academy, Institute of Neuroscience and Physiology, Gothenburg, Sweden.,Region Västra Götaland, Psykiatri Affektiva, Department of Psychiatry, Sahlgrenska University Hospital, Gothenburg, Sweden
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49
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Hu B, Liu C, Mou T, Luo F, Lv T, Qian C, Zhang J, Ye M, Liu Z. Meta-Analysis of Sleep Deprivation Effects on Patients With Depression. Front Psychiatry 2021; 12:783091. [PMID: 34916978 PMCID: PMC8669147 DOI: 10.3389/fpsyt.2021.783091] [Citation(s) in RCA: 7] [Impact Index Per Article: 1.8] [Reference Citation Analysis] [Abstract] [Key Words] [Track Full Text] [Download PDF] [Figures] [Journal Information] [Submit a Manuscript] [Subscribe] [Scholar Register] [Received: 10/01/2021] [Accepted: 11/08/2021] [Indexed: 11/13/2022] Open
Abstract
Objective: Depression is a common disorder with a high recurrence rate. Since the effect of sleep deprivation on depression in existing studies were inconsistent, the present study aimed to reassess the effects of SD on patients by performing a meta-analysis of updated research. Methods: PubMed, Embase, the Cochrane Library, and Web of Science were searched for articles before January 20th, 2021. Data on participant characteristics, SD characteristics, adjunctive method and tests for depression were extracted. A comprehensive analysis was conducted to assess the effect of SD on depression and subgroup analysis was used to determine the sources of heterogeneity. Results: In total, 8 articles were included. An SD time of <7 days slightly worsened depression levels [0.24 (-0.21, 0.69); I 2 = 0%; P = 0.43], a time of 7-14 days had antidepressant effects [-1.52 (-2.07, -0.97); I 2 = 19.6%; P = 0.288], and a time of more than 14 days also worsened depression [0.76 (0.12, 1.40); I 2 = 43.7%; P = 0.169]. Conclusion: SD may serve as an effective antidepressant measure in humans when the time was 7-14 days, while a time of <7 days and more than 14 days worsened depression.
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Affiliation(s)
- Baiqi Hu
- Department of Psychiatry, Shaoxing Seventh People's Hospital, Affiliated Mental Health Center, Medical College of Shaoxing University, Shaoxing, China.,Department of Behavioral Neurosciences, Science Research Center of Medical School, Shaoxing University, Shaoxing, China.,Department of Neurology, Shaoxing Hospital, China Medical University, Shaoxing, China
| | - Chunyan Liu
- Department of Orthopedics, Shaoxing People's Hospital, The First Affiliated Hospital of Shaoxing University, Shaoxing, China
| | - Tingting Mou
- Department of Behavioral Neurosciences, Science Research Center of Medical School, Shaoxing University, Shaoxing, China
| | - Fangyi Luo
- Department of Behavioral Neurosciences, Science Research Center of Medical School, Shaoxing University, Shaoxing, China
| | - Tingting Lv
- Department of Behavioral Neurosciences, Science Research Center of Medical School, Shaoxing University, Shaoxing, China
| | - Chao Qian
- Department of Psychiatry, Shaoxing Seventh People's Hospital, Affiliated Mental Health Center, Medical College of Shaoxing University, Shaoxing, China
| | - Jian Zhang
- Department of Behavioral Neurosciences, Science Research Center of Medical School, Shaoxing University, Shaoxing, China
| | - Mengfei Ye
- Department of Psychiatry, Shaoxing Seventh People's Hospital, Affiliated Mental Health Center, Medical College of Shaoxing University, Shaoxing, China
| | - Zheng Liu
- Department of Behavioral Neurosciences, Science Research Center of Medical School, Shaoxing University, Shaoxing, China
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50
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Bhat A, Pires AS, Tan V, Babu Chidambaram S, Guillemin GJ. Effects of Sleep Deprivation on the Tryptophan Metabolism. Int J Tryptophan Res 2020; 13:1178646920970902. [PMID: 33281456 PMCID: PMC7686593 DOI: 10.1177/1178646920970902] [Citation(s) in RCA: 36] [Impact Index Per Article: 7.2] [Reference Citation Analysis] [Abstract] [Key Words] [Track Full Text] [Download PDF] [Figures] [Journal Information] [Subscribe] [Scholar Register] [Received: 02/27/2020] [Accepted: 10/12/2020] [Indexed: 12/11/2022] Open
Abstract
Sleep has a regulatory role in maintaining metabolic homeostasis and cellular functions. Inadequate sleep time and sleep disorders have become more prevalent in the modern lifestyle. Fragmentation of sleep pattern alters critical intracellular second messengers and neurotransmitters which have key functions in brain development and behavioral functions. Tryptophan metabolism has also been found to get altered in SD and it is linked to various neurodegenerative diseases. The kynurenine pathway is a major regulator of the immune response. Adequate sleep alleviates neuroinflammation and facilitates the cellular clearance of metabolic toxins produced within the brain, while sleep deprivation activates the enzymatic degradation of tryptophan via the kynurenine pathway, which results in an increased accumulation of neurotoxic metabolites. SD causes increased production and accumulation of kynurenic acid in various regions of the brain. Higher levels of kynurenic acid have been found to trigger apoptosis, leads to cognitive decline, and inhibit neurogenesis. This review aims to link the impact of sleep deprivation on tryptophan metabolism and associated complication in the brain.
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Affiliation(s)
- Abid Bhat
- Department of Pharmacology, JSS College of Pharmacy, JSS Academy of Higher Education & Research, Mysuru, Karnataka, India.,Department of Biomedical Sciences, Faculty of Medicine and Health Sciences, Macquarie University, Sydney, Australia
| | - Ananda Staats Pires
- Department of Biomedical Sciences, Faculty of Medicine and Health Sciences, Macquarie University, Sydney, Australia
| | - Vanessa Tan
- Department of Biomedical Sciences, Faculty of Medicine and Health Sciences, Macquarie University, Sydney, Australia
| | - Saravana Babu Chidambaram
- Department of Pharmacology, JSS College of Pharmacy, JSS Academy of Higher Education & Research, Mysuru, Karnataka, India
| | - Gilles J Guillemin
- Department of Biomedical Sciences, Faculty of Medicine and Health Sciences, Macquarie University, Sydney, Australia
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