Marco Menchetti, Francesco Biscarini, Giombattista Sallemi, Elena Antelmi, Christian Franceschini, Stefano Vandi, Giulia Neccia, Valentina Baldini, Giuseppe Plazzi, Fabio Pizza
Study objectives: Pseudocataplexy is a rare functional neurological disorder that mimics cataplexy, pathognomonic for narcolepsy type 1 (NT1). We describe the psychiatric comorbidity and personality traits of patients with pseudocataplexy versus NT1 cases.
Methods: The case-control observational study enrolled consecutive patients with pseudocataplexy and a control group of age-matched consecutive NT1 patients. The diagnostic work-up included a structured interview, 48-hour polysomnography, multiple sleep latency test, cataplexy provoking test, and hypocretin-1 measurement in cerebrospinal fluid. All participants were administered Beck Depression Inventory, State-Trait Anxiety Inventory, Patient Health Questionnaire-15 (PHQ-15), Personality Inventory for DSM-5 brief form, and quality-of-life (QoL) measurement by 36-item Short Form health survey (SF-36).
Results: Fifteen patients with pseudocataplexy and 30 with NT1 were included. Despite the suspicion of possible cataplexy, none of the pseudocataplexy participants fulfilled international diagnostic criteria for NT1. Pseudocataplexy patients presented higher rates of moderate state anxiety (40% vs. 10%, p = 0.018), medium level of somatic symptoms, defined by PHQ-15 score > 10 (66.7% vs. 16.7%, p = 0.003), and a trend towards moderate-to-severe depressive symptoms (33.3% vs. 10%, p = 0.054) compared to NT1. No significant differences in personality traits emerged. Pseudocataplexy patients had worse QoL profiles in almost all SF-36 domains including physical (mean ± SD: 37.7 ± 9.88 vs. 51.13 ± 7.81, p < 0.001) and mental (mean ± SD: 33.36 ± 12.69 vs.42.76 ± 11.34, p = 0.02) summary scores.
Conclusions: Patients with pseudocataplexy present more severe psychiatric symptoms and a lower QoL profile in comparison with patients with NT1. The severe somatoform and affection impairment in pseudocataplexy may explain the poorer QoL and should require a tailored therapeutic approach.
{"title":"Phenomenology and psychiatric correlates of pseudocataplexy.","authors":"Marco Menchetti, Francesco Biscarini, Giombattista Sallemi, Elena Antelmi, Christian Franceschini, Stefano Vandi, Giulia Neccia, Valentina Baldini, Giuseppe Plazzi, Fabio Pizza","doi":"10.1093/sleep/zsad234","DOIUrl":"10.1093/sleep/zsad234","url":null,"abstract":"<p><strong>Study objectives: </strong>Pseudocataplexy is a rare functional neurological disorder that mimics cataplexy, pathognomonic for narcolepsy type 1 (NT1). We describe the psychiatric comorbidity and personality traits of patients with pseudocataplexy versus NT1 cases.</p><p><strong>Methods: </strong>The case-control observational study enrolled consecutive patients with pseudocataplexy and a control group of age-matched consecutive NT1 patients. The diagnostic work-up included a structured interview, 48-hour polysomnography, multiple sleep latency test, cataplexy provoking test, and hypocretin-1 measurement in cerebrospinal fluid. All participants were administered Beck Depression Inventory, State-Trait Anxiety Inventory, Patient Health Questionnaire-15 (PHQ-15), Personality Inventory for DSM-5 brief form, and quality-of-life (QoL) measurement by 36-item Short Form health survey (SF-36).</p><p><strong>Results: </strong>Fifteen patients with pseudocataplexy and 30 with NT1 were included. Despite the suspicion of possible cataplexy, none of the pseudocataplexy participants fulfilled international diagnostic criteria for NT1. Pseudocataplexy patients presented higher rates of moderate state anxiety (40% vs. 10%, p = 0.018), medium level of somatic symptoms, defined by PHQ-15 score > 10 (66.7% vs. 16.7%, p = 0.003), and a trend towards moderate-to-severe depressive symptoms (33.3% vs. 10%, p = 0.054) compared to NT1. No significant differences in personality traits emerged. Pseudocataplexy patients had worse QoL profiles in almost all SF-36 domains including physical (mean ± SD: 37.7 ± 9.88 vs. 51.13 ± 7.81, p < 0.001) and mental (mean ± SD: 33.36 ± 12.69 vs.42.76 ± 11.34, p = 0.02) summary scores.</p><p><strong>Conclusions: </strong>Patients with pseudocataplexy present more severe psychiatric symptoms and a lower QoL profile in comparison with patients with NT1. The severe somatoform and affection impairment in pseudocataplexy may explain the poorer QoL and should require a tailored therapeutic approach.</p>","PeriodicalId":49514,"journal":{"name":"Sleep","volume":null,"pages":null},"PeriodicalIF":5.3,"publicationDate":"2024-11-08","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"10316192","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Study objectives: Restless legs syndrome (RLS) is a circadian rhythm related sensorimotor disorder due to brain iron deficiency, with lesion sites at the putamen and substantia nigra. However, epilepsy is a disease with abnormal electric discharge from the cortex and can be triggered with iron disequilibrium. We designed a case-control study to discover the association between epilepsy and RLS.
Methods: A total of 24 patients with epilepsy and RLS and 72 patients with epilepsy without RLS were included. Most of the patients underwent polysomnography and video electroencephalogram tests and took sleep questionnaires. We collected information on seizure characteristics, including general or focal onset, epileptogenic focus, current antiseizure medications, medically responsive epilepsy or refractory epilepsy, and nocturnal attacks. The sleep architectures of the two groups were compared. We analyzed the risk factors for RLS using multivariate logistic regression.
Results: Among the patients with epilepsy, the occurrence of RLS was associated with refractory epilepsy (OR 6.422, p = 0.002) and nocturnal seizures (OR 4.960, p = 0.005). Sleep parameters were not significantly associated with RLS status. Quality of life was significantly impaired in the group with RLS in both the physical and mental domains.
Conclusions: Refractory epilepsy and nocturnal seizures were strongly correlated with RLS in patients with epilepsy. RLS should be considered a predictable comorbidity in patients with epilepsy. The management of RLS not only led to better control of the patient's epilepsy but also improved their quality of life.
{"title":"Restless legs syndrome in patients with epilepsy: risk analysis, polysomnography, and quality of life evaluation.","authors":"Ying-Sheng Li, Wei-Chih Yeh, Ya-Hsien Chang, Chung-Yao Hsu","doi":"10.1093/sleep/zsad054","DOIUrl":"10.1093/sleep/zsad054","url":null,"abstract":"<p><strong>Study objectives: </strong>Restless legs syndrome (RLS) is a circadian rhythm related sensorimotor disorder due to brain iron deficiency, with lesion sites at the putamen and substantia nigra. However, epilepsy is a disease with abnormal electric discharge from the cortex and can be triggered with iron disequilibrium. We designed a case-control study to discover the association between epilepsy and RLS.</p><p><strong>Methods: </strong>A total of 24 patients with epilepsy and RLS and 72 patients with epilepsy without RLS were included. Most of the patients underwent polysomnography and video electroencephalogram tests and took sleep questionnaires. We collected information on seizure characteristics, including general or focal onset, epileptogenic focus, current antiseizure medications, medically responsive epilepsy or refractory epilepsy, and nocturnal attacks. The sleep architectures of the two groups were compared. We analyzed the risk factors for RLS using multivariate logistic regression.</p><p><strong>Results: </strong>Among the patients with epilepsy, the occurrence of RLS was associated with refractory epilepsy (OR 6.422, p = 0.002) and nocturnal seizures (OR 4.960, p = 0.005). Sleep parameters were not significantly associated with RLS status. Quality of life was significantly impaired in the group with RLS in both the physical and mental domains.</p><p><strong>Conclusions: </strong>Refractory epilepsy and nocturnal seizures were strongly correlated with RLS in patients with epilepsy. RLS should be considered a predictable comorbidity in patients with epilepsy. The management of RLS not only led to better control of the patient's epilepsy but also improved their quality of life.</p>","PeriodicalId":49514,"journal":{"name":"Sleep","volume":null,"pages":null},"PeriodicalIF":5.6,"publicationDate":"2024-06-13","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"10819151","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Christopher M Carosella, Rebecca F Gottesman, Anna Kucharska-Newton, Pamela L Lutsey, Adam P Spira, Naresh M Punjabi, Andrea L C Schneider, Kelsie M Full, Emily L Johnson
Study objective: Sleep apnea is associated with unexplained epilepsy in older adults in small studies. We sought to determine the relationship between sleep apnea and additional sleep characteristics and late-onset epilepsy (LOE), adjusting for comorbidities, using data from the large, prospective Atherosclerosis Risk in Communities (ARIC) Study cohort.
Methods: We used Medicare claims to identify cases of LOE in ARIC participants. We used polysomnography data from 1309 ARIC participants who also participated in the Sleep Heart Health Study in 1995-1998, and demographic and comorbidity data from ARIC. Later risk of LOE was evaluated using survival analysis with a competing risk of death. We also used survival analysis in 2672 ARIC participants to identify the association between self-reported obstructive sleep apnea (2011-2013), and the risk of subsequent LOE.
Results: Late-midlife oxygen desaturation to less than 80% during sleep was associated with subsequent development of LOE, adjusted subhazard ratio 3.28 (1.18-9.08), but the apnea-hypopnea index was not related. Participant report of diagnosis of sleep apnea in 2011-2013 was also associated with subsequent LOE, adjusted subhazard ratio 2.59 (1.24-5.39).
Conclusions: Sleep apnea and oxygen saturation nadir during sleep are associated with LOE, independently of hypertension and other comorbidities. These potentially modifiable risk factors could have large clinical implications for LOE.
{"title":"Sleep apnea, hypoxia, and late-onset epilepsy: the Atherosclerosis Risk in Communities study.","authors":"Christopher M Carosella, Rebecca F Gottesman, Anna Kucharska-Newton, Pamela L Lutsey, Adam P Spira, Naresh M Punjabi, Andrea L C Schneider, Kelsie M Full, Emily L Johnson","doi":"10.1093/sleep/zsad233","DOIUrl":"10.1093/sleep/zsad233","url":null,"abstract":"<p><strong>Study objective: </strong>Sleep apnea is associated with unexplained epilepsy in older adults in small studies. We sought to determine the relationship between sleep apnea and additional sleep characteristics and late-onset epilepsy (LOE), adjusting for comorbidities, using data from the large, prospective Atherosclerosis Risk in Communities (ARIC) Study cohort.</p><p><strong>Methods: </strong>We used Medicare claims to identify cases of LOE in ARIC participants. We used polysomnography data from 1309 ARIC participants who also participated in the Sleep Heart Health Study in 1995-1998, and demographic and comorbidity data from ARIC. Later risk of LOE was evaluated using survival analysis with a competing risk of death. We also used survival analysis in 2672 ARIC participants to identify the association between self-reported obstructive sleep apnea (2011-2013), and the risk of subsequent LOE.</p><p><strong>Results: </strong>Late-midlife oxygen desaturation to less than 80% during sleep was associated with subsequent development of LOE, adjusted subhazard ratio 3.28 (1.18-9.08), but the apnea-hypopnea index was not related. Participant report of diagnosis of sleep apnea in 2011-2013 was also associated with subsequent LOE, adjusted subhazard ratio 2.59 (1.24-5.39).</p><p><strong>Conclusions: </strong>Sleep apnea and oxygen saturation nadir during sleep are associated with LOE, independently of hypertension and other comorbidities. These potentially modifiable risk factors could have large clinical implications for LOE.</p>","PeriodicalId":49514,"journal":{"name":"Sleep","volume":null,"pages":null},"PeriodicalIF":5.3,"publicationDate":"2024-06-13","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11168763/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"10165442","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Mark W DiFrancesco, Maryam Alsameen, Marie-Pierre St-Onge, Kara M Duraccio, Dean W Beebe
Study objectives: Poor sleep in adolescents can increase the risk of obesity, possibly due to changes in dietary patterns. Prior neuroimaging evidence, mostly in adults, suggests that lacking sleep results in increased response to food cues in reward-processing brain regions. Needed is a clarification of the mechanisms by which food reward processing is altered by the kind of chronic sleep restriction (SR) typically experienced by adolescents. This study aimed to elucidate the impact of sleep duration on response to visual food stimuli in healthy adolescents using functional neuroimaging, hypothesizing increased reward processing response after SR compared to a well-rested condition.
Methods: Thirty-nine healthy adolescents, 14-17 years old, completed a 3-week protocol: (1) sleep phase stabilization; (2) SR (~6.5 h nightly); and (3) healthy sleep (HS) duration (~9 h nightly). Participants underwent functional MRI while performing a visual food paradigm. Contrasts of food versus nonfood responses were compared within-subject between conditions of SR and HS.
Results: Under SR, there was a greater response to food stimuli compared to HS in a voxel cluster including the left ventral tegmental area and substantia nigra. No change in food appeal rating due to the sleep manipulation was detected.
Conclusions: Outcomes of this study suggest that SR, as commonly experienced by healthy adolescents, results in the elevated dopaminergic drive of the reward network that may augment motivation to seek food in the context of individual food appeal and inhibitory profiles. Countermeasures that reduce food salience could include promoting consistent HS habits.
{"title":"Altered neuronal response to visual food stimuli in adolescents undergoing chronic sleep restriction.","authors":"Mark W DiFrancesco, Maryam Alsameen, Marie-Pierre St-Onge, Kara M Duraccio, Dean W Beebe","doi":"10.1093/sleep/zsad036","DOIUrl":"10.1093/sleep/zsad036","url":null,"abstract":"<p><strong>Study objectives: </strong>Poor sleep in adolescents can increase the risk of obesity, possibly due to changes in dietary patterns. Prior neuroimaging evidence, mostly in adults, suggests that lacking sleep results in increased response to food cues in reward-processing brain regions. Needed is a clarification of the mechanisms by which food reward processing is altered by the kind of chronic sleep restriction (SR) typically experienced by adolescents. This study aimed to elucidate the impact of sleep duration on response to visual food stimuli in healthy adolescents using functional neuroimaging, hypothesizing increased reward processing response after SR compared to a well-rested condition.</p><p><strong>Methods: </strong>Thirty-nine healthy adolescents, 14-17 years old, completed a 3-week protocol: (1) sleep phase stabilization; (2) SR (~6.5 h nightly); and (3) healthy sleep (HS) duration (~9 h nightly). Participants underwent functional MRI while performing a visual food paradigm. Contrasts of food versus nonfood responses were compared within-subject between conditions of SR and HS.</p><p><strong>Results: </strong>Under SR, there was a greater response to food stimuli compared to HS in a voxel cluster including the left ventral tegmental area and substantia nigra. No change in food appeal rating due to the sleep manipulation was detected.</p><p><strong>Conclusions: </strong>Outcomes of this study suggest that SR, as commonly experienced by healthy adolescents, results in the elevated dopaminergic drive of the reward network that may augment motivation to seek food in the context of individual food appeal and inhibitory profiles. Countermeasures that reduce food salience could include promoting consistent HS habits.</p>","PeriodicalId":49514,"journal":{"name":"Sleep","volume":null,"pages":null},"PeriodicalIF":5.6,"publicationDate":"2024-04-12","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11009031/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"10748953","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Xiang Fu, Xiao-Jie Wan, Jun-Yi Liu, Qian Sun, Yun Shen, Jie Li, Cheng-Jie Mao, Quan-Hong Ma, Fen Wang, Chun-Feng Liu
Study objectives: Mounting evidence indicated the correlation between sleep and cerebral small vessel disease (CSVD). However, little is known about the exact causality between poor sleep and white matter injury, a typical signature of CSVD, as well as the underlying mechanisms.
Methods: Spontaneously hypertensive rats (SHR) and control Wistar Kyoto rats were subjected to sleep fragmentation (SF) for 16 weeks. The effects of chronic sleep disruption on the deep white matter and cognitive performance were observed.
Results: SHR were validated as a rat model for CSVD. Fragmented sleep induced strain-dependent white matter abnormalities, characterized by reduced myelin integrity, impaired oligodendrocytes precursor cells (OPC) maturation and pro-inflammatory microglial polarization. Partially reversible phenotypes of OPC and microglia were observed in parallel following sleep recovery.
Conclusions: Long-term SF-induced pathological effects on the deep white matter in a rat model of CSVD. The pro-inflammatory microglial activation and the block of OPC maturation may be involved in the mechanisms linking sleep to white matter injury.
{"title":"Effects of sleep fragmentation on white matter pathology in a rat model of cerebral small vessel disease.","authors":"Xiang Fu, Xiao-Jie Wan, Jun-Yi Liu, Qian Sun, Yun Shen, Jie Li, Cheng-Jie Mao, Quan-Hong Ma, Fen Wang, Chun-Feng Liu","doi":"10.1093/sleep/zsad225","DOIUrl":"10.1093/sleep/zsad225","url":null,"abstract":"<p><strong>Study objectives: </strong>Mounting evidence indicated the correlation between sleep and cerebral small vessel disease (CSVD). However, little is known about the exact causality between poor sleep and white matter injury, a typical signature of CSVD, as well as the underlying mechanisms.</p><p><strong>Methods: </strong>Spontaneously hypertensive rats (SHR) and control Wistar Kyoto rats were subjected to sleep fragmentation (SF) for 16 weeks. The effects of chronic sleep disruption on the deep white matter and cognitive performance were observed.</p><p><strong>Results: </strong>SHR were validated as a rat model for CSVD. Fragmented sleep induced strain-dependent white matter abnormalities, characterized by reduced myelin integrity, impaired oligodendrocytes precursor cells (OPC) maturation and pro-inflammatory microglial polarization. Partially reversible phenotypes of OPC and microglia were observed in parallel following sleep recovery.</p><p><strong>Conclusions: </strong>Long-term SF-induced pathological effects on the deep white matter in a rat model of CSVD. The pro-inflammatory microglial activation and the block of OPC maturation may be involved in the mechanisms linking sleep to white matter injury.</p>","PeriodicalId":49514,"journal":{"name":"Sleep","volume":null,"pages":null},"PeriodicalIF":5.6,"publicationDate":"2024-04-12","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"10075521","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Marieclaire Overton, Johan Skoog, Erika J Laukka, Timothy Hadarsson Bodin, Alexander Darin Mattsson, Linnea Sjöberg, Scott M Hofer, Lena Johansson, Jenni Kulmala, Miia Kivipelto, Alina Solomon, Ingmar Skoog, Ingemar Kåreholt, Shireen Sindi
Study objectives: We examined and compared cross-sectional and longitudinal associations between self-reported sleep disturbances and various cognitive domains in five separate Nordic European longitudinal aging studies (baseline N = 5631, mean age = 77.7, mean follow-up = 4.16 years).
Methods: Comparable sleep parameters across studies included reduced sleep duration/quality, insomnia symptoms (sleep latency, waking up at night, and early awakenings), short and long sleep duration, and daytime napping. The cognitive domains were episodic memory, verbal fluency, perceptual speed, executive functioning, and global cognition (aggregated measure). A series of mixed linear models were run separately in each study and then compared to assess the level and rate of change in cognitive functioning across each sleep disturbance parameter. Models were adjusted for age, sex, education, hypnotic usage, depressive symptoms, lifestyle factors, cardiovascular, and metabolic conditions. By using a coordinated analytic approach, comparable construct-level measurements were generated, and results from identical statistical models were qualitatively compared across studies.
Results: While the pattern of statistically significant results varied across studies, subjective sleep disturbances were consistently associated with worse cognition and steeper cognitive decline. Insomnia symptoms were associated with poorer episodic memory and participants sleeping less or more than 7-8 hours had a steeper decline in perceptual speed. In addition, daytime napping (>2 hours) was cross-sectionally and longitudinally associated with all examined cognitive domains. Most observed associations were study-specific (except for daytime napping), and a majority of association estimates remained significant after adjusting for covariates.
Conclusion: This rigorous multicenter investigation further supports the importance of sleep disturbance, including insomnia, long and short sleep duration, and daytime napping on baseline cognitive functioning and rate of change among older adults. These sleep factors may be targeted in future lifestyle interventions to reduce cognitive decline.
{"title":"Sleep disturbances and change in multiple cognitive domains among older adults: a multicenter study of five Nordic cohorts.","authors":"Marieclaire Overton, Johan Skoog, Erika J Laukka, Timothy Hadarsson Bodin, Alexander Darin Mattsson, Linnea Sjöberg, Scott M Hofer, Lena Johansson, Jenni Kulmala, Miia Kivipelto, Alina Solomon, Ingmar Skoog, Ingemar Kåreholt, Shireen Sindi","doi":"10.1093/sleep/zsad244","DOIUrl":"10.1093/sleep/zsad244","url":null,"abstract":"<p><strong>Study objectives: </strong>We examined and compared cross-sectional and longitudinal associations between self-reported sleep disturbances and various cognitive domains in five separate Nordic European longitudinal aging studies (baseline N = 5631, mean age = 77.7, mean follow-up = 4.16 years).</p><p><strong>Methods: </strong>Comparable sleep parameters across studies included reduced sleep duration/quality, insomnia symptoms (sleep latency, waking up at night, and early awakenings), short and long sleep duration, and daytime napping. The cognitive domains were episodic memory, verbal fluency, perceptual speed, executive functioning, and global cognition (aggregated measure). A series of mixed linear models were run separately in each study and then compared to assess the level and rate of change in cognitive functioning across each sleep disturbance parameter. Models were adjusted for age, sex, education, hypnotic usage, depressive symptoms, lifestyle factors, cardiovascular, and metabolic conditions. By using a coordinated analytic approach, comparable construct-level measurements were generated, and results from identical statistical models were qualitatively compared across studies.</p><p><strong>Results: </strong>While the pattern of statistically significant results varied across studies, subjective sleep disturbances were consistently associated with worse cognition and steeper cognitive decline. Insomnia symptoms were associated with poorer episodic memory and participants sleeping less or more than 7-8 hours had a steeper decline in perceptual speed. In addition, daytime napping (>2 hours) was cross-sectionally and longitudinally associated with all examined cognitive domains. Most observed associations were study-specific (except for daytime napping), and a majority of association estimates remained significant after adjusting for covariates.</p><p><strong>Conclusion: </strong>This rigorous multicenter investigation further supports the importance of sleep disturbance, including insomnia, long and short sleep duration, and daytime napping on baseline cognitive functioning and rate of change among older adults. These sleep factors may be targeted in future lifestyle interventions to reduce cognitive decline.</p>","PeriodicalId":49514,"journal":{"name":"Sleep","volume":null,"pages":null},"PeriodicalIF":5.6,"publicationDate":"2024-03-11","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC10925948/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"10241671","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Study objectives: Little empirical work has investigated the associations between life stress (LS), insomnia, depression, and suicidality in multi-wave longitudinal studies. With three waves of data collection 1-year apart, this longitudinal study with a large sample of adolescents examined the predicting effects of LS on suicidality 1-year later and 2 years later and the mediating roles of insomnia and depression in the LS-suicidality link.
Methods: A total of 6995 adolescents (mean age = 14.86 years, 51.4% male) participated in a three-wave longitudinal study of behavior and health in Shandong, China. A self-administered structured questionnaire and standardized scales were used to assess suicidality (including suicidal thought [ST], suicide plan [SP], and suicide attempt [SA]), LS, insomnia, and depression in 2015 (T1), 1-year later (T2), and 2 years later (T3). Mediation effects were examined with path models.
Results: The overall prevalence rates of past-year suicidality were 13.4% at T1, 10.0% at T2, and 9.5% at T3, respectively. The prevalence rates of suicidality across T1-T3 significantly increased with elevated levels of baseline LS, insomnia, and depression (p < .001). Path models indicated that the relationship between baseline LS and suicidal ideation (i.e., ST/SP) 2 years later was significantly mediated by both insomnia and depression. Depression was also a significant mediator between LS and SA.
Conclusions: LS is a significant predictor of suicidality 1-2 years later in adolescents. Depression mediates the association between LS and suicidal ideation and suicide attempt while insomnia appears to be a mediator for suicidal ideation rather than suicide attempt.
{"title":"Life stress and suicidality mediated by insomnia and depressive symptoms in adolescents: a three-wave longitudinal study.","authors":"Xianchen Liu, Yanyun Yang, Zhen-Zhen Liu, Cun-Xian Jia","doi":"10.1093/sleep/zsad121","DOIUrl":"10.1093/sleep/zsad121","url":null,"abstract":"<p><strong>Study objectives: </strong>Little empirical work has investigated the associations between life stress (LS), insomnia, depression, and suicidality in multi-wave longitudinal studies. With three waves of data collection 1-year apart, this longitudinal study with a large sample of adolescents examined the predicting effects of LS on suicidality 1-year later and 2 years later and the mediating roles of insomnia and depression in the LS-suicidality link.</p><p><strong>Methods: </strong>A total of 6995 adolescents (mean age = 14.86 years, 51.4% male) participated in a three-wave longitudinal study of behavior and health in Shandong, China. A self-administered structured questionnaire and standardized scales were used to assess suicidality (including suicidal thought [ST], suicide plan [SP], and suicide attempt [SA]), LS, insomnia, and depression in 2015 (T1), 1-year later (T2), and 2 years later (T3). Mediation effects were examined with path models.</p><p><strong>Results: </strong>The overall prevalence rates of past-year suicidality were 13.4% at T1, 10.0% at T2, and 9.5% at T3, respectively. The prevalence rates of suicidality across T1-T3 significantly increased with elevated levels of baseline LS, insomnia, and depression (p < .001). Path models indicated that the relationship between baseline LS and suicidal ideation (i.e., ST/SP) 2 years later was significantly mediated by both insomnia and depression. Depression was also a significant mediator between LS and SA.</p><p><strong>Conclusions: </strong>LS is a significant predictor of suicidality 1-2 years later in adolescents. Depression mediates the association between LS and suicidal ideation and suicide attempt while insomnia appears to be a mediator for suicidal ideation rather than suicide attempt.</p>","PeriodicalId":49514,"journal":{"name":"Sleep","volume":null,"pages":null},"PeriodicalIF":5.6,"publicationDate":"2024-03-11","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"9475663","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Courtney M Quinlan, Xiao Chang, Michael March, Frank D Mentch, Hui-Qi Qu, Yichuan Liu, Joseph Glessner, Patrick M A Sleiman, Hakon Hakonarson
Study objectives: To identify genetic susceptibility variants in pediatric obstructive sleep apnea in European American and African American children.
Methods: A phenotyping algorithm using electronic medical records was developed to recruit cases with OSA and control subjects from the Center for Applied Genomics at Children's Hospital of Philadelphia (CHOP). Genome-wide association studies (GWAS) were performed in pediatric OSA cases and control subjects with European American (EA) and African American (AA) ancestry followed by meta-analysis and sex stratification.
Results: The algorithm accrued 1486 subjects (46.3% European American, 53.7% African American). We identified genomic loci at 1p36.22 and 15q26.1 that associated with OSA risk in EA and AA, respectively. We also revealed a shared risk locus at 18p11.32 (rs114124196, p = 1.72 × 10-8) across EA and AA populations. Additionally, association at 1q43 (rs12754698) and 2p25.1 (rs72775219) was identified in the male-only analysis of EA children with OSA, while association at 8q21.11 (rs6472959), 11q24.3 (rs4370952) and 15q21.1 (rs149936782) was detected in the female-only analysis of EA children and association at 18p11.23 (rs9964029) was identified in the female-only analysis of African-American children. Moreover, the 18p11.32 locus was replicated in an EA cohort (rs114124196, p = 8.8 × 10-3).
Conclusions: We report the first GWAS for pediatric OSA in European Americans and African Americans. Our results provide novel insights to the genetic underpins of pediatric OSA.
研究目的确定欧洲裔美国儿童和非洲裔美国儿童患小儿阻塞性睡眠呼吸暂停的遗传易感性变异:对具有欧洲裔美国人(EA)和非洲裔美国人(AA)血统的小儿OSA病例和对照受试者进行全基因组关联研究(GWAS),然后进行荟萃分析和性别分层:该算法共收集了 1,486 名受试者(46.3% 为欧洲裔美国人,53.7% 为非洲裔美国人)。我们确定了 1p36.22 和 15q26.1 基因组位点,这两个位点分别与欧裔美国人和非裔美国人的 OSA 风险有关。我们还在 EA 和 AA 人群中发现了一个位于 18p11.32 的共享风险位点(rs114124196,P =1.72 ×10 -8)。此外,在对患有 OSA 的 EA 儿童进行的男性分析中,发现了 1q43 (rs12754698) 和 2p25.1 (rs72775219),而 8q21.11 (rs6472959)、11q24.3 (rs4370952) 和 15q21.1 (rs149936782) 的关联,而在对非裔美国儿童进行的女性分析中则发现了 18p11.23 (rs9964029) 的关联。此外,18p11.32位点在EA队列中得到了复制(rs114124196,P =8.8 ×10 -3):我们报告了首个针对欧洲裔美国人和非洲裔美国人小儿 OSA 的 GWAS。结论:我们首次报告了欧洲裔美国人和非洲裔美国人小儿 OSA 的 GWAS,我们的研究结果为小儿 OSA 的遗传基础提供了新的见解。
{"title":"Identification of novel loci in obstructive sleep apnea in European American and African American children.","authors":"Courtney M Quinlan, Xiao Chang, Michael March, Frank D Mentch, Hui-Qi Qu, Yichuan Liu, Joseph Glessner, Patrick M A Sleiman, Hakon Hakonarson","doi":"10.1093/sleep/zsac182","DOIUrl":"10.1093/sleep/zsac182","url":null,"abstract":"<p><strong>Study objectives: </strong>To identify genetic susceptibility variants in pediatric obstructive sleep apnea in European American and African American children.</p><p><strong>Methods: </strong>A phenotyping algorithm using electronic medical records was developed to recruit cases with OSA and control subjects from the Center for Applied Genomics at Children's Hospital of Philadelphia (CHOP). Genome-wide association studies (GWAS) were performed in pediatric OSA cases and control subjects with European American (EA) and African American (AA) ancestry followed by meta-analysis and sex stratification.</p><p><strong>Results: </strong>The algorithm accrued 1486 subjects (46.3% European American, 53.7% African American). We identified genomic loci at 1p36.22 and 15q26.1 that associated with OSA risk in EA and AA, respectively. We also revealed a shared risk locus at 18p11.32 (rs114124196, p = 1.72 × 10-8) across EA and AA populations. Additionally, association at 1q43 (rs12754698) and 2p25.1 (rs72775219) was identified in the male-only analysis of EA children with OSA, while association at 8q21.11 (rs6472959), 11q24.3 (rs4370952) and 15q21.1 (rs149936782) was detected in the female-only analysis of EA children and association at 18p11.23 (rs9964029) was identified in the female-only analysis of African-American children. Moreover, the 18p11.32 locus was replicated in an EA cohort (rs114124196, p = 8.8 × 10-3).</p><p><strong>Conclusions: </strong>We report the first GWAS for pediatric OSA in European Americans and African Americans. Our results provide novel insights to the genetic underpins of pediatric OSA.</p>","PeriodicalId":49514,"journal":{"name":"Sleep","volume":null,"pages":null},"PeriodicalIF":5.6,"publicationDate":"2024-03-11","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"40653101","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Aurelio Vidal-Ortiz, Carlos Blanco-Centurion, Priyattam J Shiromani
To determine how a waking brain falls asleep researchers have monitored and manipulated activity of neurons and glia in various brain regions. While imaging Gamma-Aminobutyric Acid (GABA) neurons in the zona incerta (ZI) we found a subgroup that anticipates onset of NREM sleep (Blanco-Centurion C, Luo S, Vidal-Ortiz A, Swank C, Shiromani PJ. Activity of a subset of vesicular GABA-transporter neurons in the ventral ZI anticipates sleep onset. Sleep. 2021;44(6):zsaa268. doi:10.1093/sleep/zsaa268.). To differentiate the GABA subtype we now image and optogenetically manipulate the ZI neurons containing the transcription factor, Lhx6. In the first study, Lhx6-cre mice (n = 5; female = 4) were given rAAV-DJ-EF1a-DIO-GCaMP6M into the ZI (isofluorane anesthesia), a GRIN lens implanted, and 21days later sleep and fluorescence in individual Lhx6 neurons were recorded for 4 hours. Calcium fluorescence was detected in 132 neurons. 45.5% of the Lhx6 neurons were REM-max; 30.3% were wake-max; 11.4% were wake + REM max; 9% were NREM-max; and 3.8% had no change. The NREM-max group of neurons fluoresced 30 seconds ahead of sleep onset. The second study tested the effects of unilateral optogenetic stimulation of the ZI Lhx6 neurons (n = 14 mice) (AAV5-Syn-FLEX-rc[ChrimsonR-tdTomato]. Stimulation at 1 and 5 Hz (1 minute on- 4 minutes off) significantly increased percent REM sleep during the 4 hours stimulation period (last half of day cycle). The typical experimental approach is to stimulate neurons in both hemispheres, but here we found that low-frequency stimulation of ZI Lhx6 neurons in one hemisphere is sufficient to shift states of consciousness. Detailed mapping combined with mechanistic testing is necessary to identify local nodes that can shift the brain between wake-sleep states.
为了确定清醒的大脑是如何进入睡眠状态的,研究人员对不同脑区的神经元和神经胶质细胞的活动进行了监测和操作。在对内侧透明带(ZI)的 GABA 神经元进行成像时,我们发现了一个亚群,它能预测 NREM 睡眠的开始 1。为了区分 GABA 亚型,我们现在对含有转录因子 Lhx6 的 ZI 神经元进行成像和光遗传操作。在第一项研究中,将rAAV-DJ-EF1a-DIO-GCaMP6M注入ZI(异氟烷麻醉),植入GRIN透镜,21d后记录单个Lhx6神经元的睡眠和荧光4小时。在132个神经元中检测到了钙荧光。45.5%的Lhx6神经元为REM-max;30.3%为Wake-max;11.4%为wake+REM-max;9%为NREM-max;3.8%无变化。NREM-max神经元组在睡眠开始前30秒发出荧光。第二项研究测试了单侧光遗传刺激 ZI Lhx6 神经元(n=14 只小鼠)(AAV5-Syn-FLEX-rc[ChrimsonR-tdTomato])的效果。1赫兹和5赫兹的刺激(1分钟开4分钟关)显著增加了4小时刺激期(一天周期的后半段)的快速眼动睡眠百分比。典型的实验方法是刺激两个半球的神经元,但在这里我们发现,低频刺激一个半球的 ZI Lhx6 神经元足以改变意识状态。有必要绘制详细的地图,并进行机理测试,以确定能够在清醒-睡眠状态之间转换大脑的局部节点。
{"title":"Unilateral optogenetic stimulation of Lhx6 neurons in the zona incerta increases REM sleep.","authors":"Aurelio Vidal-Ortiz, Carlos Blanco-Centurion, Priyattam J Shiromani","doi":"10.1093/sleep/zsad217","DOIUrl":"10.1093/sleep/zsad217","url":null,"abstract":"<p><p>To determine how a waking brain falls asleep researchers have monitored and manipulated activity of neurons and glia in various brain regions. While imaging Gamma-Aminobutyric Acid (GABA) neurons in the zona incerta (ZI) we found a subgroup that anticipates onset of NREM sleep (Blanco-Centurion C, Luo S, Vidal-Ortiz A, Swank C, Shiromani PJ. Activity of a subset of vesicular GABA-transporter neurons in the ventral ZI anticipates sleep onset. Sleep. 2021;44(6):zsaa268. doi:10.1093/sleep/zsaa268.). To differentiate the GABA subtype we now image and optogenetically manipulate the ZI neurons containing the transcription factor, Lhx6. In the first study, Lhx6-cre mice (n = 5; female = 4) were given rAAV-DJ-EF1a-DIO-GCaMP6M into the ZI (isofluorane anesthesia), a GRIN lens implanted, and 21days later sleep and fluorescence in individual Lhx6 neurons were recorded for 4 hours. Calcium fluorescence was detected in 132 neurons. 45.5% of the Lhx6 neurons were REM-max; 30.3% were wake-max; 11.4% were wake + REM max; 9% were NREM-max; and 3.8% had no change. The NREM-max group of neurons fluoresced 30 seconds ahead of sleep onset. The second study tested the effects of unilateral optogenetic stimulation of the ZI Lhx6 neurons (n = 14 mice) (AAV5-Syn-FLEX-rc[ChrimsonR-tdTomato]. Stimulation at 1 and 5 Hz (1 minute on- 4 minutes off) significantly increased percent REM sleep during the 4 hours stimulation period (last half of day cycle). The typical experimental approach is to stimulate neurons in both hemispheres, but here we found that low-frequency stimulation of ZI Lhx6 neurons in one hemisphere is sufficient to shift states of consciousness. Detailed mapping combined with mechanistic testing is necessary to identify local nodes that can shift the brain between wake-sleep states.</p>","PeriodicalId":49514,"journal":{"name":"Sleep","volume":null,"pages":null},"PeriodicalIF":5.3,"publicationDate":"2024-03-11","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11502959/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"10034097","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Véronique Latreille, Tamir Avigdor, John Thomas, Joelle Crane, Viviane Sziklas, Marilyn Jones-Gotman, Birgit Frauscher
Seminal animal studies demonstrated the role of sleep oscillations such as cortical slow waves, thalamocortical spindles, and hippocampal ripples in memory consolidation. In humans, whether ripples are involved in sleep-related memory processes is less clear. Here, we explored the interactions between sleep oscillations (measured as traits) and general episodic memory abilities in 26 adults with drug-resistant temporal lobe epilepsy who performed scalp-intracranial electroencephalographic recordings and neuropsychological testing, including two analogous hippocampal-dependent verbal and nonverbal memory tasks. We explored the relationships between hemispheric scalp (spindles, slow waves) and hippocampal physiological and pathological oscillations (spindles, slow waves, ripples, and epileptic spikes) and material-specific memory function. To differentiate physiological from pathological ripples, we used multiple unbiased data-driven clustering approaches. At the individual level, we found material-specific cerebral lateralization effects (left-verbal memory, right-nonverbal memory) for all scalp spindles (rs > 0.51, ps < 0.01) and fast spindles (rs > 0.61, ps < 0.002). Hippocampal epileptic spikes and short pathological ripples, but not physiological oscillations, were negatively (rs > -0.59, ps < 0.01) associated with verbal learning and retention scores, with left lateralizing and antero-posterior effects. However, data-driven clustering failed to separate the ripple events into defined clusters. Correlation analyses with the resulting clusters revealed no meaningful or significant associations with the memory scores. Our results corroborate the role of scalp spindles in memory processes in patients with drug-resistant temporal lobe epilepsy. Yet, physiological and pathological ripples were not separable when using data-driven clustering, and thus our findings do not provide support for a role of sleep ripples as trait-like characteristics of general memory abilities in epilepsy.
{"title":"Scalp and hippocampal sleep correlates of memory function in drug-resistant temporal lobe epilepsy.","authors":"Véronique Latreille, Tamir Avigdor, John Thomas, Joelle Crane, Viviane Sziklas, Marilyn Jones-Gotman, Birgit Frauscher","doi":"10.1093/sleep/zsad228","DOIUrl":"10.1093/sleep/zsad228","url":null,"abstract":"<p><p>Seminal animal studies demonstrated the role of sleep oscillations such as cortical slow waves, thalamocortical spindles, and hippocampal ripples in memory consolidation. In humans, whether ripples are involved in sleep-related memory processes is less clear. Here, we explored the interactions between sleep oscillations (measured as traits) and general episodic memory abilities in 26 adults with drug-resistant temporal lobe epilepsy who performed scalp-intracranial electroencephalographic recordings and neuropsychological testing, including two analogous hippocampal-dependent verbal and nonverbal memory tasks. We explored the relationships between hemispheric scalp (spindles, slow waves) and hippocampal physiological and pathological oscillations (spindles, slow waves, ripples, and epileptic spikes) and material-specific memory function. To differentiate physiological from pathological ripples, we used multiple unbiased data-driven clustering approaches. At the individual level, we found material-specific cerebral lateralization effects (left-verbal memory, right-nonverbal memory) for all scalp spindles (rs > 0.51, ps < 0.01) and fast spindles (rs > 0.61, ps < 0.002). Hippocampal epileptic spikes and short pathological ripples, but not physiological oscillations, were negatively (rs > -0.59, ps < 0.01) associated with verbal learning and retention scores, with left lateralizing and antero-posterior effects. However, data-driven clustering failed to separate the ripple events into defined clusters. Correlation analyses with the resulting clusters revealed no meaningful or significant associations with the memory scores. Our results corroborate the role of scalp spindles in memory processes in patients with drug-resistant temporal lobe epilepsy. Yet, physiological and pathological ripples were not separable when using data-driven clustering, and thus our findings do not provide support for a role of sleep ripples as trait-like characteristics of general memory abilities in epilepsy.</p>","PeriodicalId":49514,"journal":{"name":"Sleep","volume":null,"pages":null},"PeriodicalIF":5.3,"publicationDate":"2024-02-08","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC10851866/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"10499260","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}