Sleep−wake cycle dysregulation in idiopathic REM sleep behaviour disorder

Alteration of the circadian sleep-wake rhythm has been suggested in patients affected by idiopathic rapid eye movement sleep behaviour disorder. Because actigraphy is the validated instrument to monitor the sleep-wake cycle, the aim of the present study was to investigate the circadian sleep-wake rhythm in patients with idiopathic rapid eye movement sleep behaviour disorder compared with healthy aged controls. Fourteen-day actigraphic recording, a comprehensive sleep interview, and cognitive and behavioural domains were investigated in patients affected by idiopathic rapid eye movement sleep behaviour disorder, and compared with controls similar for age, sex and cognitive performances. Patients with idiopathic rapid eye movement sleep behaviour disorder showed reduced relative amplitude and alteration of both sleep and wake compared with controls. Patients with idiopathic rapid eye movement sleep behaviour disorder also showed subjective sleep and wake complaints, and higher scores at the Beck Depression Inventory, compared with controls. Beck Depression Inventory scores correlated with sleep actigraphic parameters, such as sleep latency, sleep efficiency, time in bed, and relative amplitude. Therefore, the present study showed the dysregulation of the sleep-wake cycle in patients with idiopathic rapid eye movement behaviour disorder. Moreover, depressive symptoms documented in patients with idiopathic rapid eye movement sleep behaviour disorder correlated with the sleep-wake rhythm dysregulation

Sleep-wake cycle dysregulation in idiopathic REM sleep behaviour disorder

Alteration of the circadian sleep-wake rhythm has been suggested in patients affected by idiopathic rapid eye movement sleep behaviour disorder. Because actigraphy is the validated instrument to monitor the sleep-wake cycle, the aim of the present study was to investigate the circadian sleep-wake rhythm in patients with idiopathic rapid eye movement sleep behaviour disorder compared with healthy aged controls. Fourteen-day actigraphic recording, a comprehensive sleep interview, and cognitive and behavioural domains were investigated in patients affected by idiopathic rapid eye movement sleep behaviour disorder, and compared with controls similar for age, sex and cognitive performances. Patients with idiopathic rapid eye movement sleep behaviour disorder showed reduced relative amplitude and alteration of both sleep and wake compared with controls. Patients with idiopathic rapid eye movement sleep behaviour disorder also showed subjective sleep and wake complaints, and higher scores at the Beck Depression Inventory, compared with controls. Beck Depression Inventory scores correlated with sleep actigraphic parameters, such as sleep latency, sleep efficiency, time in bed, and relative amplitude. Therefore, the present study showed the dysregulation of the sleep-wake cycle in patients with idiopathic rapid eye movement behaviour disorder. Moreover, depressive symptoms documented in patients with idiopathic rapid eye movement sleep behaviour disorder correlated with the sleep-wake rhythm dysregulation

Correction to: Sleep dysregulation, memory impairment, and CSF biomarkers during different levels of neurocognitive functioning in Alzheimer's disease course

An amendment to this paper has been published and can be accessed via the original article

Depressive symptoms in patients with epilepsy and clinically associated features in a single tertiary center

Although depressive symptoms are the most common psychiatric comorbidity in epilepsy, they remain underestimated and untreated in a large proportion of patients. The purpose of this study was to evaluate depression severity and related clinical features in people with epilepsy using a well-reliable self-report index of mood, the Beck Depression Inventory-II (BDI-II). One-hundred seventeen adult patients with epilepsy were recruited from a tertiary epilepsy center and completed the BDI-II. A single-item analysis of the 21 questions of the BDI-II was computed and differences between women and men in each depressive symptom were evaluated. Correlation and regression analyses were used to identify clinical features associated with the severity of depression. Results showed gender differences in some items, with women reporting overall higher depression severity than men. The most common symptoms regarded domains of sleeping patterns, tiredness, and loss of energy. Regression evidence suggested that being female, having an epilepsy duration < 10 years, as well as being treated with psychotropic drugs and reporting generalized seizure, were associated with higher depression severity. Despite its cross-sectional nature, this study reinforces the importance of investigating and possibly treating depressive symptoms in adult patients with epilepsy, since they negatively impact well-being, daytime activities, and sleep. Further studies identifying pharmacological and non-pharmacological treatments for depression in epilepsy need to be planned

Sleep-disordered breathing and the risk of Alzheimer's disease

Sleep-disordered breathing is highly prevalent in the elderly population. Obstructive sleep apnea (OSA) represents the most common sleep disorder among the adult and elderly population. Recently, OSA diagnosis has been associated with an increased risk of developing cognitive decline and dementia, including vascular dementia and Alzheimer's disease (AD). Subsequently, there have been studies on AD biomarkers investigating cerebrospinal fluid, blood, neuroimaging, and nuclear medicine biomarkers in patients with OSA. Furthermore, studies have attempted to assess the possible effects of continuous positive airway pressure (CPAP) treatment on the cognitive trajectory and AD biomarkers in patients with OSA. This review summarizes the findings of studies on each AD biomarker (cognitive, biofluid, neuroimaging, and nuclear medicine imaging) in patients with OSA, also accounting for the related effects of CPAP treatment. In addition, the hypothetical model connecting OSA to AD in a bi-directional interplay is analyzed. Finally, the sex-based differences in prevalence and clinical symptoms of OSA between men and women have been investigated in relation to AD risk. Further studies investigating AD biomarkers changes in patients with OSA and the effect of CPAP treatment should be auspicated in future for identifying strategies to prevent the development of AD

Sleep disorders and late-onset epilepsy of unknown origin: Understanding new trajectories to brain amyloidopathy

The intertwining between epilepsy, sleep disorders and beta amyloid pathology has been progressively highlighted, as early identification and stratification of patients at high risk of cognitive decline is the need of the hour. Modification of the sleep-wake activity, such as sleep impairment or excessive daytime sleepiness, can critically affect cerebral beta amyloid levels. Both mice models and human studies have demonstrated a substantial increase in the burden of beta amyloid pathology after sleep-deprivation, with potential negative effects partially restored by sleep recovery. The accumulation of beta amyloid has been shown to be an early event in the course of Alzheimer's disease dementia. Beta amyloid accumulation has been linked to epileptic seizures epileptic seizures, with beta amyloid being itself pro-epileptogenic in mice models already at oligomeric stage, well before plaque deposition. Further supporting a potential relationship between beta amyloid and epilepsy: i) seizures happen in 1 out of oofut 10 patients with Alzheimer's disease in the prodromal stage, ii) epileptic activity accelerates cognitive decline in Alzheimer's disease, iii) people with late-onset epilepsy present a critically high risk of developing dementia. In this Review we highlight the role of beta amyloid as a potential shared mechanisms between sleep disorders, late-onset epilepsy, and cognitive decline

Derivation and Validation of a Phenoconversion-Related Pattern in Idiopathic Rapid Eye Movement Behavior Disorder

Background: Idiopathic rapid eye movement sleep behavior disorder (iRBD) represents the prodromal stage of α-synucleinopathies. Reliable biomarkers are needed to predict phenoconversion. Objective: The aim was to derive and validate a brain glucose metabolism pattern related to phenoconversion in iRBD (iRBDconvRP) using spatial covariance analysis (Scaled Subprofile Model and Principal Component Analysis [SSM-PCA]). Methods: Seventy-six consecutive iRBD patients (70 ± 6 years, 15 women) were enrolled in two centers and prospectively evaluated to assess phenoconversion (30 converters, 73 ± 6 years, 14 Parkinson's disease and 16 dementia with Lewy bodies, follow-up time: 21 ± 14 months; 46 nonconverters, 69 ± 6 years, follow-up time: 33 ± 19 months). All patients underwent [ 18F]FDG-PET ( 18F-fluorodeoxyglucose positron emitting tomography) to investigate brain glucose metabolism at baseline. SSM-PCA was applied to obtain the iRBDconvRP; nonconverter patients were considered as the reference group. Survival analysis and Cox regression were applied to explore prediction power. Results: First, we derived and validated two distinct center-specific iRBDconvRP that were comparable and significantly able to predict phenoconversion. Then, SSM-PCA was applied to the whole set, identifying the iRBDconvRP. The iRBDconvRP included positive voxel weights in cerebellum; brainstem; anterior cingulate cortex; lentiform nucleus; and middle, mesial temporal, and postcentral areas. Negative voxel weights were found in posterior cingulate, precuneus, middle frontal gyrus, and parietal areas. Receiver operating characteristic analysis showed an area under the curve of 0.85 (sensitivity: 87%, specificity: 72%), discriminating converters from nonconverters. The iRBDconvRP significantly predicted phenoconversion (hazard ratio: 7.42, 95% confidence interval: 2.6–21.4). Conclusions: We derived and validated an iRBDconvRP to efficiently discriminate converter from nonconverter iRBD patients. [ 18F]FDG-PET pattern analysis has potential as a phenoconversion biomarker in iRBD patients