9 research outputs found

    Excessive Daytime Sleepiness and REM Sleep Behavior Disorders in Parkinson's Disease: A Narrative Review on Early Intervention With Implications to Neuroprotection

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    Sleep contributes to the consolidation of our memory and facilitates learning. Short term sleep deprivation temporarily reduces mnestic capacity, whereas long lasting sleep deprivation is associated with structural changes in the hippocampus and cortical areas. However, it is unknown whether early intervention and treatment of sleep disorders could have a neuroprotective effect. In neurodegenerative diseases sleep disorders can occur at preclinical stages and are frequently observed in patients with established Parkinson's disease (PD) and other α-synucleinopathies. REM sleep behavior disorder (RBD) is recognized as a hallmark for the development of α-synucleinopathies and may predict early cognitive decline, while excessive daytime sleepiness (EDS) is present in 12% of patients with PD before treatment initiation and increases continuously over time, causing substantial restrictions for the patients' social life. In more advanced disease, EDS is associated with dementia. Even though well recognized, limited attention has been given to genetics or the treatment of RBD and EDS in early PD. Systematic screening and early intervention can be expected to increase the patients' quality of life, but it remains unclear if this will also impact disease progression. Intervention studies in preclinical and early stages of α-synucleinopathies are needed to increase our understanding of the underlying pathomechanisms and may also provide important inroads to help clarify whether sleep disturbances are secondary to the neurodegenerative process or also contribute to disease exacerbation

    The European Insomnia Guideline : An update on the diagnosis and treatment of insomnia 2023

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    Publisher Copyright: © 2023 The Authors. Journal of Sleep Research published by John Wiley & Sons Ltd on behalf of European Sleep Research Society.Progress in the field of insomnia since 2017 necessitated this update of the European Insomnia Guideline. Recommendations for the diagnostic procedure for insomnia and its comorbidities are: clinical interview (encompassing sleep and medical history); the use of sleep questionnaires and diaries (and physical examination and additional measures where indicated) (A). Actigraphy is not recommended for the routine evaluation of insomnia (C), but may be useful for differential-diagnostic purposes (A). Polysomnography should be used to evaluate other sleep disorders if suspected (i.e. periodic limb movement disorder, sleep-related breathing disorders, etc.), treatment-resistant insomnia (A) and for other indications (B). Cognitive-behavioural therapy for insomnia is recommended as the first-line treatment for chronic insomnia in adults of any age (including patients with comorbidities), either applied in-person or digitally (A). When cognitive-behavioural therapy for insomnia is not sufficiently effective, a pharmacological intervention can be offered (A). Benzodiazepines (A), benzodiazepine receptor agonists (A), daridorexant (A) and low-dose sedating antidepressants (B) can be used for the short-term treatment of insomnia (≤ 4 weeks). Longer-term treatment with these substances may be initiated in some cases, considering advantages and disadvantages (B). Orexin receptor antagonists can be used for periods of up to 3 months or longer in some cases (A). Prolonged-release melatonin can be used for up to 3 months in patients ≥ 55 years (B). Antihistaminergic drugs, antipsychotics, fast-release melatonin, ramelteon and phytotherapeutics are not recommended for insomnia treatment (A). Light therapy and exercise interventions may be useful as adjunct therapies to cognitive-behavioural therapy for insomnia (B).Peer reviewe

    Excessive Daytime Sleepiness and REM Sleep Behavior Disorders in Parkinson's Disease: A Narrative Review on Early Intervention With Implications to Neuroprotection

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    Sleep contributes to the consolidation of our memory and facilitates learning. Short term sleep deprivation temporarily reduces mnestic capacity, whereas long lasting sleep deprivation is associated with structural changes in the hippocampus and cortical areas. However, it is unknown whether early intervention and treatment of sleep disorders could have a neuroprotective effect. In neurodegenerative diseases sleep disorders can occur at preclinical stages and are frequently observed in patients with established Parkinson's disease (PD) and other α-synucleinopathies. REM sleep behavior disorder (RBD) is recognized as a hallmark for the development of α-synucleinopathies and may predict early cognitive decline, while excessive daytime sleepiness (EDS) is present in 12% of patients with PD before treatment initiation and increases continuously over time, causing substantial restrictions for the patients' social life. In more advanced disease, EDS is associated with dementia. Even though well recognized, limited attention has been given to genetics or the treatment of RBD and EDS in early PD. Systematic screening and early intervention can be expected to increase the patients' quality of life, but it remains unclear if this will also impact disease progression. Intervention studies in preclinical and early stages of α-synucleinopathies are needed to increase our understanding of the underlying pathomechanisms and may also provide important inroads to help clarify whether sleep disturbances are secondary to the neurodegenerative process or also contribute to disease exacerbation.publishedVersio

    REM sleep behavior disorder is not associated with a more rapid cognitive decline in mild dementia

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    Objectives: REM sleep behavior disorder (RBD) is associated with cognitive dysfunctions and is a risk factor for development of mild cognitive impairment and dementia. However, it is unknown whether RBD is associated with faster cognitive decline in already established dementia. The main goal of this study was to determine if patients with mild dementia with and without RBD differ in progression rate and in specific neuropsychological measures over 4-year follow-up. Methods: This longitudinal, prospective study based on data from the DemVest study compares neuropsychological measures in a mild dementia cohort. A diagnosis of probable RBD (pRBD) was made based on the Mayo Sleep Questionnaire. Neuropsychological domains were assessed by Mini Mental State Examination, total score and figure copying, California Verbal Learning Test-II, Visual Object and Space Perception Cube and Silhouettes, Boston Naming Test, Stroop test, Verbal Category Fluency, Trail Making Test A and B. Results: Among the 246 subjects, 47 (19.1%) had pRBD at the baseline, and pRBD group was younger and with male predominance. During 4-year follow-up, we did not observe any significant differences in the rate of decline in neuropsychological measures. Patients with pRBD performed generally poorer in visuoconstructional, visuoperceptual, and executive/attention tests in comparison to RBD negative. Conclusion: We did not find any significant differences in progression rate of neurocognitive outcomes between dementia patients with and without RBD

    European guideline for the diagnosis and treatment of insomnia

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    This European guideline for the diagnosis and treatment of insomnia was developed by a task force of the European Sleep Research Society, with the aim of providing clinical recommendations for the management of adult patients with insomnia. The guideline is based on a systematic review of relevant meta-analyses published till June 2016. The target audience for this guideline includes all clinicians involved in the management of insomnia, and the target patient population includes adults with chronic insomnia disorder. The GRADE (Grading of Recommendations Assessment, Development and Evaluation) system was used to grade the evidence and guide recommendations. The diagnostic procedure for insomnia, and its co-morbidities, should include a clinical interview consisting of a sleep history (sleep habits, sleep environment, work schedules, circadian factors), the use of sleep questionnaires and sleep diaries, questions about somatic and mental health, a physical examination and additional measures if indicated (i.e. blood tests, electrocardiogram, electroencephalogram; strong recommendation, moderate- to high-quality evidence). Polysomnography can be used to evaluate other sleep disorders if suspected (i.e. periodic limb movement disorder, sleep-related breathing disorders), in treatment-resistant insomnia, for professional at-risk populations and when substantial sleep state misperception is suspected (strong recommendation, high-quality evidence). Cognitive behavioural therapy for insomnia is recommended as the first-line treatment for chronic insomnia in adults of any age (strong recommendation, high-quality evidence). A pharmacological intervention can be offered if cognitive behavioural therapy for insomnia is not sufficiently effective or not available. Benzodiazepines, benzodiazepine receptor agonists and some antidepressants are effective in the short-term treatment of insomnia (≤4 weeks; weak recommendation, moderate-quality evidence). Antihistamines, antipsychotics, melatonin and phytotherapeutics are not recommended for insomnia treatment (strong to weak recommendations, low- to very-low-quality evidence). Light therapy and exercise need to be further evaluated to judge their usefulness in the treatment of insomnia (weak recommendation, low-quality evidence). Complementary and alternative treatments (e.g. homeopathy, acupuncture) are not recommended for insomnia treatment (weak recommendation, very-low-quality evidence)
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