Effects of various factors on sleep disorders and quality of life in Parkinson’s disease

Telarović, Srđana; Mijatović, Davor; Telarović, Irma

doi:10.1007/s13760-015-0478-0

Cited by 6 publications

(2 citation statements)

References 31 publications

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“…Others reported a close correlation between low sleep quality, chronic insomnia and restless legs syndrome symptoms [23]. Insomnia in PD seems to be associated with age [24], disease duration, female sex, use of dopamine agonists [25] as well as neuropsychological symptoms such as depression/anxiety, even in de novo PD patients at an early disease stage [26,27]. In a Dutch longitudinal, prospective, cohort-study insomnia was also associated with motor fluctuations, autonomic dysfunction and hallucinations [28].…”

Section: Insomnia In Neurodegenerative Movement Disordersmentioning

confidence: 94%

Insomnia in neurological diseases

Mayer

Happe²,

Evers

et al. 2021

Neurol. Res. Pract.

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Insomnia is defined as difficulties of initiating and maintaining sleep, early awakening and poor subjective sleep quality despite adequate opportunity and circumstances for sleep with impairment of daytime performance. These components of insomnia – namely persistent sleep difficulties despite of adequate sleep opportunity resulting in daytime dysfunction - appear secondary or co-morbid to neurological diseases. Comorbid insomnia originates from neurodegenerative, inflammatory, traumatic or ischemic changes in sleep regulating brainstem and hypothalamic nuclei with consecutive changes of neurotransmitters. Symptoms of neurological disorders (i.e motor deficits), co-morbidities (i.e. pain, depression, anxiety) and some disease-specific pharmaceuticals may cause insomnia and/or other sleep problems.This guideline focuses on insomnias in headaches, neurodegenerative movement disorders, multiple sclerosis, traumatic brain injury, epilepsies, stroke, neuromuscular disease and dementia.The most important new recommendations are: Cognitive behavioral therapy (CBTi) is recommended to treat acute and chronic insomnia in headache patients. Insomnia is one of the most frequent sleep complaints in neurodegenerative movement disorders. Patients may benefit from CBTi, antidepressants (trazodone, doxepin), melatonin and gaba-agonists. Insomnia is a frequent precursor of MS symptoms by up to 10 years. CBTi is recommended in patients with MS, traumatic brain injury and. Melatonin may improve insomnia symptoms in children with epilepsies. Patients with insomnia after stroke can be treated with benzodiazepine receptor agonists and sedating antidepressants. For patients with dementia suffering from insomnia trazodone, light therapy and physical exercise are recommended.

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Section: Insomnia In Neurodegenerative Movement Disordersmentioning

confidence: 94%

Insomnia in neurological diseases

Mayer

Happe²,

Evers

et al. 2021

Neurol. Res. Pract.

View full text Add to dashboard Cite

show abstract

“…Several lines of evidence suggest that DA signals are closely associated with regulation of sleep-wake activity [8, 9]. In humans, malfunction of the brain DA system is associated with neuropsychopathy, with disruption of sleep as one symptom [10]. Systemic administration of a selective D 1 receptor agonist induced an increase of wakefulness (W) and a reduction of slow wave sleep (SWS) and REM sleep.…”

Section: Introductionmentioning

confidence: 99%

Activation of the ventral tegmental area increased wakefulness in mice

Sun

Wang

et al. 2017

Sleep Biol. Rhythms

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The ventral tegmental area (VTA) is crucial for brain functions, such as voluntary movement and cognition; however, the role of VTA in sleep-wake regulation when directly activated or inhibited remains unknown. In this study, we investigated the effects of activation or inhibition of VTA neurons on sleep-wake behavior using the pharmacogenetic “designer receptors exclusively activated by designer drugs (DREADD)” approach. Immunohistochemistry staining was performed to confirm the microinjection sites, and combined with electrophysiological experiments, to determine whether the VTA neurons were activated or inhibited. The hM3Dq-expressing VTA neurons were excited confirmed by clozapine-N-oxide (CNO)-driven c-Fos expression and firing in patch-clamp recordings; whereas the hM4Di-expressing VTA neurons inhibited by reduction of firing. Compared with controls, the activation of VTA neurons at 9:00 (inactive period) produced a 120.1% increase in the total wakefulness amount for 5 h, whereas NREM and REM sleep were decreased by 62.5 and 92.2%, respectively. Similarly, when VTA neurons were excited at 21:00 (active period), the total wakefulness amount increased 81.5%, while NREM and REM sleep decreased 64.6 and 93.8%, respectively, for 8 h. No difference of the amount and EEG power density of the NREM sleep was observed following the arousal effects of CNO. The inhibition of VTA neurons during active or inactive periods gave rise to no change in the time spent in the wakefulness, REM, and NREM sleep compared with control. The results indicated that VTA neurons activated pharmacogentically played important roles in promoting wakefulness.

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S2k-Leitlinie: Insomnie bei neurologischen Erkrankungen

Mayer

2020

DGNeurologie

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Effects of various factors on sleep disorders and quality of life in Parkinson’s disease

Cited by 6 publications

References 31 publications

Insomnia in neurological diseases

Insomnia in neurological diseases

Activation of the ventral tegmental area increased wakefulness in mice

S2k-Leitlinie: Insomnie bei neurologischen Erkrankungen

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