Effects of parkinsonian medication on sleep

Schäfer, D.; Greulich, W.

doi:10.1007/pl00007770

Cited by 27 publications

(19 citation statements)

References 6 publications

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“…A correlation between reduced night sleep duration and decreased daytime sleep latency was ruled out suggesting that sleepiness might be disease-related (ibid.). Some authors compared PD psychosis with narcolepsy-like REM sleep disorder with the hallucinations coinciding with daytime REM episodes or hypnagogic states (Schafer and Greulich, 2000). Hypnagogic phenomena and cataplexy also resemble narcoleptic symptoms.…”

Section: Abnormalities Of Neuronal Circuits In Pd: Psychotic and Cognmentioning

confidence: 98%

Dopaminergic dysbalance in distinct basal ganglia neurocircuits: Implications for the pathophysiology of parkinson’s disease, schizophrenia and attention deficit hyperactivity disorder

Riederer²,

2006

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The basal ganglia form a forebrain system that collects signals from a large part of the neocortex, redistributes these cortical inputs both with respect to one another and with respect to inputs from the limbic system, and then focuses the inputs of this redistributed, integrated signals into particular regions of the frontal lobes and brainstem involved in aspects of motor planning and motor memory. Movement disorders associated with basal ganglia dysfunction comprise a spectrum of abnormalities that range from the hypokinetic disorder (from which Parkinson's disease, PD, is the best-known-example) at one extreme to the hyperkinetic disorder (exemplified by Huntington's disease and hemiballism) at the other. In addition to disorders of movement, major mental disorders including schizophrenic-like states and attention deficit hyperactivity disorder (ADHD) have been linked to abnormalities in the basal ganglia and their allied nuclei. In this paper we discuss recent evidence indicating that a dopamine-induced dysbalance of basal ganglia neurocircuitries may be an important pathophysiological component in PD, schizophrenia and ADHD. According to our model, the deprivation of dopaminergic nigro-striatal input, as in PD, reduces the positive feedback via the direct system, and increases the negative feedback via the indirect system. The critical consequences are an overactivity of the basal ganglia output sites with the resulting inhibition of thalamo-cortical drive. In schizophrenia the serious cognitive deficits might be partly a result of a hyperactivity of the inhibitory dopamine D(2) transmission system. Through this dysinhibition, the thalamus exhibits hyperactivity that overstimulates the cortex resulting in dysfunctions of perception, attention, stimulus distinction, information processing and affective regulation (inducing hallucinations and delusions) and motor disabilities. Recent studies have strongly suggested that a disturbance of the dopaminergic system is also involved in the pathophysiology of ADHD. The most convincing evidence comes from the demonstration of the efficacy of psychostimulants such as the dopamine transporter (DAT) blocker methylphenidate in the symptomatic treatment of ADHD. Genetic studies have shown an association between ADHD and genes involved in dopaminergic neurotransmission (for example the dopamine receptor genes DRD4 and DRD5, and the DAT gene DAT1). DAT knockout mice display a phenotype with increased locomotor activity, which is normalized by psychostimulant treatment. Finally, imaging studies demonstrated an increased density of DAT in the striatum of ADHD patients. Which system is disturbed and whether this system is hyper- or hypoactive is not unambiguously known yet.

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Section: Abnormalities Of Neuronal Circuits In Pd: Psychotic and Cognmentioning

confidence: 98%

Dopaminergic dysbalance in distinct basal ganglia neurocircuits: Implications for the pathophysiology of parkinson’s disease, schizophrenia and attention deficit hyperactivity disorder

Riederer²,

2006

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“…There are distinct patterns of release of various hormones (including cortisol, growth hormone, and corticotrophin) during the sleep cycle, with the potential existence of common regulatory pathways of the sleep EEG and the nocturnal hormone secretion [ 42,43 ] .There is consensus that both abnormal sleep and impaired daytime alertness occur in the majority of PD patients [ 44 ] ; clinical observations of sleepiness in PD further support the role of DA in the sleep-wake cycle [ 31 ] . The effects of levodopa and DA agonists on sleep [ 45 ] also point toward a role of dopaminergic systems in sleep. Thus it is not surprising that most PD patients experience dif fi culties with sleep due to the disease, its treatment, or both [ 46 ] .…”

Section: Sleep Physiologymentioning

confidence: 95%

“…The effects of levodopa on sleep are nonspeci fi c, exerted through pre-and postsynaptic mechanisms, as well as through interaction with different neurotransmitters [ 69 ] . Levodopa suppresses REM sleep and delays REM sleep latency [ 45,83 ] ; it has improved daytime vigilance in narcoleptic patients [ 84 ] . In a questionnaire study, the use and duration of levodopa therapy in patients with PD were associated with a higher frequency of sleep disruption, with sleep fragmentation being the most common sleep complaint [ 85 ] .…”

Section: Effects Of Antiparkinsonian Treatmentmentioning

confidence: 99%

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Insomnia in Parkinson’s Disease

Moro-de-Casillas

Riley

2012

Parkinson’s Disease and Nonmotor Dysfunction

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The International Classi fi cation of Sleep Disorders (ICSD) de fi nes insomnia simply as "dif fi culty in initiating and/or maintaining sleep". Other de fi nitions exist, and there is no clear consensus in this matter. The core elements of insomnia are an inadequate quantity or quality of sleep, with both nocturnal and daytime consequences. Traditionally, insomnia has been subgrouped into sleep-onset insomnia, sleep-maintaining insomnia, and insomnia with early morning awakening; however, there is extensive overlap, and most insomniacs fi t into more than one subgroup.Sleep disorders, particularly in the elderly, are strongly associated with increased morbidity and mortality, signi fi cant limitations in activities of daily living, and impaired quality of life. Aside from the obvious complications of daytime fatigue and somnolence, insomniacs have an increased incidence of psychiatric disorders such as depression and anxiety, increased use of over-the-counter medications and alcohol, and a higher incidence of accidents and unemployment. Chronic sleep loss has multisystem consequences and may represent a risk factor for obesity, insulin resistance, and Type 2 diabetes. However, the brunt of negative effects of sleep deprivation is borne by the brain. Chronic insomnia independently predicts incident cognitive decline in older men, but it also has been suggested that some degree of apparent age-related cognitive decline may be due to treatable insomnia.

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“…Впервые ДС привлекла к себе внимание ученых после того, как в 90-е годы XX века появились со-общения о возникновении императивных засыпа-ний у больных БП, принимающих агонисты дофа-миновых рецепторов (АДР) [12][13][14][15]. Одно из пер-вых сообщений принадлежало S. Frucht и соавт.…”

Section: дс -побочный эффект дофаминергической терапии?unclassified

Heterogeneity of excessive daytime sleepiness in Parkinson’s disease

2016

Z. nevrol. psikhiatr. im. S.S. Korsakova

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Effects of parkinsonian medication on sleep

Cited by 27 publications

References 6 publications

Dopaminergic dysbalance in distinct basal ganglia neurocircuits: Implications for the pathophysiology of parkinson’s disease, schizophrenia and attention deficit hyperactivity disorder

Dopaminergic dysbalance in distinct basal ganglia neurocircuits: Implications for the pathophysiology of parkinson’s disease, schizophrenia and attention deficit hyperactivity disorder

Insomnia in Parkinson’s Disease

Heterogeneity of excessive daytime sleepiness in Parkinson’s disease

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