Approaching disturbed sleep in late Parkinson's Disease: first step toward a proposal for a revised UPDRS

Askenasy, J. J. M.

doi:10.1016/s1353-8020(01)00026-8

Cited by 36 publications

(18 citation statements)

References 73 publications

Supporting

Mentioning

Contrasting

Unclassified

Order By: Relevance

“…Disturbances of sleep are highly prevalent in PD, affecting up to 88% of patients in a community-based study (Factor et al, 1990), although a range of 55–98% has been reported across various studies (Larsen and Tandberg, 2001; Kaynak et al, 2005; Gjerstad et al, 2007). However, the interaction between PD and sleep is complex because PD patients may also have primary sleep disturbances such as rapid eye movement (REM) sleep behavior disorder, periodic limb movements during sleep and restless legs syndrome (Askenasy, 2001). Other factors such as depression, reactions to medications, nocturia, akinesia, pain, and dystonia may also underlie their sleep disturbances (Dhawan et al, 2006; Chaudhuri and Schapira, 2009).…”

Section: Implications Of the Bg In Sleep–wake Controlmentioning

confidence: 99%

Role of Basal Ganglia in Sleep–Wake Regulation: Neural Circuitry and Clinical Significance

et al. 2010

View full text Add to dashboard Cite

Researchers over the last decade have made substantial progress toward understanding the roles of dopamine and the basal ganglia (BG) in the control of sleep–wake behavior. In this review, we outline recent advancements regarding dopaminergic modulation of sleep through the BG and extra-BG sites. Our main hypothesis is that dopamine promotes sleep by its action on the D2 receptors in the BG and promotes wakefulness by its action on D1 and D2 receptors in the extra-BG sites. This hypothesis implicates dopamine depletion in the BG (such as in Parkinson's disease) in causing frequent nighttime arousal and overall insomnia. Furthermore, the arousal effects of psychostimulants (methamphetamine, cocaine, and modafinil) may be linked to the ventral periaquductal gray (vPAG) dopaminergic circuitry targeting the extra-BG sleep–wake network.

show abstract

Section: Implications Of the Bg In Sleep–wake Controlmentioning

confidence: 99%

Role of Basal Ganglia in Sleep–Wake Regulation: Neural Circuitry and Clinical Significance

et al. 2010

View full text Add to dashboard Cite

show abstract

“…Sleep problems occur in at least 75% of PD patients over the course of the disease (Factor et al 1990; Goetz et al 2005; Lees et al 1988), including sleep fragmentation, sleep-related breathing disorders, restless legs/periodic leg movements, REM sleep behavior disorder, sleep-related psychosis (nocturnal hallucinations), and altered sleep-wake cycle (Askenasy 2001; Fahn 2003; Gunn et al 2010). Relatedly, patients with PD experience disturbances of arousal, including excessive daytime sleepiness (Askenasy 1993; Fahn 2003; Gunn et al 2010).…”

Section: Hemispheric Effects On Sleep and Mood In Pdmentioning

confidence: 99%

Parkinson’s Disease as a Disconnection Syndrome

Cronin‐Golomb

2010

Neuropsychol Rev

103

View full text Add to dashboard Cite

Parkinson’s disease (PD) is a major neuro-degenerative disorder that is usually considered in terms of midbrain and basal ganglia dysfunction. Regarding PD instead as a disconnection syndrome may prove beneficial to understanding aspects of cognition, perception, and other neuropsychological domains in the disease. PD is usually of unilateral onset, providing evidence of intrahemispheric dissociations and an imbalance in the usual relative strengths of the right and left hemispheres. Hence, in order to appreciate the neuropsychology of PD, it is important to apply to this disease our understanding of hemispheric lateralization effects and within-hemisphere circuitry from brainstem to higher-order association cortex. The focus of this review is on the relevance of PD-related disconnections among subcortical and cortical structures to cognition, perception, emotion, and associated brainstem-based domains such as sleep and mood disturbance. Besides providing information on disease characteristics, regarding PD as a disconnection syndrome allows us to more completely understand normal brain-behavior relations in general.

show abstract

“…Severely disturbed sleep is characteristic of progressive neurodegenerative diseases such as Alzheimer's disease, Parkinson's disease, and Huntington's disease (HD) (Askenasy, 2001;Bates et al, 2002;Hatfield et al, 2004). When patients with long-term neurological illnesses have disrupted sleep, this becomes a problem not only for the patient but also for their carers (Bianchetti et al, 1995;Van Someren, 2000).…”

Section: Introductionmentioning

confidence: 99%

Disintegration of the Sleep-Wake Cycle and Circadian Timing in Huntington's Disease

Morton¹,

Wood²,

Hastings³

et al. 2005

J. Neurosci.

379

295

View full text Add to dashboard Cite

Sleepdisturbancesinneurologicaldisordershaveadevastatingimpactonpatientandcareralike.However,theirpathologicaloriginisunknown.Here we show that patients with Huntington's disease (HD) have disrupted night-day activity patterns. This disruption was mirrored in a transgenic model of HD (R6/2 mice) in which daytime activity increased and nocturnal activity fell, eventually leading to the complete disintegration of circadian behavior. The behavioral disturbance was accompanied by marked disruption of expression of the circadian clock genes mPer2 and mBmal1 in the suprachiasmatic nuclei (SCN), the principal circadian pacemaker in the brain. The circadian peak of expression of mPer2 was prematurely truncated, and the mRNA levels of mBmal1 were attenuated and failed to exhibit a significant circadian oscillation. Circadian cycles of gene expression in the motor cortex and striatum, markers of behavioral activation in wild-type mice, were also suppressed in the R6/2 mice, providing a neural correlate of the disturbed activity cycles. Increased daytime activity was also associated with reduced SCN expression of prokineticin 2, a transcriptional target of mBmal1 encoding a neuropeptide that normally suppresses daytime activity in nocturnal mammals. Together, these molecular abnormalities could explain the pathophysiological changes in circadian behavior. We propose that circadian sleep disturbances are an important pathological feature of HD, that they arise from pathology within the SCN molecular oscillation, and that their treatment will bring appreciable benefits to HD patients.

show abstract

Approaching disturbed sleep in late Parkinson's Disease: first step toward a proposal for a revised UPDRS

Cited by 36 publications

References 73 publications

Role of Basal Ganglia in Sleep–Wake Regulation: Neural Circuitry and Clinical Significance

Role of Basal Ganglia in Sleep–Wake Regulation: Neural Circuitry and Clinical Significance

Parkinson’s Disease as a Disconnection Syndrome

Disintegration of the Sleep-Wake Cycle and Circadian Timing in Huntington's Disease

Contact Info

Product

Resources

About