Parkinson’s disease and sleepiness

Arnulf, Isabelle; Konofal, Éric; Merino-Andreu, Milagros; Houeto, Jean Luc; Mesnage, Valérie; Welter, Marie‐Laure; Lacomblez, L.; Golmard, Jean‐Louis; Derenne, Jean‐Philippe; Agid, Yves

doi:10.1212/wnl.58.7.1019

Cited by 482 publications

(373 citation statements)

References 24 publications

Supporting

Mentioning

322

Contrasting

Unclassified

Order By: Relevance

“…Conventional antiparkinsonism drugs effectively ameliorate the symptoms of patients with PD during the initial several years of onset, but become increasingly less effective and induce motor fluctuations including wearing-off, on-off, dopa-induced dyskinesia, and agonist-induced sleep attack (Arnulf et al, 2002;Comella, 2002;Hobson et al, 2002;Ondo et al, 2001;Pahwa et al, 2006 Smet, 2002). Traditional Chinese medicines (TCM) ameliorate various symptoms, particularly the ageing-related symptoms, and hence are likely to be beneficial for chronic diseases such as PD (Iwasaki et al, 2004;2005a;2005b).…”

Section: Evaluation Of Effects Of Traditional Chinese Medicine On Parmentioning

confidence: 99%

Objective Evaluation of the Severity of Parkinsonism Using Power-Law Temporal Auto-Correlation of Activity

Pan¹,

Yamamoto²,

Kwak³

2011

Diagnostics and Rehabilitation of Parkinson's Disease

View full text Add to dashboard Cite

Section: Evaluation Of Effects Of Traditional Chinese Medicine On Parmentioning

confidence: 99%

Objective Evaluation of the Severity of Parkinsonism Using Power-Law Temporal Auto-Correlation of Activity

Pan¹,

Yamamoto²,

Kwak³

2011

Diagnostics and Rehabilitation of Parkinson's Disease

View full text Add to dashboard Cite

“…Wisor et al (2001) found that mice with deletion of the DA transporter gene have 20% more wakefulness than control mice and do not respond to psychostimulant drugs such as amphetamine or modafinil, indicating that the DA transporter is involved in the control of wakefulness and is required for modafinil-and amphetamine-induced arousal. Patients with Parkinson's disease who have extensive loss of dopaminergic cells in the substantia nigra (SN; A9), and less extensive loss in the A10 dopaminergic group in the ventral tegmental area (VTA), often have increased sleepiness, which is made worse by D 2 receptor (autoreceptor) agonists (Larsen and Tandberg, 2001;Arnulf et al, 2002). Despite this evidence, the specific population of dopaminergic neurons responsible for arousal is not known.…”

Section: Introductionmentioning

confidence: 99%

Identification of Wake-Active Dopaminergic Neurons in the Ventral Periaqueductal Gray Matter

Lü

Jhou²,

Saper³

2006

J. Neurosci.

410

309

View full text Add to dashboard Cite

Recent evidence suggests that dopamine plays an important role in arousal, but the location of the dopaminergic neurons that may regulate arousal remains unclear. It is sometimes assumed that the dopaminergic neurons in the ventral tegmental area that project to the prefrontal cortex and striatum may regulate the state of arousal; however, the firing of these dopaminergic neurons does not correlate with overall levels of behavioral wakefulness. We identified wake-active dopaminergic neurons by combining immunohistochemical staining for Fos and tyrosine hydroxylase (TH) in awake and sleeping rats. Approximately 50% of the TH-immunoreactive (TH-ir) cells in the ventral periaqueductal gray matter (vPAG) expressed Fos protein during natural wakefulness or wakefulness induced by environmental stimulation, but none expressed Fos during sleep. Fos immunoreactivity was not seen in the substantia nigra TH-immunoreactive cells in either condition. Injections of 6-hydroxydopamine into the vPAG, which killed 55-65% of wake-active TH-ir cells but did not injure nearby serotoninergic cells, increased total daily sleep by ϳ20%. By combining retrograde and anterograde tracing, we showed that these wake-active dopaminergic cells have extensive reciprocal connections with the sleep-wake regulatory system. The vPAG dopaminergic cells may provide the long-sought ascending dopaminergic waking influence. In addition, their close relationship with the dorsal raphe nucleus will require reassessment of previous studies of the role of the dorsal raphe nucleus in sleep, because many of those experiments may have been confounded by the then-unrecognized presence of intermingled wake-active dopaminergic neurons.

show abstract

“…11 Sleep disorders such as obstructive sleep apnea (OSA), restless legs syndrome (RLS), periodic limb movements syndrome (PLMS), and REM sleep behavior disorder (RBD) are commonly reported in patients with PD in rates similar or higher than in the general older adult population. [12][13][14][15][16][17][18][19][20][21][22][23][24][25] Sleep disorders result in complaints about disturbed sleep, excessive daytime sleepiness, cognitive decline, and depression, all of which are also recognized as NMS of PD. [26][27][28][29] Additionally, sleep disorders have been shown to substantially impact healthrelated quality of life in patients with PD.…”

mentioning

confidence: 99%

Effects of Sleep Disorders on the Non-Motor Symptoms of Parkinson Disease

Neikrug

Maglione

Liu³

et al. 2013

Journal of Clinical Sleep Medicine

102

106

View full text Add to dashboard Cite

Study Objectives: To evaluate the impact of sleep disorders on non-motor symptoms in patients with Parkinson disease (PD). Design: This was a cross-sectional study. Patients with PD were evaluated for obstructive sleep apnea (OSA), restless legs syndrome (RLS), periodic limb movement syndrome (PLMS), and REM sleep behavior disorder (RBD). Cognition was assessed with the Montreal Cognitive Assessment and patients completed self-reported questionnaires assessing non-motor symptoms including depressive symptoms, fatigue, sleep complaints, daytime sleepiness, and quality of life. Setting: Sleep laboratory. Participants: 86 patients with PD (mean age = 67.4 ± 8.8 years; range: 47-89; 29 women). Interventions: N/A. Measurements and Results: Having sleep disorders was a predictor of overall non-motor symptoms in PD (R 2 = 0.33, p < 0.001) while controlling for age, PD severity, and dopaminergic therapy. These analyses revealed that RBD (p = 0.006) and RLS (p = 0.014) were signifi cant predictors of increased non-motor symptoms, but OSA was not. More specifi cally, having a sleep disorder signifi cantly predicted sleep complaints (ΔR 2 = 0.13, p = 0.006), depressive symptoms (ΔR 2 = 0.01, p = 0.03), fatigue (ΔR 2 = 0.12, p = 0.007), poor quality of life (ΔR 2 = 0.13, p = 0.002), and cognitive decline (ΔR 2 = 0.09, p = 0.036). Additionally, increasing number of sleep disorders (0, 1, or ≥ 2 sleep disorders) was a signifi cant contributor to non-motor symptom impairment (R 2 = 0.28, p < 0.001). Conclusion: In this study of PD patients, presence of comorbid sleep disorders predicted more non-motor symptoms including increased sleep complaints, more depressive symptoms, lower quality of life, poorer cognition, and more fatigue. RBD and RLS were factors of overall increased non-motor symptoms, but OSA was not. S C I E N T I F I C I N V E S T I G A T I O N SP arkinson disease (PD) is a progressive neurodegenerative disorder primarily characterized by motor symptoms and increasing motor-related disability, including bradykinesia, rigidity, and tremor.1 Non-motor symptoms (NMS) such as sleep dysfunction, sleepiness, fatigue, pain, and depressive symptoms, are common in PD. In a large multicenter study, NMS were reported by 99% of 1072 PD patients.2 The presentation of NMS in PD is highly variable, and the understanding of such heterogeneity in PD is limited and incomplete.3,4 Chaudhuri et al. 4 suggested that NMS dominate the clinical picture in patients with PD and contribute to the severe disability these patients experience, impair quality of life, and even shorten life expectancy. Studies have suggested that NMS, more than motor symptoms, may impact caregiver distress, quality of life, institutionalization rates, and overall costs related to PD .4-6 A 15-year follow-up study of patients with PD reported that the NMS that did not respond to dopamine therapy (e.g., dementia, sleep disruption) were "more disabling than endof-dose failure or dyskinesia" and were the major cause of morbidity and mortality. Sixty to 98% of pati...

show abstract

Parkinson’s disease and sleepiness

Cited by 482 publications

References 24 publications

Objective Evaluation of the Severity of Parkinsonism Using Power-Law Temporal Auto-Correlation of Activity

Objective Evaluation of the Severity of Parkinsonism Using Power-Law Temporal Auto-Correlation of Activity

Identification of Wake-Active Dopaminergic Neurons in the Ventral Periaqueductal Gray Matter

Effects of Sleep Disorders on the Non-Motor Symptoms of Parkinson Disease

Contact Info

Product

Resources

About