Levodopa‐induced dyskinesia in Parkinson disease: Sleep matters

Objective The spectrum of clinical symptom changes during the course of Parkinson disease (PD). Levodopa therapy, while offering remarkable control of classical motor symptoms, causes abnormal involuntary movements as the disease progresses. This levodopa‐induced dyskinesia (LID) has been associated...

Celý popis

Uloženo v:
Podrobná bibliografie
Vydáno v:Annals of neurology Ročník 84; číslo 6; s. 905 - 917
Hlavní autoři: Amato, Ninfa, Manconi, Mauro, Möller, Jens C., Sarasso, Simone, Stanzione, Paolo, Staedler, Claudio, Kaelin‐Lang, Alain, Galati, Salvatore
Médium: Journal Article
Jazyk:angličtina
Vydáno: United States Wiley Subscription Services, Inc 01.12.2018
Témata:
Cortex
Disease control
Dyskinesia
EEG
Electroencephalography
Excitability
Eye movements
Levodopa
Motor task performance
Movement disorders
Neurodegenerative diseases
Neuroplasticity
NREM sleep
Parkinson's disease
Patients
Sleep
Synaptic strength
ISSN:0364-5134, 1531-8249, 1531-8249
On-line přístup:Získat plný text
Tagy: Přidat tag
Žádné tagy, Buďte první, kdo vytvoří štítek k tomuto záznamu!
Popis
Shrnutí:Objective The spectrum of clinical symptom changes during the course of Parkinson disease (PD). Levodopa therapy, while offering remarkable control of classical motor symptoms, causes abnormal involuntary movements as the disease progresses. This levodopa‐induced dyskinesia (LID) has been associated with abnormal cortical plasticity. Because slow wave activity (SWA) of nonrapid eye movement (NREM) sleep underlies adjustment of cortical excitability, we sought to elucidate the relationship between this physiological process and LID. Methods Thirty‐six patients at different stages of PD underwent whole‐night video polysomnography–high‐density electroencephalography (vPSG‐hdEEG), preceded by 1 week of actigraphy. To represent the broad spectrum of the disease, patients were divided into 3 groups by disease stage—(1) de novo (n = 9), (2) advanced (n = 13), and (3) dyskinetic (DYS; n = 14)—were compared to an age‐matched control group (n = 12). The SWA‐NREM content of the vPSG‐hdEEG was then temporally divided into 10 equal parts, from T1 to T10, and power and source analyses were performed. T2‐T3‐T4 were considered early sleep and were compared to T7‐T8‐T9, representing late sleep. Results We found that all groups, except the DYS group, manifested a clear‐cut SWA decrease between early and late sleep. Interpretation Our data demonstrate a strong pathophysiological association between sleep and PD. Given that SWA may be a surrogate for synaptic strength, our data suggest that DYS patients do not have adequate synaptic downscaling. Further analysis is needed to determine the effect of drugs that can enhance cortical SWA in LID. Ann Neurol 2018;84:905–917
Bibliografie:ObjectType-Article-1
SourceType-Scholarly Journals-1
ObjectType-Feature-2
content type line 14
content type line 23
ISSN:0364-5134
1531-8249
1531-8249
DOI:10.1002/ana.25360