Phasic muscle activity in sleep and clinical features of Parkinson disease
Article first published online: 12 JUL 2010
Copyright © 2010 American Neurological Association
Annals of Neurology
Volume 68, Issue 3, pages 353–359, September 2010
How to Cite
Bliwise, D. L., Trotti, L. M., Greer, S. A., Juncos, J. J. and Rye, D. B. (2010), Phasic muscle activity in sleep and clinical features of Parkinson disease. Ann Neurol., 68: 353–359. doi: 10.1002/ana.22076
- Issue published online: 30 AUG 2010
- Article first published online: 12 JUL 2010
- Manuscript Accepted: 30 APR 2010
- Manuscript Revised: 25 MAR 2010
- Manuscript Received: 4 SEP 2009
The absence of atonia during rapid eye movement (REM) sleep and dream-enactment behavior (REM sleep behavior disorder [RBD]) are common features of sleep in the alpha-synucleinopathies. This study examined this phenomenon quantitatively, using the phasic electromyographic metric (PEM), in relation to clinical features of idiopathic Parkinson disease (PD). Based on previous studies suggesting that RBD may be prognostic for the development of later parkinsonism, we hypothesized that clinical indicators of disease severity and more rapid progression would be related to PEM.
A cross-sectional convenience sample of 55 idiopathic PD patients from a movement disorders clinic in a tertiary care medical center underwent overnight polysomnography. PEM, the percentage of 2.5-second intervals containing phasic muscle activity, was quantified separately for REM and non-REM (NREM) sleep from 5 different electrode sites.
Higher PEM rates were seen in patients with symmetric disease, as well as in akinetic-rigid versus tremor-predominant patients. Men had higher PEM relative to women. Results occurred in all muscle groups in both REM and NREM sleep.
Although our data were cross-sectional, phasic muscle activity during sleep suggests disinhibition of descending motor projections in PD broadly reflective of more advanced and/or progressive disease. Elevated PEM during sleep may represent a functional window into brainstem modulation of spinal cord activity and is broadly consistent with the early pathologic involvement of non-nigral brainstem regions in PD, as described by Braak. ANN NEUROL 2010