TY  - JOUR
PY  - 2017//
TI  - Bicycling suppresses abnormal beta synchrony in the Parkinsonian basal ganglia
JO  - Annals of neurology
A1  - Storzer, Lena
A1  - Butz, Markus
A1  - Hirschmann, Jan
A1  - Abbasi, Omid
A1  - Gratkowski, Maciej
A1  - Saupe, Dietmar
A1  - Vesper, Jan
A1  - Dalal, Sarang S.
A1  - Schnitzler, Alfons
SP  - 592
EP  - 601
VL  - 82
IS  - 4
N2  - OBJECTIVE: Freezing of gait is a poorly understood symptom of Parkinson's disease, and can severely disrupt the locomotion of affected patients. However, bicycling ability remains surprisingly unaffected in most patients suffering from freezing suggesting functional differences in the motor network. The purpose of this study was to characterize and contrast the oscillatory dynamics underlying bicycling and walking in the basal ganglia. <br><br>METHODS: We present the first local field potential recordings directly comparing bicycling and walking in Parkinson's disease patients with electrodes implanted in the subthalamic nuclei for deep brain stimulation. Low (13-22 Hz) and high (23-35 Hz) beta power changes were analyzed in 22 subthalamic nuclei from 13 Parkinson's disease patients (57.5 +/- 5.9 years, four female). The study group consisted of five patients with and eight patients without freezing of gait. <br><br>RESULTS: In patients without freezing of gait, both bicycling and walking led to a suppression of subthalamic beta power (13-35 Hz), and this suppression was stronger for bicycling. Freezers showed a similar pattern in general. Superimposed on this pattern, however, we observed a movement-induced, narrowband power increase around 18 Hz, which was evident even in the absence of freezing. <br><br>INTERPRETATION: These results indicate that bicycling facilitates overall suppression of beta power. Furthermore, movement leads to exaggerated synchronization in the low beta band specifically within the basal ganglia of patients susceptible to freezing. Abnormal ∼18 Hz oscillations are implicated in the pathophysiology of freezing of gait, and suppressing them may form a key strategy in developing potential therapies. This article is protected by copyright. All rights reserved.<br><br>© 2017 American Neurological Association.<p />  <p>Language: en</p>
LA  - en
SN  - 0364-5134
UR  - http://dx.doi.org/10.1002/ana.25047
ID  - ref1
ER  -