TY - JOUR
T1 - Cortical correlates of susceptibility to upper limb freezing in Parkinson's disease
AU - Scholten, Marlieke
AU - Govindan, Rathinaswamy B.
AU - Braun, Christoph
AU - Bloem, Bastiaan R.
AU - Plewnia, Christian
AU - Krüger, Rejko
AU - Gharabaghi, Alireza
AU - Weiss, Daniel
N1 - Publisher Copyright:
© 2016 International Federation of Clinical Neurophysiology.
PY - 2016/6/1
Y1 - 2016/6/1
N2 - Objective: Freezing behavior is an unmet symptom in Parkinson's disease (PD), which reflects its complex pathophysiology. Freezing behavior can emerge when attentional capacity is reduced, i.e. under dual task interference. In this study, we characterized the cortical network signatures underlying the susceptibility to freezing during continuous finger tapping. Methods: Fourteen PD patients with STN-DBS and thirteen age- and gender-matched healthy controls performed continuous tapping with the index finger as single motor task and during dual tasking. Synchronized EEG and mechanogram of the finger tapping were recorded. Subsequently, we analyzed cortical activity and cortico-cortical phase synchronization. We correlated these spectral measures with the biomechanically confirmed numbers of freezing episodes during finger tapping. Results: During dual tasking compared to the single motor task, PD patients showed an increase of cortico-cortical phase synchronization over the left prefrontal area from 13 to 30 Hz. This correlated with increased occurrence of freezing episodes. Interestingly, PD patients lacked the increase of prefrontal cortico-cortical synchronization from 4 to 7 Hz during dual tasking as observed in healthy controls. Conclusion: Dual task interference led to an increase of left prefrontal beta band synchronization (13-30 Hz) in PD and this increment predicted the number of freezing episodes. This increment may underscore the relevance of prefrontal executive dysfunction in freezing susceptibility. Significance: These findings enhance our understanding of the pathological network mechanisms behind increased susceptibility to freezing behavior.
AB - Objective: Freezing behavior is an unmet symptom in Parkinson's disease (PD), which reflects its complex pathophysiology. Freezing behavior can emerge when attentional capacity is reduced, i.e. under dual task interference. In this study, we characterized the cortical network signatures underlying the susceptibility to freezing during continuous finger tapping. Methods: Fourteen PD patients with STN-DBS and thirteen age- and gender-matched healthy controls performed continuous tapping with the index finger as single motor task and during dual tasking. Synchronized EEG and mechanogram of the finger tapping were recorded. Subsequently, we analyzed cortical activity and cortico-cortical phase synchronization. We correlated these spectral measures with the biomechanically confirmed numbers of freezing episodes during finger tapping. Results: During dual tasking compared to the single motor task, PD patients showed an increase of cortico-cortical phase synchronization over the left prefrontal area from 13 to 30 Hz. This correlated with increased occurrence of freezing episodes. Interestingly, PD patients lacked the increase of prefrontal cortico-cortical synchronization from 4 to 7 Hz during dual tasking as observed in healthy controls. Conclusion: Dual task interference led to an increase of left prefrontal beta band synchronization (13-30 Hz) in PD and this increment predicted the number of freezing episodes. This increment may underscore the relevance of prefrontal executive dysfunction in freezing susceptibility. Significance: These findings enhance our understanding of the pathological network mechanisms behind increased susceptibility to freezing behavior.
KW - Cortical activity
KW - Electroencephalography
KW - Global phase synchronization
KW - Parkinson's disease
KW - Subthalamic nucleus deep brain stimulation
KW - Upper limb freezing
UR - http://www.scopus.com/inward/record.url?scp=84963567661&partnerID=8YFLogxK
U2 - 10.1016/j.clinph.2016.01.028
DO - 10.1016/j.clinph.2016.01.028
M3 - Article
C2 - 27178857
AN - SCOPUS:84963567661
SN - 1388-2457
VL - 127
SP - 2386
EP - 2393
JO - Clinical Neurophysiology
JF - Clinical Neurophysiology
IS - 6
ER -