Neural correlates of rate-dependent finger-tapping in Parkinson’s disease
- First Online:
- Cite this article as:
- Wurster, C.D., Graf, H., Ackermann, H. et al. Brain Struct Funct (2015) 220: 1637. doi:10.1007/s00429-014-0749-1
- 441 Downloads
Functional imaging demonstrated hemodynamic activation within specific brain areas that contribute to frequency-dependent movement control. Previous investigations demonstrated a linear relationship between movement and hemodynamic response rates within cortical regions, whereas the basal ganglia displayed an inverse neural activation pattern. We now investigated neural correlates of frequency-related finger movements in patients with Parkinson’s disease (PD) to further elucidate the neurofunctional alterations in cortico-subcortical networks in that disorder. We studied ten PD patients (under dopaminergic medication) and ten healthy subjects using a finger-tapping task at three different frequencies (1–4 Hz), implemented in an event-related, sparse sampling fMRI design. FMRI data were analyzed by means of a parametric approach to relate movement rates and regional BOLD signal alteration. Compared to healthy controls, PD patients showed higher tapping response rates only during the lower 1 Hz condition. FMRI analysis revealed a rate-dependent neural activity within the supplemental motor area, primary sensorimotor cortex, thalamus and the cerebellum with higher neural activity at higher frequency conditions in both groups. Within the putamen/pallidum, an inverse neural activity and frequency response correlation could be observed in healthy subjects with higher BOLD signal responses in slow frequencies, whereas this relationship was not evident in PD patients. We could demonstrate similar behavioral responses and neural activation patterns at the level both of frontal and cerebellar areas in PD compared to healthy controls, whereas regions like the putamen/pallidum appear to be still dysfunctional under medication regarding frequency-related neural activation. These findings may, potentially, serve as a neural signature of basal ganglia dysfunctions in frequency-related task requirements.