6533b7d4fe1ef96bd1261f8e

RESEARCH PRODUCT

Attenuated beta rebound to proprioceptive afferent feedback in Parkinson's disease.

Mikkel C. VindingPer SvenningssonHarri PiitulainenMartin IngvarVeikko JousmäkiVeikko JousmäkiVeikko JousmäkiDaniel LundqvistJosefine BlumePanagiota Tsitsi

subject

0301 basic medicineMaleParkinson's diseaselcsh:MedicineStimulationAntiparkinson AgentsLevodopa0302 clinical medicineFeedback SensoryMedicine:Science::Medicine [DRNTU]lcsh:Science0303 health sciencesMultidisciplinarymedicine.diagnostic_testMotor CortexMagnetoencephalographyParkinson DiseaseMiddle Aged3. Good healthProprioceptive functioncortexmedicine.anatomical_structureFemaleMotor cortexmedicine.drugAdultLevodopaParkinsonin tautiSensory systemArticle03 medical and health sciencesmotor cortexMotor systemHumans030304 developmental biologyAgedProprioceptionbusiness.industrylcsh:RMagnetoencephalographyIndex fingermedicine.diseaseProprioceptionaivokuori030104 developmental biologylcsh:QbusinessBeta RhythmNeuroscience030217 neurology & neurosurgery

description

AbstractMotor symptoms are defining traits in the diagnosis of Parkinson’s disease (PD). A crucial component in motor function and control of movements is the integration of efferent signals from the motor network to the peripheral motor system, and afferent proprioceptive sensory feedback. Previous studies have indicated abnormal movement-related cortical oscillatory activity in PD, but the role of the proprioceptive afference on abnormal oscillatory activity in PD has not been elucidated. In the present study, we examine the role of proprioception by studying the cortical processing of proprioceptive stimulation in PD patients, ON/OFF levodopa medication, as compared to that of healthy controls (HC). We used a proprioceptive stimulator that generated precisely controlled passive movements of the index finger and measured the induced cortical oscillatory responses following the proprioceptive stimulation using magnetoencephalography (MEG). Both PD patients and HC showed a typical initial mu/beta-band (8–30 Hz) desynchronization during the passive movement. However, the subsequent beta rebound after the passive movement that was apparent in HC was much attenuated and almost absent in PD patients. Furthermore, we found no difference in the degree of beta rebound attenuation between patients ON and OFF levodopa medication. Our results hence demonstrate a disease-related deterioration in cortical processing of proprioceptive afference in PD, and further suggest that such disease-related loss of proprioceptive function is due to processes outside the dopaminergic system affected by levodopa medication.

10.1038/s41598-019-39204-3https://pubmed.ncbi.nlm.nih.gov/30796340