The unstable bridge from stimulus processing to correct responding in Parkinson's disease.
It has been assumed that the basal ganglia implement links between stimulus (S) processing and motor response (R). It has also been proposed that the P3b component of the event-related EEG potential, which is usually as large in R- as in S-locked averages over trials, is a candidate marker to reveal integrity of S-R links. Therefore, the P3 complex (consisting of P3a and P3b) was here measured in averages over trials time-locked either to S or to the key-press R. P3b was expected to be equally large in healthy participants' R- and S-locked averages but to be smaller in R-locked than S-locked averages of patients with Parkinson's disease (PD) (n=12 each), reflecting the loss of S-R links in PD. It has been further assumed that the basal ganglia extract unambiguous results from complex signal patterns thereby resolving discrepancies between competing responses. If so, signals arriving at PD patients' cortex may still be discrepant and produce conflicts, as indicated by error-negativity (NE)-type components even with PD patients' correct responses. As expected, healthy persons had equal S- and R- locked P3b amplitudes and topographies, and PD patients had smaller P3b amplitudes in R-locked than S-locked averages. This latter result was due to an R-related fronto-central negative shift, overlapping PD patients' P3b in the final 100 ms before overt responding. This negativity might indicate response conflict even with correct responses. In line with this interpretation, PD patients had an N(E)-type signal in error trials not only in R-locked averages, like healthy participants, but in S-locked averages as well. These findings support the discrepancy-resolving hypothesis of the basal ganglia and suggest that the overlap of P3b by N(E)-type components, related both to S and R, may reflect a major pathophysiological feature in Parkinson's disease.
Department of Neurology, University of Lübeck, D 23538 Lübeck, Germany. Electronic address: rolf.verleger@neuro.uni-luebeck.de.
Rolf
R
Verleger
Henning
H
Schroll
Fred H
FH
Hamker
D000368:Aged; D000704:Analysis of Variance; D001931:Brain Mapping; D002540:Cerebral Cortex / Q000503:physiopathology; D004569:Electroencephalography; D018913:Event-Related Potentials, P300 / Q000502:physiology*; D005260:Female; D007839:Functional Laterality; D006801:Humans; D008297:Male; D008875:Middle Aged; D010300:Parkinson Disease / Q000503:physiopathology*; D010364:Pattern Recognition, Visual / Q000502:physiology; D010775:Photic Stimulation; D011930:Reaction Time / Q000502:physiology; D013997:Time Factors
Action selection; Basal ganglia; N(E); N-120; P300; Parkinson's disease