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PreprintCC BYmedRxiv

Reactive Compensation for Proactive Deficits in Parkinsons Disease

  1. 1Department of Neurology, School of Medicine and Health Science, Carl von Ossietzky University of Oldenburg, 26046 Oldenburg, Germany

Abstract

The dual mechanisms of control (DMC) framework distinguishes between proactive (anticipatory) and reactive (post-conflict) adaptive cognitive control mechanisms. Evidence for proactive deficits in Parkinsons disease (PD) is inconsistent, and the neurophysiological underpinnings remain poorly understood. We investigated adaptive control in 30 PD patients and 30 demographically similar healthy controls. Adaptive cognitive control was tested using a numerical Stroop test that included manipulations sensitive to proactive and reactive control. In both behavioral and EEG analyses, inducer items that trigger control adaptation were distinguished from diagnostic items, allowing adaptation to be assessed independently of learning effects. Event-related potentials (ERPs) derived from electroencephalography (EEG) captured signatures of proactive (N450) and reactive (Late Positive Complex, LPC) control.

The HC group showed robust proactive control with faster responses compared to reaction times to reactive control condition, whereas PD revealed reduced proactive control, particularly for diagnostic items. ERP analysis indicated a clear N450 in the HC group, whereas the N450 was absent in the PD group. Both groups displayed LPC activity during reactive control, but PD also showed LPC activity in the adaptive proactive control condition, suggesting compensatory reliance on reactive mechanisms. Both, behavioural and ERP analyses provide insights into the dissociation of reactive and proactive control processes in PD. Our findings indicate selective impairments in proactive control, along with preserved reactive control, in patients with PD. Moreover, the presence of the LPC during proactive control trials suggests that the recruitment of reactive control mechanisms may compensate deficits in proactive control in PD.

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BibTeX
@misc{ficke2026reactive,
  title = {{Reactive Compensation for Proactive Deficits in Parkinsons Disease}},
  author = {J. Ficke and J. Kricheldorff and S. Debener and K. Janitzky and K. Witt},
  howpublished = {medRxiv},
  year = {2026},
  month = sep,
  doi = {10.64898/2026.09.10.26362782},
  url = {https://www.medrxiv.org/content/10.64898/2026.09.10.26362782v1},
  note = {CC BY},
}
RIS
TY  - UNPB
TI  - Reactive Compensation for Proactive Deficits in Parkinsons Disease
AU  - J. Ficke
AU  - J. Kricheldorff
AU  - S. Debener
AU  - K. Janitzky
AU  - K. Witt
PY  - 2026
DA  - 2026/09/10
PB  - medRxiv
DO  - 10.64898/2026.09.10.26362782
UR  - https://www.medrxiv.org/content/10.64898/2026.09.10.26362782v1
AB  - The dual mechanisms of control (DMC) framework distinguishes between proactive (anticipatory) and reactive (post-conflict) adaptive cognitive control mechanisms. Evidence for proactive deficits in Parkinsons disease (PD) is inconsistent, and the neurophysiological underpinnings remain poorly understood. We investigated adaptive control in 30 PD patients and 30 demographically similar healthy controls. Adaptive cognitive control was tested using a numerical Stroop test that included manipulations sensitive to proactive and reactive control. In both behavioral and EEG analyses, inducer items that trigger control adaptation were distinguished from diagnostic items, allowing adaptation to be assessed independently of learning effects. Event-related potentials (ERPs) derived from electroencephalography (EEG) captured signatures of proactive (N450) and reactive (Late Positive Complex, LPC) control.  The HC group showed robust proactive control with faster responses compared to reaction times to reactive control condition, whereas PD revealed reduced proactive control, particularly for diagnostic items. ERP analysis indicated a clear N450 in the HC group, whereas the N450 was absent in the PD group. Both groups displayed LPC activity during reactive control, but PD also showed LPC activity in the adaptive proactive control condition, suggesting compensatory reliance on reactive mechanisms. Both, behavioural and ERP analyses provide insights into the dissociation of reactive and proactive control processes in PD. Our findings indicate selective impairments in proactive control, along with preserved reactive control, in patients with PD. Moreover, the presence of the LPC during proactive control trials suggests that the recruitment of reactive control mechanisms may compensate deficits in proactive control in PD.
ER  -