Cerebral Compensation in Parkinson’s Disease: BOLD Activation in the Oculomotor Network after Perturbation of the Parietal Eye Fields: Implications for Parkinson’s Disease

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Parkinson’s disease is characterized by bradykinsesia and akinesia, caused by degeneration of the dopaminergic neurons in the substantia nigra, causing problems in voluntary movement. To overcome these problems patients with Parkinson’s desease can develop compensational strategies in which they are helped by visual information to initiate movements. However, these compensatory mechanisms are not always beneficial as strong visual cues can trigger freezing. In previous eye movement experiments patients with Parkinson’s disease are shown to be more reflexive at pro-saccades, but they have problems in inhibiting these reflexes at anti-saccades. Neuroimaging evidence revealed reduced activity in movement programming regions (frontal eye fields), but increased activity in parietal/occipital visual regions. The aim of the current project is to establish whether this parietal hyperactivity is compensational or pathological. To this end we disrupted activity in the right IPS (parietal eye fields). 2 Parkinson’s patients and 7 healthy controls were tested in a pro- and anti-saccade task in 3 sessions (baseline, after cTBS to IPS and after cTBS to a control region, S1). The BOLD activity in left and right parietal eye fields, frontal eye fields and dorsolateral prefrontal cortex after cTBS to IPS was compared to cTBS to S1. In healthy controls we found increased activity in right FEF after cTBS to right IPS (PEF), suggesting compensation of right FEF. These results are discussed in relation to previous TMS studies, compensation and Parkinson’s disease.
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