P07-F Event related EEG brain oscillations differentiate cognitive decline in patients with Parkinson’s disease

Güntekin, Bahar; Aktürk, Tuba; Yıldırım, Ebru; Mantar, Nagihan; Çadırcı, Fadime; Hanoğlu, Lütfü

doi:10.1016/j.clinph.2019.04.460

Cited by 2 publications

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“…Such changes are reported early in disease progression, and can be measured regardless of disease duration, stage, severity, or medication level [44]. A number of studies demonstrate that in PD, global changes in oscillatory power are correlated with cognitive dysfunction as well (for a review, see [45][46][47][48][49]). Attenuated desynchronization of both beta band [22] and higher alpha band [50] EEG has been reported in people with PD during Go and Nogo trials [51].…”

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confidence: 99%

Cortical oscillatory dysfunction in Parkinson disease during movement activation and inhibition

et al. 2022

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Response activation and inhibition are functions fundamental to executive control that are disrupted in Parkinson disease (PD). We used magnetoencephalography to examine event related changes in oscillatory power amplitude, peak latency and frequency in cortical networks subserving these functions and identified abnormalities associated with PD. Participants (N = 18 PD, 18 control) performed a cue/target task that required initiation of an un-cued movement (activation) or inhibition of a cued movement. Reaction times were variable but similar across groups. Task related responses in gamma, alpha, and beta power were found across cortical networks including motor cortex, supplementary and pre- supplementary motor cortex, posterior parietal cortex, prefrontal cortex and anterior cingulate. PD-related changes in power and latency were noted most frequently in the beta band, however, abnormal power and delayed peak latency in the alpha band in the pre-supplementary motor area was suggestive of a compensatory mechanism. PD peak power was delayed in pre-supplementary motor area, motor cortex, and medial frontal gyrus only for activation, which is consistent with deficits in un-cued (as opposed to cued) movement initiation characteristic of PD.

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