Electrophysiological signatures of visual cortical dysfunction in Parkinson's disease: An integrative EEG-based review.
Electrophysiological signatures of visual cortical dysfunction in Parkinson's disease: An integrative EEG-based review.
Where did the research take place?
The study site has not been established. Author addresses may differ from where the research occurred.
Universidad, ES · Author affiliation
Universidad del Atlántico Medio, Carretera de Quilmes 37, 35017 Tafira Baja, Las Palmas de Gran Canaria, Spain. Electronic address: emilia.samit@pdi.atlanticomedio.es.Location evidence
Las Palmas de Gran Canaria, ES · Author affiliation
Universidad del Atlántico Medio, Carretera de Quilmes 37, 35017 Tafira Baja, Las Palmas de Gran Canaria, Spain. Electronic address: emilia.samit@pdi.atlanticomedio.es.Location evidence
Rio Grande, BR · Author affiliation
Universidade Federal do Rio Grande, Campus Carreiros, Av. Itália, km 8, Carreiros, Rio Grande, RS, 96203-900, Brazil.Location evidence
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Original abstract
Parkinson's disease (PD) can disrupt retinal, early cortical, oscillatory, and distributed visuoperceptual processing. This structured integrative review synthesized human evidence from pattern electroretinography (PERG), electroretinography (ERG), optical coherence tomography (OCT)-linked and conventional visual evoked potentials (VEPs), visual event-related potentials (ERPs), electroencephalography (EEG), steady-state visual evoked potentials (ssVEPs), and occipital transcranial magnetic stimulation-electroencephalography (TMS-EEG), with searches verified up to 18 July 2026. Findings were organized into four domains: 1) Retinal and retinocortical contributions: retinal dysfunction can delay or attenuate afferent input, yet concurrent retinal physiology is rarely measured; therefore VEP abnormalities cannot generally be assigned specifically to cortex. 2) Early visual encoding: prolonged pattern-reversal P100 latency is the most reproducible finding, including a pooled 6.04-ms delay across 20 case-control studies, whereas amplitude findings are inconsistent. 3) Oscillatory dynamics: PD-specific ssVEP evidence suggests altered contextual gain, but it derives from one small unreplicated study; gamma-band and task-EEG findings remain sparse and confound-sensitive. 4) Higher-order and network-level processing: visual ERPs, resting microstates, and occipital TMS-EEG indicate possible associations with hallucinations, cognition, and network connectivity, but current studies are cross-sectional or unreplicated. Overall, PD is characterized by multilevel visual-pathway dysfunction rather than a single cortex-specific biomarker. Ophthalmic status, retinal physiology, medication state, cognition, mood, sleep, and recording quality should be controlled before electrophysiological measures are used for localization, stratification, or prognosis.