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.