This review synthesizes ocular, visuoperceptual, and visuospatial disturbances in Parkinson’s disease (PD) across disease stages, linking bedside task performance with structural/functional brain changes and neurochemistry. Oculomotor problems (impaired saccades, convergence, blinking) are common. PD also shows early retinal thinning and ganglion loss on optical coherence tomography (OCT)/electrophysiology, plus reduced visual acuity (especially low contrast), contrast sensitivity, and color vision. Models implicate degraded bottom-up input with aberrant top-down attention/default-mode activity, involving dopaminergic, cholinergic, and serotonergic systems. Visuospatial/visuoperceptual impairments are common even without dementia, vary by side of onset and motor phenotype, and show sex effects.
Neuroanatomically, poorer visual cognition correlates with cortical thinning and hypometabolism across occipital, parietal, temporal, and frontostriatal networks, worsening with mild cognitive impairment and dementia. Neurochemically, dopamine loss (including retinal) interacts with cholinergic, serotonergic, GABAergic, and noradrenergic systems. Clinically, visual dysfunction is prevalent, under-recognized, and prognostic—linked to hallucinations and elevated dementia risk. This supports routine visual screening (OCT, contrast/color tests, targeted cognitive tasks), attention to sleep/psychosis management, and development of imaging/genetic biomarkers to stratify risk and guide trials.
Reference: Nieto-Escamez F, Obrero-Gaitán E, Cortés-Pérez I. Visual Dysfunction in Parkinson’s Disease. Brain Sci. 2023;13(8):1173. doi: 10.3390/brainsci13081173.
