Visuo-perceptual deficits and visual hallucinations (VHs) are common disturbances in patients with dementia with Lewy bodies (DLB) and those with Parkinson’s disease (PD). In particular, delays in visual evoked potential (VEP), reversed by l-dopa administration, have previously been observed in PD patients. Impairment in metabolic functions of dopaminergic amacrine cells within the inner plexiform layer of the retina has been largely documented and has been posited as the underlying cause of visual and retinal alterations in PD. The aims of the present study were to investigate the presence of VEP abnormalities in DLB patients, as compared to a PD control group, and to assess the presence of significant correlations between neurophysiological measures and clinical symptoms (i.e., presence of visuospatial deficits and/or visual hallucinations).

Fifteen DLB patients and fifteen matched PD patients underwent pattern reversal before and after l-dopa administration, and a short neuropsychological assessment.

In DLB patients, we observed delay of the P100 latency to foveal stimuli in both eyes compared to normative values. Compared to PD, DLB patients showed higher values of the P100 latency for foveal stimulation from the right eye prior to l-dopa administration (p = 0.018). No correlations between VEP alterations, visuo-spatial deficit and visual hallucinations were found.

Our findings demonstrated a longer P100 delay in DLB than in PD patients, especially along the right visual pathway. In contrast to previous studies, which focused on a dopaminergic pre-geniculate impairment of visual pathways, our evidence suggests that other mechanisms, possibly relying on thalamic involvement, which is known to be dysfunctional in DLB, can interfere with VEP abnormalities.