Although VH are common among patients with PD, the underlying pathophysiological mechanisms of the symptom are unclear. However, one theory suggests dysfunction of attentional networks, in addition to ambiguous visual input, may contribute to VH when remembered images intrude into patients’ consciousness.
During the course of PD, “minor hallucinations may first evolve into VH with retained insight and, subsequently, into multimodality hallucinations with loss of insight and delusions, corresponding to the development of the disease process from the brainstem, through the basal forebrain and ultimately involving widespread cortical brain areas,” authors explained.
To better understand the association between the presence of VH, the ganglion cell layer-inner plexiform layer (GCL-IPL), and visual acuity, researchers collected clinical and demographic data from 40 patients with PD and 22 age- and sex-matched controls. All patients with PD were older than 50 years and had a disease duration of at least 3 years. Patients also exhibited a modified Hoehn and Yahr (mHY) stage between 2 and 5.
Patients’ cognitive functions were evaluated via the Montreal Cognitive Assessment (MoCA) while neurologists interviewed each patient to determine the presence of VH during the last 6 months. Best-corrected visual acuity (BCVA), intraocular pressure, and other ophthalmologic characteristics were also assessed.
Overall, researchers found patients with PD had a lower MoCA score compared with controls and lower intraocular pressure. Fourteen patients (35%) had VH which occurred daily in 50% of patients, weekly in 25%, and monthly in 25% of patients.
Additional analyses revealed:
- Patients with VH had a thinner GCL-IPL than patients without VH, which persisted after correction for age, disease stage, levodopa equivalent daily dose (LED) and cognitive function
- BCVA was lower in PD patients (median [IQR]: 1.0 [0.3]) than in controls (median: 1.1 [0.3]; P < .01)
- disease stage (mHY) was inversely correlated with GCL-IPL thickness (although only at trend level) and with BCVA
Findings suggest ocular pathology may play a role in the development of VH in patients with PD, researchers wrote. They continued, “Our findings are in line with histopathological research showing that PD pathology (i.e. degeneration of amacrine cells and abnormal alpha synuclein depositions) is mainly located in the GCL-IPL.” When compared with other retinal layers, GCL-IPL is also most strongly associated with visual dysfunction.
Because presence of VH was subjective to patients’ recall, bias may have been present, marking a limitation to the study. Authors also cautioned a causal relationship could not be determined due to the nature of the study. Future longitudinal studies in this population, combining repeated measurements of retinal layer thickness and parallel assessments of the presence of visual hallucinations over time, ought to be carried out.
Visser F, Apostolov VI, Vlaar AMM, Twisk JWR, Weinstein HC, and Berendse HW. Visual hallucinations in Parkinson’s disease are associated with thinning of the inner retina. Sci Rep. Published online December 3, 2020. doi:10.1038/s41598-020-77833-1