Independent patterns of damage within magno-, parvo- and koniocellular pathways in Parkinson's disease

• Autor(a) principal: Silva, M. F.
• Data de Publicação: 2005
• Outros Autores: Faria, P., Regateiro, F. S., Forjaz, V., Januário, C., Freire, A., Castelo-Branco, M.
• Tipo de documento: Artigo
• Idioma: eng
• Título da fonte: Repositório Científico de Acesso Aberto de Portugal (Repositórios Cientìficos)
• Texto Completo: http://hdl.handle.net/10316/12650; https://doi.org/10.1093/brain/awl292
• topic: Contrast sensitivity; Koniocellular; Magnocellular; Parkinson’s disease; Parvocellular

Sensory deficits have been documented in Parkinson's disease, in particular within the visual domain. However, ageing factors related to the brain and to neural and non-neural ocular structures could explain some of the previously reported results, in particular the claimed impairment within the koniocellular pathway. This study addressed visual impairment attributable to the magno- (luminance), parvo- (red-green) and koniocellular (blue-yellow) pathways in a population of Parkinson's disease patients. To avoid potentially confounding factors, all subjects underwent a full neurophthalmological assessment which led to exclusion of subjects with increased intraocular pressure, diabetes even in the absence of retinopathy, and ocular abnormalities (from a total of 72 patients' eyes, 12 were excluded). Both parvo- and koniocellular pathways were studied by means of contrast sensitivity (CS) measurements along protan, tritan and deutan axes and also by fitting chromatic discrimination ellipses using eight measured contrast axes. Magnocellular function was assessed, using stimuli that induce a frequency doubling illusion, in 17 locations in the fovea and periphery. Achromatic (luminance modulation) thresholds were significantly higher in Parkinson's disease both in foveal and peripheral locations. A significant impairment was observed along protan and deutan axes, but only marginally along the tritan axis. These results were corroborated by a significant elongation of chromatic discrimination ellipses in our Parkinson's disease group. Correlation analysis showed that achromatic and chromatic CS measures were independent, which implies that multiple visual pathways are affected independently in Parkinson's disease. Magnocellular impairment was significantly correlated with age and disease stage, in contrast to the measured chromatic deficits. We conclude that in Parkinson's disease, independent damage occurs in the early magno- and parvocellular pathways. Furthermore, traditional koniocellular probing strategies in Parkinson's disease may be confounded by ageing factors, which may reconcile the previously reported controversial findings concerning chromatic impairment in Parkinson's disease