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Magnocellular and Parvocellular Mediated Luminance Contrast Discrimination in Severe Alcohol Use Disorder
Author(s) -
Creupelandt Coralie,
Maurage Pierre,
Lenoble Quentin,
Lambot Carine,
Geus Christophe,
D’Hondt Fabien
Publication year - 2021
Publication title -
alcoholism: clinical and experimental research
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.267
H-Index - 153
eISSN - 1530-0277
pISSN - 0145-6008
DOI - 10.1111/acer.14541
Subject(s) - parvocellular cell , contrast (vision) , luminance , psychology , neuroscience , audiology , medicine , optics , physics , central nervous system
Background Severe alcohol use disorder (SAUD) is associated with widespread cognitive impairments, including low‐level visual processing deficits that persist after prolonged abstinence. However, the extent and characteristics of these visual deficits remain largely undetermined, impeding the identification of their underlying mechanisms and influence on higher‐order processing. In particular, little work has been conducted to assess the integrity of the magnocellular (MC) and parvocellular (PC) visual pathways, namely the 2 main visual streams that convey information from the retina up to striate, extrastriate, and dorsal/ventral cerebral regions. Methods We investigated achromatic luminance contrast processing mediated by inferred MC and PC pathways in 33 patients with SAUD and 32 matched healthy controls using 2 psychophysical pedestal contrast discrimination tasks that promote responses of inferred MC or PC pathways. We relied on a staircase procedure to assess participants’ ability to detect small changes in luminance within an array of 4 gray squares that were either continuously presented (steady pedestal, MC‐biased) or briefly flashed (pulsed pedestal, PC‐biased). Results We replicated the expected pattern of MC and PC contrast responses in healthy controls. We found preserved dissociation of MC and PC contrast signatures in SAUD but higher MC‐mediated mean contrast discrimination thresholds combined with a steeper PC‐mediated contrast discrimination slope compared with healthy controls. Conclusion These findings indicate altered MC‐mediated contrast sensitivity and PC‐mediated contrast gain, confirming the presence of early sensory disturbances in individuals with SAUD. Such low‐level deficits, while usually overlooked, might influence higher‐order abilities (e.g., memory, executive functions) in SAUD by disturbing the “coarse‐to‐fine” tuning of the visual system, which relies on the distinct functional properties of MC and PC pathways and ensures proper and efficient monitoring of the environment.