Brain Networks Implicated in Cerebral Achromatopsia
Mazzy Marcucci1, Elijah Baughan1, Owen Benzley1, Keaton Helquist1, Frederic Schaper2, Michael Ferguson2, Jared Nielsen1
1Brigham Young University, 2Brigham and Women's Hospital, Harvard Medical School
Objective:

To identify the brain regions and networks involved in lesion induced cerebral achromatopsia.

Background:

Cerebral achromatopsia is a perceptual disorder characterized by the partial or complete loss of color vision. It typically results in experiencing the world in shades of gray or sepia tones without damaging other aspects of perceptual vision. Cerebral achromatopsia can be caused by brain lesions such as strokes, encephalitis, tumors, or traumatic brain injuries. Previous research using voxel-wise lesion overlap analysis, which only relies on the lesion site, found evidence of lesion overlap in the ventro-medial occipital, temporal lobes, and fusiform gyri. However, symptoms may better localize to brain networks instead of brain regions.

Design/Methods:

We utilized lesion network mapping, a method that identifies the brain regions functionally connected to the lesion site rather than focusing on the lesion location itself. We performed a systematic literature review to identify relevant case studies including patients showing signs and symptoms of cerebral achromatopsia (n=16). Lesion network mapping analysis was performed on the achromatopsia cases, using a large resting state functional connectivity dataset derived from healthy controls (n=1000). Many of the cases included in the analysis where due to ischemic stroke, while others were incidents from hemorrhagic strokes, brain trauma, encephalitis, or tumors.

Results:

The analysis showed functional connectivity of the fusiform gyrus and anterior lobe of the cerebellum. While our results align with previous reports finding lesions in the fusiform gyrus, the anterior cerebellum was identified as a novel region in the network of cerebral achromatopsia.

Conclusions:

Further research is necessary to determine the specific roles that these networks play and how they might interact with each other to cause cerebral achromatopsia.

 

10.1212/WNL.0000000000205532