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Published on: April 14, 2014
Tri-modal assessment reveals early visual pathway degeneration in patients with MSA-C
Chunrong Wang1, Feiyan Deng2, Zhao Chen3
1Department of Neurology, Xiangya Hospital, Central South University, Changsha, Hunan, China; Department of Pathology, Xiangya Hospital, Central South University, Changsha, Hunan, China; Key Laboratory of Hunan Province in Neurodegenerative Disorders, Central South University, Changsha, Hunan, China; Bioinformatics Center & National Clinical Research Center for Geriatric Disorders, Xiangya Hospital, Central South University, Changsha, Hunan, China.
Background And Objectives:
Post-mortem evidence suggests neurodegeneration in the visual pathway in multiple system atrophy-cerebellar type (MSA-C), yet robust in vivo evidence remains scarce. This study aimed to characterize these visual pathway changes in MSA-C patients by integrating optical coherence tomography (OCT), visual evoked potential (VEP), and magnetic resonance imaging (MRI).
Methods:
This cross-sectional study prospectively recruited 156 participants, including 53 healthy controls and 103 early-stage MSA-C patients (mean disease duration: approx. 2 years). All participants underwent retinal layer evaluation using OCT. A randomly selected subset of 34 MSA-C patients and 19 controls also received VEP and MRI to assess visual pathway structure and function comprehensively.
Results:
OCT analysis revealed significant parafoveal thinning within the 3-mm inner ring in MSA-C patients, predominantly affecting the ganglion cell layer (GCL) (P < 0.001) and inner plexiform layer (IPL) (P < 0.001). VEP recordings demonstrated significantly prolonged P100 latency (P < 0.001). MRI confirmed reduced cerebellar volume (P < 0.001). DTI detected microstructural degeneration in the cerebellum and visual pathways, with increased mean and axial diffusivity in optic tracts and radiation. Notably, retinal thinning correlated significantly with longer P100 latency (GCL: r = 0.49, P = 0.003; IPL: r = 0.41, P = 0.015) and cerebellar atrophy (GCL: r = 0.53, P = 0.001; IPL: r = 0.49, P = 0.003), indicating integrated visual pathway degeneration.
Conclusions:
This large-scale multimodal study provides robust in vivo evidence that MSA-C involves early retinal neurodegeneration, functional conduction delay, and central white matter degeneration. The convergence of OCT, VEP, and DTI parameters suggests bidirectional retinocortical degeneration. Our findings support the potential of these parameters for early detection and highlight the visual pathway as a promising potential biomarker in synucleinopathies.
