Abstract

The mechanism of bitemporal hemianopia arising as a result of chiasmal compression is unknown. In this study, we combined an ex vivo experiment and finite element modelling (FEM) to investigate its potential mechanism. A cadaveric human optic chiasm was scanned using micro-CT before and after deformation by inflation of Foley catheter, to simulate tumour growth from beneath. The geometry of the same chiasm was reconstructed and simulated using finite element analysis. Chiasmal deformations were extracted from the simulation and compared with those observed during micro-CT scanning. In addition, nerve fibre models examining variation in local fibre distribution patterns of the chiasm were incorporated to investigate the strain (deformation) distributions of the chiasm at an axonal level. The FEM model matched the micro-CT scans well both qualitatively and quantitatively. Compression of the chiasm induced high strains in the paracentral portions of the chiasm where the crossing optic nerve fibres are located. At an axonal level, the magnitude of strains affecting crossed fibres were greater than those affecting uncrossed fibres. The high strains in the paracentral portions of the chiasm, combined with the differences in strain between crossed and uncrossed nerve fibres, are consistent with a biomechanical explanation for the pattern of visual field loss seen in chiasmal compression.

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