The effect of traumatic brain injury on the visual system: a morphologic characterization of reactive axonal change.

Reactive axonal changes following fluid-percussion brain injury were studied in the highly organized afferent pathways of the cat visual system. The visual system offers several features advantageous to the study of traumatic brain injury. Specifically, as the retinal cells of origin of the optic nerve and tract are isolated from the employed fluid-percussion injury, concomitant traumatically induced somatic change is not a confounding variable. Additionally, the existence of axons of varying diameters and topographic localization within the visual pathways allows the relationship between both fiber size and distribution and their predilection for traumatically induced change to be considered. Since the visual pathway is a highly organized sensory pathway, data obtained in this system can be compared with similar studies previously conducted in motor systems. In these experiments, 20 adult cats were subjected to brain injury and killed at posttraumatic survival periods ranging from 2 to 60 days. Six cats received intravitreous injections of horseradish peroxidase (HRP) to aid in the recognition of axonal change. At the designated survival time, all animals were perfused with aldehydes. The visual system from optic chiasm to lateral geniculate was sectioned and prepared for routine light (LM) and electron microscopic (TEM) study. Animals injected with HRP were processed for the LM and TEM visualization of HRP reaction products. By the second posttraumatic day, reactive axonal swellings were observed in the optic tracts as they entered the medial intralaminar nuclei of the lateral geniculate bodies. Proximal segments of the reactive axons showed enlargement and lobulation, whereas the distal segments underwent wallerian degeneration. Over a 2 week posttraumatic course, some axonal swelling persisted unchanged, some degenerated, and others initiated regenerative sprouting. with continued survival, however, all the reactive swellings manifested only progressive degenerative change. These reactive axonal changes appeared to constitute a primary response to the traumatic episode and occurred without concomitant damage to either the related brain parenchyma or its intrinsic vasculature. Although these findings replicate many of those previously described in motor pathways, new conceptual information has been provided. These studies preclude concomitant somal damage as a confounding variable and suggest that large-caliber axons are susceptible to the shear and tensile forces of traumatic brain injury.