Traumatically induced axonal damage without concomitant change in focally related neuronal somata and dendrites.

Traumatic head injury has long been associated with the genesis of reactive axonal change, which many believe to be a major factor in influencing neurological outcome. Although much significance has been attached to such a traumatically induced axonal change, little information exists as to whether such a reactive change occurs as an isolated event or rather as an event associated with concomitant focal tissue damage, possibly involving related neuronal somal and dendritic elements. This issue was critically assessed in mechanically brain-injured cats in which the anterograde axonal transport of horseradish peroxidase was employed to detect reactive axonal change. Following such traumatically induced reactive axonal change over a 21-day post-traumatic period, altered axons were consistently observed within the red, vestibular and reticular nuclei and any evidence for concomitant change within the related neuronal somal and dendritic elements was assessed using light and electron microscopy. Typically, such axonal change occurred without any evidence of focally related somatic or dendritic alteration. Isolated examples of reactive axons approximating neurons undergoing chromatolysis were observed. However, such neuronal chromatolytic change appeared not to be a primary response to trauma, but rather a response secondary to severence of these neurons' axonal projections. The results of this study demonstrate that, in mild to moderate head injury, reactive axonal change does occur in isolation from other forms of focal parenchymal abnormality. This finding, therefore, emphasizes the concept that the number of axons damaged is most likely related to the magnitude of any ensuing neurological abnormality.