Traumatic damage to the nodal axolemma: an early, secondary injury

Electronmicroscopical investigations were made in a model of optic nerve damage in guinea-pigs on the development of acute axonal damage on an ultrastructural basis. It was expected to obtain thereby further information on mechanisms underlying axonal damage in traumatic brain injury. For that purpose an injury apparatus was employed to deliver defined elongation and/or tensile strains to the optic nerve. Transmission electronmicrographs were examined of longitudinal and transverse nerve sections throughout its entire length. The most severe abnormalities were identified in the prechiasmatic portion of the nerve. Among others, elongations of the nodes of Ranvier were encountered, swollen axons with accumulation of organelles, and even disrupted axons having a morphology similar to retraction balls. In all instances, abnormal axons were found together with axons having a normal structural appearance. Nodes of Ranvier demonstrated outward dilatations of the nodal axolemma and of the adjacent axoplasm, which are named as nodal blebs. Nodal blebs occurred already 15 min after injury, and were fully developed at 6 or 24 hrs. The blebs had disappeared again after 5-7 days. The axoplasm in the blebs demonstrated considerable disorganization of cytoskeletal elements with an array of amorphous material appearing as granular degeneration. Taken together, the present experimental model is a useful approach to analyse axonal damage at the ultrastructural level as it may occur in white matter of the central nervous system.