Harris P. Mosher Award thesis. The recovery potential of the optic nerve.

Abstract

Optic nerve dysfunction can be secondary to mass lesions, osseous compression states, inflammatory disorders, ischemia, increased cerebrospinal fluid pressure, and trauma. Representative clinical material from each of these areas is described, with an institutional review of 70 cases that were managed surgically. It is evident that compromise of optic nerve function can resolve with medical and surgical therapy. This clinical review is designed to highlight factors that favor this recovery. Although each condition has unique characteristics, an evaluation of clinical disorders that affect the nerve from globe to optic chiasm is presented as a comprehensive review of optic neuropathy. It is apparent from the literature that many questions need to be answered concerning the pathophysiology of optic nerve injury and the factors that influence recovery. A basic animal model for the analysis of these questions has been developed. An optic nerve injury produced in the cat leads to progressive loss of myelin but preservation of axons, the precise theoretic state that may be reversible with corticosteroid therapy or surgical management. Finally, the model may allow future study of the biochemical mediators of injury and the factors that promote recovery.