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The observed differences in temporal responses to rhEPO between the models could be explained by the magnitude of delayed injury. Specifically, the aneurysm clip model produces a compressive/occlusive injury characterized by transient vascular occlusion and pressure-related block of axonal conduction, but often with minimal disruption of myelin. Restoration of axonal conduction is likely to occur sooner for an axon possessing an intact myelin sheath. In contrast, the impactor model, being primarily mechanical in nature, differentially injures large myelinated fibers, with the most severe damage occurring at the nodes of Ranvier, and tends to spare smaller axons (20). Additionally, significant hemorrhage occurs from the severe parenchymal disruption caused by absorption of kinetic energy. Therefore, in the later stages of response to injury caused by contusion, cellular debris and grossly disrupted axons elicit pronounced inflammatory and degenerative processes that initiate a secondary phase of injury.