An experimental study of the evolution of focal axonal injury

Uniaxial stretch of the optic nerve of the albino guinea pig can reproduce the axonal damage as demonstrated in prolonged traumatic coma in humans and primates. By morphological and neurophysiological approaches we have demonstrated that in the acute phase (24 hrs after injury) axonal lesions are characterized by terminal clubs and focal axonal enlargements along with an elongation of visual evoked potentials (VEPs). In this model, in which the lesion is distributed along the entire nerve, the velocity of the fast phase of axoplasmic transport in injured nerves was increased (218 mm/day vs. 176 mm/day in controls) and so was the amount of transported proteins. There was no accumulation and a block of protein uptake at the site of the lesion as demonstrated in other biological models. One week after injury, axonal lesions observed in the acute phase and alterations of VEPs disappeared, whereas the rate of axonal transport and the amount of protein uptake were persistently increased. Therefore in this model, an increase of anterograde fast transport was demonstrated both in acute and chronic phases. Since regeneration of optic axons was never evident on morphological study, the restoration of axonal function and the persistence of active axonal transport one week after injury support that spontaneous reparative processes occurred in lesioned axons.