Photochemically induced experimental ischemic neuropathy: a clinical, electrophysiological and immunohistochemical study.

A new experimental model of focal peripheral nerve infarction is presented. Ischemia was produced in 12 rats by intravascular thrombosis induced by the photochemical reaction of systemically injected rose bengal to the local application of light from a cold light source. Clinical, electrophysiological and immunohistochemical techniques were used to monitor the pathology and the time course of experimental ischemic neuropathy (EIN) of the sciatic nerve. Primary axonal neurofilament disintegration was detectable 4-24 h after illumination and was followed by wallerian degeneration within the first week. At 7 days, there was a secondary disruption of myelin sheaths accompanied by massive infiltration of macrophages and phagocytosis of the necrotic debris. The majority of detected macrophages were derived from circulating blood monocytes which had invaded the nerve. Two weeks after the initial lesions, degeneration had advanced without any signs of regeneration or remyelination. Electrophysiological recordings corroborate the findings of primary axonal degeneration and failure of regeneration up to 2 weeks after the lesion.