Incomplete infarction of the tibial nerve was produced in 37 rats by injecting arachidonic acid into the femoral artery. Sciatic-tibial motor nerve conduction studies were performed 1, 2, 3 and 7 days later. In all animals the evoked motor responses were of low amplitude and morphological examination showed axonal degeneration. In 20 rats the response elicited by proximal stimulation was of lower amplitude than the distal response indicating focal conduction block in a proportion of those axons which had survived the ischemia and were not degenerating distally. The conduction block resolved over several days and in all but one rat had disappeared by 7 days. Morphological examination of semithin sections and single teased myelinated axons revealed no evidence of segmental demyelination. The rapid resolution of conduction block and the lack of significant segmental demyelination suggest that it has a metabolic basis. We suggest that hypoperfusion of the subperineurial region of the proximal tibial nerve, the region surrounding the infarct through which surviving axons pass, may be sufficient to temporarily block impulse transmission in these surviving axons without producing morphological changes.