Nerve and muscle in steroid-induced weakness in the rabbit.

The purpose of this study was (1) to produce a cortisone induced myopathy, (2) to find out whether or not there is an associated neuropathy, and (3) if a cortisone induced neuropathy is produced, to determine its temporal relation to the myopathy. Several corticosteroid preparations were administered to rabbits, in different dosages and for different periods of time in an attempt to produce maximal effects. Decadron and cortisone acetate in doses of 0.8 mg/kg of body weight and 10 mg/kg of body weight respectively, proved most effective in producing a myopathy. Higher dosages of decadron were fatal, and hydrocortisome, 10 mg/kg of body weight, was not effective. Experimental animals receiving effective doses of decadron, cortisone acetate, and hydrocortisone lost weight, became less agile and, with continued administration of corticosteroids, became immobile. Hind limbs were affected earlier than forelimbs. The muscle lesion consisted of Z-line irregularity and streaming, vacuolation, variation in fiber size, fragmentation and phagocytosis. Cytologic alterations consisted of Z-line streaming, mitochondrial and lipid aggregates and myofilamentous disarray and disorganization. Sciatic nerve histological and cytological findings were not different from controls. They consisted of minor degrees of thickening and tortuosity of myelin sheaths which occurred in both controls and experimental animals. The electron microscopic findings in the sciatic nerve following cortisone administration have not heretofore been reported in the literature. It is concluded that cortisone myopathy is due to a primary effect of cortisone on skeletal muscle and not secondary to a peripheral nerve lesion.