It has been shown that in diabetic patients, peripheral nerve function is retained during ischemia longer than in normal subjects, indicating some resistance to ischemia. The purpose of the present study was to investigate the mixed nerve function of the median nerve before, during and after 30 min of ischemia, and to evaluate the relations between changes in peripheral nerve function during ischemia and other manifestations of diabetes.
Forty-three diabetics and 9 normal subjects were examined. In order to produce ischemia, a pneumatic cuff was applied around the upper arm, and the pressure was raised to at least 60 mmHg above systolic pressure. Median nerve action potentials (NAP) were evoked by electrical stimulation at the wrist and were recorded with surface electrodes at the elbow every minute during and after the 30min of induced ischemia.
Normal subjects complained of paresthesia soon after the beginning of ischemia, followed by hypesthesia and anesthesia. The amplitudes of the NAP decreased rapidly and disappeared within 18 to 20 min after the beginning of pressure application. On the other hand, ischemia-induced paresthesia and hypesthesia were remarkably reduced in all diabetics. The preischemic amplitudes of the NAP were smaller than those in normal subjects (p<0.005). However, the potential amplitudes during ischemia decreased more slowly than in the controls (after 15 min of ischemia; p<0.001). The disappearance time of NAP during ischemia was longer than 22 min in all diabetics. In only 6 patients, the disappearance time was between 23 and 29 min. The amplitudes of the NAP in the remaining 37 diabetics (86.0%) persisted even after 30 min. This phenomenon was observed in diabetics with no clinical findings or slowing in the nerve conduction studies suggestive of diabetic neuropathy, and was also observed in diabetics with a diabetic history of less than 1 year including 3 patients with IDDM. The amplitudes of the NAP after 15 and 30 min, and the disappearance time of NAP correlated significantly with the HbA1c and HbA1 levels. In addition, the disappearance time of NAP during ischemia improved in patients in optimal glucose control after diet alone or combined with insulin therapy.
It was concluded that the abnormal resistance to ischemia in diabetics could represent one of the earliest manifestations of peripheral nerve dysfunction prior to the appearance of clinical abnormalities and slowed nerve conduction, and might be affected by metabolic defects. The present method is simple and readily available. For its routine clinical use, at least 15 min of ischemia is sufficient to distinguish diabetics from normal subjects.