¹⁸F-FDG positron emission tomography as a novel diagnostic tool for peripheral nerve injury

Glucose hypermetabolism in denervated skeletal muscle suggests the potential for developing a diagnostic tool for peripheral nerve injuries. Herein, we investigated the characteristics and molecular mechanism of this phenomenon.

Temporal course of glucose hypermetabolism and development of abnormal spontaneous activities (ASA) through electromyography (EMG) were investigated in rats with complete sciatic nerve injuries. Rats with partial sciatic nerve injuries were used to investigate the relationship between nerve injury severity and change in glucose metabolism. Rapamycin-treated rats were used to study molecular mechanism. Mean lesion-to-normal count ratios (LNR_mean) was calculated as a numeric value of the ¹⁸F-FDG uptake.

Glucose hypermetabolism began 2 days after nerve injury and lasted up to 12 weeks, with the maximum increase at 1 week after denervation (10-fold increase compared to sham-operated muscle; LNR_mean, sham, 1.360 ± 0.452; denervation, 10.340 ± 4.094; n = 5; P < 0.05). The metabolic changes showed similar temporal characteristics to ASA on EMG. The signal intensity of ¹⁸F-FDG uptake in denervated skeletal muscle was strongly related to nerve injury severity in a partial nerve injury model (Pearson correlation coefficient 0.63, P < 0.05). Suppression of mTOR by rapamycin treatment reduced the increase in peak glucose hypermetabolism in muscle denervation.

Metabolic changes in ¹⁸F-FDG PET scans have a wider time span than abnormalities on EMG after denervation and it is correlated with the severity of nerve injury assessed by NCS.

¹⁸F-FDG PET may be used to diagnose and evaluate peripheral nerve injuries.