Experimental motor neuropathy in diabetes.

Motor dysfunction in diabetes is less prevalent than sensory symptoms but still remains an important clinical complication. Experimental studies using rodent models have shed light on several key components that likely contribute to motor dysfunction. Measurements of motor nerve conduction velocities have been a standard for identifying motor dysfunction; however, the validity and relevance of these early changes in axon conduction velocities to human diabetic neuropathy is questionable. This is supported by difficulties in establishing causative pathologic alterations in motor neurons or motor axons in rodents. This caveat has led to identification of additional mechanisms that contribute to motor dysfunction, including diabetes-associated abnormalities in motor units, innervation of the neuromuscular junction, and intrinsic problems in skeletal muscle. In addition, deficiencies in sensory feedback from skeletal muscles may contribute to changes in motor control. It is clear that increased studies of experimental interventions are needed, and future studies should account for diabetes-induced changes at multiple sites of motor control, ranging from the motor neurons to skeletal muscle. In addition, future experimental studies should be encouraged to extend beyond measurements of conduction velocity and include modern behavioral and imaging techniques to identify causative mechanisms and validate experimental interventions that improve motor control.