Though understudied when compared with peripheral nerve, it is clear that the spinal cord is not protected from diabetes-induced injury and that structural and functional damage is discernable in diabetic subjects. Animal models of diabetes show a number of disorders similar to those seen in humans and these changes are accompanied by neurochemical changes, which may have functional significance. Because the spinal cord is the first site of integration of sensory input from the periphery and the last site of descending control of sensory and motor systems, disruption of spinal cord function has the capacity to impede appropriate CNS control systems and contribute to apparent peripheral neuropathy. The extent to which aberrant spinal cord processing is evoked by direct metabolic consequences of diabetes or is secondary to peripheral neuropathy, is an intriguing question that has not yet been widely addressed.

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