Although myelopathy was first described in the spinal cord of diabetic patients at autopsy over 100 years ago, the impact of diabetes on this portion of the nervous system has been infrequently studied compared with the peripheral nervous system (PNS). In part, this may reflect a tendency to target the regions of the nervous system from where patients perceive pain and/or loss of sensation to emanate. The greater accessibility of the peripheral nerves to biopsy and functional studies probably also contributes to the imbalance. Recent technical advances have re-emphasized that the spinal cord is subject to injury in diabetic patients (1) and exhibits unique structural and functional features that possess both scientific and clinical significance. For example, the spinal cord lies within the blood-brain barrier and glucose levels in the cerebrospinal fluid are substantially lower than those to which peripheral nerves are exposed, both in normal and hyperglycemic conditions. Consequently, the cell body and the peripherally projecting axon of a primary sensory neuron are exposed to higher glucose concentrations
From: Contemporary Diabetes: Diabetic Neuropathy: Clinical Management, Second Edition Edited by: A. Veves and R. Malik © Humana Press Inc., Totowa, NJ
during hyperglycemia than the terminal regions of the central projection that enter the spinal cord and synapse with second-order neurons in the dorsal horn. Conversely, motor neuron cell bodies located in the ventral horn are relatively protected in comparison with the sensory cell bodies in the dorsal root ganglia and indeed relative to their own axons that leave the spinal cord and project to target organs. As hyperglycemia is widely regarded as a primary pathogenic mechanism for diabetic neuropathy, the regional variability in glucotoxic exposure may have important consequences for the manifestation of diabetic neuropathy.
There is increasing scientific interest in the spinal cord as clinical and experimental studies have revealed the extent to which it is involved in integrating and modulating both sensory input from peripheral nerves to the higher central nervous system (CNS) and also output from the CNS to peripheral organs. Phenomena such as phantom limb and some neuropathic pain states indicate that the perception and pathogenic site of a lesion do not always match. Research studies of peripheral nerve injury have also highlighted associations between the PNS and spinal cord, such that injury to the PNS can have long-acting consequences in the spinal cord that modify how future sensory input from the PNS is modulated and presented to the CNS. The extent to which the well-documented effects of diabetes on the PNS have an impact on the structure and function of the spinal cord, including its processing of sensory input, is largely unexplored. The direct effects of hyperaglycemia on spinal cord have to be incorporated into the pathogenic scheme of diabetic neuropathy.
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