Spinal Electrophysiology In Diabetes

Conduction Velocity

Slowing of large motor and sensory fiber conduction velocity has long been recognized as an early indicator of neuropathy in the PNS (41,42) and these deficits are widely used to follow progression of neuropathy and assess efficacy of therapeutic interventions. In contrast, there have been relatively few evaluations of spinal electro-physiology in diabetic subjects and such measurements are rarely included in global assessments of neuropathy. Increased latencies, indicative of conduction slowing are described in diabetic subjects (43-45), but it is not definitively established that this disorder shares a common presentation or aetiology with peripheral conduction slowing. For example, evaluation of a series of diabetic subjects indicated that relatively few showed both spinal and PNS conduction slowing, with many cases of either PNS or CNS dysfunction (46) and there is not a strong correlation between conduction slowing in the PNS and CNS (47). It had also been reported that slowing in sensory (ascending) tracts precedes that of motor (descending) tracts (48). The aetiology of CNS conduction slowing is poorly understood and the extent to which it precedes or reflects the pathological changes that occur in the spinal cord described earlier is not known.

There have been occasional reports of conduction slowing in the spinal cord of diabetic rats as early as 2 weeks after onset of hyperglycemia (49), although others reported that months of diabetes were required to show slowing in both ascending and descending tracts (50,51). Again, little is known about the pathogenesis of the disorder and the extent to which it mirrors the early metabolic and later structurally mediated aetiology of PNS conduction slowing has not been established, although conduction slowing in the PNS does appear to precede that in the CNS (51). It may be worth noting that glucose levels in spinal cerebrospinal fluid of diabetic rats are markedly lower than in plasma of the same animals (52), so that spinal axons and lower motor neuron cell bodies are exposed to less glycemic stress than their PNS counterparts.

Response Properties

Characterization of the response properties of spinal neurons that are triggered by peripheral sensory stimuli have been studied only in rats with short-term diabetes. There is agreement that spontaneous activity of the second order neurons that respond to a broad range of sensory stimuli (wide dynamic range or WDR neurons) is increased in spinal cord of diabetic rats (53,54). This could reflect diverse mechanisms including ectopic primary afferent input to the cord, rewiring of spinal synapses or altered post-synaptic signal transduction properties. Increased spontaneous activity of WDR neurons that project to the brain through the spinothalamic tract has been proposed to underlie spontaneous pain and hyperalgesia in diabetes. There is less agreement on other parameters, with a report of increased receptive field size, lower activation thresholds, and augmented responses to mechanical stimulation in ascending (sensory) spinothalamic tract neurons (54) being balanced by another showing no change in these parameters (53). Most recently, the phenomenon of spinal wind-up, where repeated electrical stimulation of C fibers leads to a frequency-dependent increase in the excitability of spinal neurons has been reported to be enhanced in short-term diabetic mice (55), further supporting the idea that spinal mediation of sensory processing is altered by diabetes.

Diabetes 2

Diabetes 2

Diabetes is a disease that affects the way your body uses food. Normally, your body converts sugars, starches and other foods into a form of sugar called glucose. Your body uses glucose for fuel. The cells receive the glucose through the bloodstream. They then use insulin a hormone made by the pancreas to absorb the glucose, convert it into energy, and either use it or store it for later use. Learn more...

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