This chapter reviews how disease of small nerve and ganglia microvessels, or microangiopathy, relates to the development of diabetic peripheral neuropathy. Microangiopathy involving vessels of the nerve trunk and those of dorsal root ganglia (that house sensory neuron cell bodies), does develop in parallel with neuropathy and is likely to eventually contribute to it. It is debatable whether early polyneuropathy in models or in humans can be exclusively linked to reductions in the blood supply of nerves. More likely, diabetes targets neural structures and vessels concurrently. There might be chronic ganglion ischemia altering neuronal function such that terminal branches of the nerve can no longer be properly supported. Downregulation, in turn, of critical structural and survival proteins in the sensory (or autonomic) neuron tree might account for early sensory dysfunction and pain (or autonomic abnormalities). There might also be exquisite sensitivity of vessels to vasoconstriction as an early functional abnormality. Rises in local endothelin levels, for example, might trigger acute nerve trunk and ganglion ischemia, and damage. Finally, failed upregulation of blood flow to injured nerves after acute injury might impair their ability to regenerate. Future therapy of diabetic polyneuropathy will require attention toward both direct neuronal degeneration and superimposed microangiopathy.

Key Words: Diabetic neuropathy; ganglion blood flow; ischemia; microangiopathy; nerve blood flow; nerve injury; regeneration; vasa nervorum.

Peripheral Neuropathy Natural Treatment Options

Peripheral Neuropathy Natural Treatment Options

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