Diabetic neuropathy involves the death of peripheral neurons caused by the pathophysiology of DM. It is the most common peripheral neuropathy in the western hemisphere. Up to 60% of individuals with diabetes mellitus will be afflicted with neuropathy after 20 years from their diagnosis.
Chronic hyperglycemia associated with diminished insulin production or function appears to be the primary initiating factor in the pathogenesis of diabetic complications.
Diabetic autonomic neuropathy (DAN) is a well-described complication in long-term diabetes. The DAN is associated with a markedly reduced quality of life and poor prognosis. The manifestations of DAN cause multiple symptoms that can involve:
(i) gastrointestinal tract: oesophageal motor dysfunction, diabetic gastroparesis, gall bladder atony, diabetic enteropathy, colonic hypomotility, anorectal dysfunction;
(ii) respiratory system: reduced ventilatory drive to hypercapnia/hypoxemia, sleep apnoea;
(iii) genitourinary tract: diabetic cystopathy, erectile dysfunction;
(iv) cardiovascular system: resting tachycardia, reduced heart rate variability and circadian rhythm of heart rate and blood pressure, painless myocardial ischaemia/infarction, orthostatic hypotension, exercise intolerance, perioperative instability, and sudden death.
Various pathological lesions are observed in animal and human models of diabetes including segmental demyelination, atrophy, loss of myelinated and unmyelinated fibres, Wallerian degeneration, segmental and paranodal demyelination and blunted nerve fibre generation.
- Axonal regeneration in the peripheral nervous system is initially robust, but it eventually fails for unclear reasons.