PATHOLOGICAL FEATURES OF DIABETIC NEUROPATHY
Abstract:
Peripheral neuropathy is the major reason for morbidity and mortality among diabetic
patients. Unfortunately, the natural history and pathogenesis of the disease are not fully known. For a
long time, hyperglicemia was viewed as a major, if not the sole factor responsible. It is obvious that
diabetic neuropathy cannot be fully understood without considering factors besides hyperglycemia.
Metabolic and vascular factors play an important role in the pathogenesis of the diabetic neuropathy.
Detailed neurophysiological studies in diabetic patients have shown that demyelination precedes axonal
loss. Experimental studies demonstrate progressive molecular alterations leading to nodal and
paranodal degeneration with axo-glial dysjunction and axonal atrophy. These alterations have not been
observed in diabetic patients. Unmyelinated fibres demonstrate both degeneration and regeneration in a
variety of clinical syndromes of the diabetic neuropathy. The occurence of demyelination in the absence
of morphologically apparent axonal damage suggest that the Schwann cell may be a primary target of
damage in diabetic neuropathy. Epidermal small nerve fibre degeneration was demonstrated in the
presence of normal vibration sensation and electrophysiology. Small fibres appear to be prone to early
damage but retain the ability to repair themselves even in chronic end-stage neuropathy. Prior to
clinically detectable neuropathy, endoneurial microangiopathy is characterised by membrane thickening
and endothelial cell hyperplasia in diabetic patients.
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