Pathology of Autonomic Neuropathy in Diabetes Mellitus

L. W. Duchen

Annals of Internal Medicine · 1980 · 251 citations · 6 references

Concepts

TL;DR

All had clinical evidence of peripheral sensorimotor neuropathy and developed autonomic disturbances such as postural hypotension, diarrhoea, bladder dysfunction, impotence, and cardiac denervation. Pathologic changes in the autonomic nervous system were studied postmortem in five early‑onset insulin‑dependent diabetes cases. Autopsy revealed giant or vacuolated sympathetic and enteric neurons, loss of myelinated fibers in the vagus and sympathetic trunks, focal hyaline degeneration of visceral smooth muscle, and inflammatory changes in ganglia, indicating multiple pathogenetic mechanisms for diabetic autonomic neuropathy.

Abstract

Pathologic changes in the autonomic nervous system were studied postmortem in five cases of insulin-dependent diabetes of early onset. All had had clinical evidence of peripheral sensorimotor neuropathy and developed disturbances of autonomic function that included postural hypotension, diarrhoea, bladder dysfunction, impotence (in the men), and signs of cardiac denervation. In coeliac and other sympathetic ganglia there were many distended ('giant') or vacuolated neurons as well as enlarged club-shaped neural processes. The vagus nerve and sympathetic trunks showed severe loss of myelinated fibres. Smooth muscle in many viscera showed a hitherto undescribed focal hyaline degeneration. There were inflammatory changes in the autonomic ganglia in all cases and in or around bundles of unmyelinated nerve fibres in many. These findings suggest that there may be several different pathogenetic mechanisms involved in the development of autonomic neuropathy in diabetes.

References

6