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Diabetes may affect both the somatosensory system causing a variable sensory and
motor deficits and the autonomic nervous system. About 30% of diabetic patients
have evidence of neuropathy on formal testing but in the vast majority it is
asymptomatic. Diabetic neuropathy may manifest clinically in one of two ways. A
focal (or occasionally multifocal) acute neuropathy in which individual nerves are
picked off by discrete, presumably, vascular insults; an acute sixth nerve palsy would
be an example. The other clinical manifestation is that of a diffuse, often symmetrical
pattern of sensory loss in which the longest nerves are often the most susceptible.
This explains why the characteristic pattern of sensory loss seen in people with
diabetes is that of a “glove and stocking” distribution. This type of neuropathy is
insidious in its onset, gradually progressive and with time leads to the loss of
cutaneous and proprioceptive sensation in a glove and stocking pattern.

Causative factors in diabetic neuropathy are thought to include hyperglycaemia and
vascular damage. Why hyperglycaemia should cause and exacerbate neuropathy is not
fully understood but glycosylation of proteins, a structural change which has
profound functional consequences, has been implicated. Vascular damage appears to
occur by two mechanisms both of which are manifestations of microvascular disease.
Diffuse occlusion of the capillaries supplying the nerves; the vasa nervorum, may lead
to its progressive ischaemia and loss of function; (this is thought to be the
pathophysiological process behind the slowly progressive glove and stocking
neuropathies). The acute palsies of the larger peripheral and cranial nerves may be due
to sudden occlusion of larger vessels causing localised infarction of the nerve.


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