Extrinsic neuropathy results in impaired GI contractility or abnormal myoelectrical control. The syndrome is typically seen in patients with type 1 or insulin-dependent diabetes mellitus (IDDM). Peripheral neuropathy is present in the majority of patients with enteropathy, and other forms of autonomic neuropathy (e.g., orthostatic hypotension) are common. Previous work has attributed these motility disorders mainly to vagal nerve dysfunction (3,30). Motor abnormalities of the small intestine observed in symptomatic diabetic patients (31,32) are often indistinguishable from those seen in patients with other syndromes affecting postganglionic sympathetic function (33). Vagal dysfunction is probably critical in gastric stasis of solid food. Electrolyte imbalances due to diabetic ketoacidosis (e.g., hypokalemia) and uremia may further aggravate impaired motor function in diabetic patients.
Vagal neuropathy is likely to impair normal gastric accommodation and compliance in diabetics (34). However, patients with diabetes and cardio-vagal neuropathy exhibit normal postprandial change in gastric volume as measured using SPECT imaging (Fig. 3) (35). This is consistent with the normalization of gastric accommodation in rats and humans after vagotomy (36). This adaptation in rats is inhibited by treatment with tetrodotoxin, suggesting that enteric neurons are involved in the adaptation to chronic vagal denervation (36).
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