Diabetic autonomic neuropathy was in the Toronto consensus defined as a disorder of the autonomic nervous system in diabetes or metabolic derangements of prediabetes, after the exclusion of other causes. It may affect the cardiac, gastrointestinal (GI), genitourinary systems, and sudomotor function.1 The prevalence of autonomic neuropathies are best described for cardiovascular autonomic neuropathy (CAN). In unselected diabetes populations, CAN was found in 17 % to 20 % of patients with diabetes, increasing with age and diabetes duration. In newly diagnosed diabetes, the prevalence was reported to be around 7 %.2

Cardiovascular autonomic reflex tests (CARTs) are considered gold standard in the diagnosis of diabetic autonomic neuropathy. They have good sensitivity, specificity, and reproducibility. Furthermore, they are non-invasive and easy to perform in a clinical setting.1 Emerging tests, measuring sudomotor function through electrical skin conductance, corneal small fiber structure by confocal microscopy, or the axon reflex-mediated neurogenic vasodilatation are increasingly available, but there is a lack of consensus on their role in the diagnostic armamentarium.3

Gastrointestinal symptoms are frequent in the general population, but even more so in people with diabetes. The prevalence of GI symptoms in unselected people with diabetes varies between 1 % and 40 % for the different symptoms.4 There are several modalities to assess gastric emptying and gastroenteric motility, but they do not always correspond with symptoms, symptom severity or CARTs.5 We have previously shown, that both gastrointestinal autonomic neuropathy as well as central neuroplastic changes are involved in the pathomechanism.6., 7. Accordingly, in addition to GI motility studies, there is a need for tools to examine both the GI autonomic nervous system and its interplay with the brain.

Investigating cerebral responses to GI tract stimulations was developed in the 1980s and has been extensively employed by our and other study groups.6., 8., 9. Rectal mucosa is innervated by visceral afferents running in both sympathetic and parasympathetic nerves. Visceral afferents consist mainly of small myelinated Aδ and unmyelinated C-fibers, with slow conduction speeds compared to somatic afferents. Hence, cerebral responses induced by visceral mechanical activation occur after 40–50 ms and should enable a reasonable separation between somatic Aβ and visceral signaling.10 Consequently, this could be an interesting method for investigating the afferent signaling from the GI tract, with the potential to better the understanding of the differences between cardiac and gastric autonomic nerve function.

In the current study, we wanted to explore a novel test measuring cortical evoked potentials (EPs) in response to rapid balloon distention in the rectum and compare it to established tests for diabetic neuropathy. As a primary outcome, we hypothesized that reduced rectal sensitivity and pathological findings in EPs were more prevalent in both longstanding as well as early diabetes, compared to controls. Secondarily, we hypothesized that different manifestations of diabetic neuropathy run in parallel, and thus, that rectal sensitivity and EPs correlate with measures from other neuropathy tests.