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PubMed · 10225611

Autonomic dysfunction and the gastrointestinal tract.

M Bittinger·J Barnert·M Wienbeck
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Abstract

Autonomic neuropathy of the gastrointestinal tract may represent a primary disorder, but much more often it is secondary due to systemic disorders like diabetes mellitus. This review gives an overview about the common clinical manifestations and the principles and limitations in diagnostic work-up of autonomic dysfunction of the gastrointestinal tract. Diagnostic evaluation usually includes a combination of screening tests for autonomic neuropathy and specialized diagnostic procedures for the detection of sequela of autonomic neuropathy in gastrointestinal motility.

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Autonomic Nervous System DiseasesDigestive SystemHumansJournal ArticleReview

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M Bittinger, J Barnert, M Wienbeck. 1999. Autonomic dysfunction and the gastrointestinal tract.. https://doi.org/10.1007/bf02311763

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Cardiovascular and cerebrovascular responses to lower body negative pressure in type 2 diabetic patients.

In diabetic patients, vascular disease and autonomic dysfunction might compromise cerebral autoregulation and contribute to orthostatic intolerance. The aim of our study was to determine whether impaired cerebral autoregulation contributes to orthostatic intolerance during lower body negative pressure in diabetic patients. Thirteen patients with early-stage type 2 diabetes were studied. We continuously recorded RR-interval, mean blood pressure and mean middle cerebral artery blood flow velocity at rest and during lower body negative pressure applied at -20 and -40 mm Hg. Spectral powers of RR-interval, blood pressure and cerebral blood flow velocity were analyzed in the sympathetically mediated low (LF: 0.04-0.15 Hz) and the high (HF: 0.15-0.5 Hz) frequency ranges. Cerebral autoregulation was assessed from the transfer function gain and phase shift between LF oscillations of blood pressure and cerebral blood flow velocity. In the diabetic patients, lower body negative pressure decreased the RR-interval, i.e. increased heart rate, while blood pressure and cerebral blood flow velocity decreased. Transfer function gain and phase shift remained stable. Lower body negative pressure did not induce the normal increase in sympathetically mediated LF-powers of blood pressure and cerebral blood flow velocity in our patients indicating sympathetic dysfunction. The stable phase shift, however, suggests intact cerebral autoregulation. The dying back pathology in diabetic neuropathy may explain an earlier and greater impairment of peripheral vasomotor than cerebrovascular control, thus maintaining cerebral blood flow constant and protecting patients from symptoms of presyncope.

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