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Updated: Dec 6, 2025

Video Imaging and Spatiotemporal Maps to Analyze Gastrointestinal Motility in Mice
Published on: February 3, 2016
Autoimmune encephalitis and gastrointestinal dysmotility: achalasia, gastroparesis, and slow transit constipation
Thomas Frieling1, Christian Kreysel1, Michael Blank1
1Department of Internal Medicine and Gastroenterology, HELIOS Clinic Krefeld, Germany.
Background:
Neurological autoimmune disorders (NAD) are caused by autoimmune inflammation triggered by specific antibody subtypes. NAD may disturb the gut-brain axis at several levels including brain, spinal cord, peripheral, or enteric nervous system.
Case Report:
We present a case with antinuclear neuronal Hu (ANNA-1)- and antiglial nuclear (SOX-1) autoimmune antibody-positive limbic encephalitis and significant gastrointestinal dysmotility consisting of achalasia type II, gastroparesis, altered small intestinal interdigestive motility, and severe slow transit constipation. The autoantibodies of the patient's serum labeled enteric neurons and interstitial cells of Cajal but no other cells in the gut wall. Achalasia was treated successfully by pneumatic cardia dilation and gastrointestinal dysmotility successfully with prucalopride.
Conclusion:
NAD may disturb gastrointestinal motility by altering various levels of the gut-brain axis.
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