Autoimmune encephalitis and gastrointestinal dysmotility: Achalasia, gastroparesis, and slow transit constipation

Translated title of the contribution: Autoimmune encephalitis and gastrointestinal dysmotility: Achalasia, gastroparesis, and slow transit constipation

Thomas Frieling, Christian Kreysel, Michael Blank, Dorothee Müller, Ilka Melchior, Philipp Euler, Rita Kuhlbusch-Zicklam, Thomas Haarmeier, Michael Schemann

Research output: Contribution to journalArticlepeer-review

4 Scopus citations

Abstract

Background Neurological autoimmune disorders (NAD) are caused by autoimmune inflammation triggered by specific antibody subtypes. NADmay 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 serumlabeled 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 NADmay disturb gastrointestinal motility by altering various levels of the gut-brain axis.

Translated title of the contributionAutoimmune encephalitis and gastrointestinal dysmotility: Achalasia, gastroparesis, and slow transit constipation
Original languageEnglish
Pages (from-to)975-981
Number of pages7
JournalZeitschrift fur Gastroenterologie
Volume58
Issue number10
DOIs
StatePublished - 1 Oct 2020

Keywords

  • ANNA-1
  • achalasia
  • anti-Hu
  • autoimmune antibodies
  • autoimmune encephalitis
  • gastroparesis
  • limbic encephalitis
  • slow transit constipation

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