Introduction
Gastroparesis is characterized by delayed gastric emptying without mechanical obstruction, causing abdominal pain, nausea, early satiety, and bloating.1,2 Psychiatric conditions like anxiety and depression may compound the severity of gastrointestinal symptoms and worsen quality of life.3 While neuromodulators for psychiatric conditions may be used off-label for gastroparesis symptoms, there is a limited understanding of how treating coexisting psychiatric conditions affect gastrointestinal symptoms. We present a case in which refractory gastroparesis symptoms resolved after treatment for catatonic depression.
Case Report
A 57-year-old woman with Sjogren’s syndrome and spasmodic dysphonia reported 7 months of vomiting, early satiety, and progressive abdominal pain with poor oral intake and weight loss after a viral illness. Abdominal CT and MRI and pelvic ultrasound were unremarkable. Gastric emptying study showed severe delayed gastric emptying (44% at 4 hours) without abnormal esophageal retention, suggestive of post-viral gastroparesis. She was prescribed metoclopramide, domperidone, and erythromycin, all with limited efficacy due to side effects (Figure). Given ongoing weight loss (baseline 56.7 kg to 43.1 kg), a nasojejunal tube was placed. Endoscopic findings were notable only for non-specific gastritis. When the nasojejunal tube clogged, she insisted on pursuing total parenteral nutrition (TPN). She then underwent gastric peroral endoscopic myotomy (G-POEM) for refractory symptoms. She developed worsening gastroesophageal reflux and constipation which were treated with proton pump inhibitors and plecanatide, respectively. Despite these interventions, her symptoms did not improve.
Figure.
Medication timeline by therapy and outcome. TID, 3 times a day; QID, 4 times a day; BID, twice a day.
Four months post-pyloromyotomy, the patient’s husband reported new progressive anxiety, depression, and insomnia alongside persistent gastrointestinal symptoms. She was admitted for failure to thrive and gastrojejunal tube placement in an effort to wean off TPN. A thiamine level was normal. She reported worsening persecutory delusions and was diagnosed with hypoactive catatonia. She was started on oral lorazepam for catatonia and anxiety, and subsequently, her motor function, appetite, and gastrointestinal symptoms improved. She passed a calorie count within 2 weeks. TPN was stopped and gastrojejunal tube placement deferred. Venlafaxine was started for maintenance therapy. She was discharged to an inpatient psychiatric facility and maintained on venlafaxine and a lorazepam taper. Six months post-hospitalization, she remains free of gastrointestinal symptoms.
Discussion
Our case demonstrates improvement in gastroparesis symptoms after treatment of catatonic depression with a psychiatric agent. Medical therapy of gastroparesis and chronic nausea and vomiting are often targeted at symptoms. In this case, prokinetics and invasive therapies were initially favored over neuromodulators such as tricyclic antidepressants or mirtazapine given the significant retention on gastric emptying study, severity of symptoms, and malnutrition. Individuals with refractory symptoms of chronic nausea and vomiting may benefit from pyloromyotomy, which has approximately a 50% response rate at 6 months.2 In this case, the beneficial effect of G-POEM may not have been manifested or realized immediately. Of the fewer than 5 cases in the literature detailing gastroparesis treatment with benzodiazepines, none to our knowledge describe a concurrent diagnosis of catatonia with depression and use of benzodiazepines for the treatment of psychiatric symptoms.
Gastroparesis symptoms can mimic or overlap with somatic manifestations of psychiatric syndromes, with nearly 50% of gastroparesis patients experiencing concurrent psychiatric disorders, more frequent imaging, and longer hospital stays.4 Benzodiazepines are sometimes used to treat chronic nausea by acting on the chemoreceptor trigger zone and reducing anticipatory nausea. They are more commonly used to treat psychiatric symptoms because of their anxiolytic properties. While it is possible that the patient’s post-viral gastrointestinal symptoms may have been exacerbated by an unrecognized underlying psychiatric condition or that her post-viral gastrointestinal symptoms may have been headed towards spontaneous resolution over this time course, the complete resolution of her gastrointestinal symptoms with psychiatric treatment suggests that a primary psychiatric condition was the driving force.5 Nevertheless, we present this case to bring awareness to psychological factors that may impact the course of gastrointestinal disease and to consider primary psychiatric conditions that manifest with somatic symptoms.
Acknowledgement
This case report has been accepted as a poster presentation at the American College of Gastroenterology Annual Meeting in October 2025 at Phoenix, Arizona.
Footnotes
Patient consent: Informed patient consent was obtained for publication of the case details.
Financial support: None.
Conflicts of interest: None.
Author contributions: Benjamin M Moy: conceptualization, data curation, formal analysis, funding acquisition, investigation, methodology, project administration, resources, software, supervision, validation, visualization, writing-original draft, writing-review and editing; Mark A Solinski: writing-review and editing; and Joy J Liu: conceptualization, data curation, formal analysis, funding acquisition, investigation, methodology, project administration, resources, software, supervision, validation, visualization, writing-review and editing.
References
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