{"title":"Unraveling Protracted Neuropsychiatric Symptoms in a Patient With Altered Post-Bariatric Pharmacokinetics: A Diagnostic Puzzle.","authors":"Akbar Ali, Christopher E Potts, Dakota May","doi":"10.1155/crps/8340699","DOIUrl":null,"url":null,"abstract":"<p><strong>Objective: </strong>To report a complex case of serotonin toxicity that evolved into a persistent neuropsychiatric syndrome, complicating the differential diagnosis between protracted toxicity, prolonged SSRI discontinuation syndrome, acute hepatic porphyria, and functional neurological disorder (FND).</p><p><strong>Method: </strong>We present the case of a 61-year-old male with a history of gastric sleeve surgery and major depressive disorder (MDD) who developed acute serotonin syndrome (SS) following the concomitant use of fluoxetine, buspirone, and linezolid.</p><p><strong>Results: </strong>While acute autonomic instability resolved upon cessation of serotonergic agents, the patient developed subacute, evolving neurological deficits. Workup revealed an <i>SLC6A4</i> polymorphism and elevated urinary porphyrins, initially prompting Hemin therapy, though genetic testing for porphyria was negative. Tertiary evaluation at the Cleveland Clinic ultimately confirmed a diagnosis of FND, psychogenic non-epileptic seizures (PNES), and chronic migraine. Management remains challenging due to medication sensitivity, including recent parasomnias during a cautious trial of vilazodone.</p><p><strong>Conclusions: </strong>This case highlights the diagnostic complexity following SS in patients with altered gastrointestinal anatomy and genetic variances. It emphasizes how an acute organic insult-whether serotonin toxicity, prolonged SSRI discontinuation, or a combination of both-can serve as a physiological trigger for complex FND and PNES, requiring multidisciplinary management. The limitations inherent in single-case observations are discussed.</p>","PeriodicalId":9631,"journal":{"name":"Case Reports in Psychiatry","volume":"2026 ","pages":"8340699"},"PeriodicalIF":0.0000,"publicationDate":"2026-06-15","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC13266407/pdf/","citationCount":"0","resultStr":null,"platform":"Semanticscholar","paperid":null,"PeriodicalName":"Case Reports in Psychiatry","FirstCategoryId":"1085","ListUrlMain":"https://doi.org/10.1155/crps/8340699","RegionNum":0,"RegionCategory":null,"ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":null,"EPubDate":"2026/1/1 0:00:00","PubModel":"eCollection","JCR":"Q4","JCRName":"Medicine","Score":null,"Total":0}
引用次数: 0
Abstract
Objective: To report a complex case of serotonin toxicity that evolved into a persistent neuropsychiatric syndrome, complicating the differential diagnosis between protracted toxicity, prolonged SSRI discontinuation syndrome, acute hepatic porphyria, and functional neurological disorder (FND).
Method: We present the case of a 61-year-old male with a history of gastric sleeve surgery and major depressive disorder (MDD) who developed acute serotonin syndrome (SS) following the concomitant use of fluoxetine, buspirone, and linezolid.
Results: While acute autonomic instability resolved upon cessation of serotonergic agents, the patient developed subacute, evolving neurological deficits. Workup revealed an SLC6A4 polymorphism and elevated urinary porphyrins, initially prompting Hemin therapy, though genetic testing for porphyria was negative. Tertiary evaluation at the Cleveland Clinic ultimately confirmed a diagnosis of FND, psychogenic non-epileptic seizures (PNES), and chronic migraine. Management remains challenging due to medication sensitivity, including recent parasomnias during a cautious trial of vilazodone.
Conclusions: This case highlights the diagnostic complexity following SS in patients with altered gastrointestinal anatomy and genetic variances. It emphasizes how an acute organic insult-whether serotonin toxicity, prolonged SSRI discontinuation, or a combination of both-can serve as a physiological trigger for complex FND and PNES, requiring multidisciplinary management. The limitations inherent in single-case observations are discussed.