Letters to the Editor
Serotonin Syndrome With Prolonged Dysphagia
Dear Editor:
Serotonin syndrome (SS) involves central nervous system (CNS) serotonergic pharmacotoxicity. Sternbach’s proposed diagnostic criteria for SS require the association of a CNS serotonergic agent with at least 3 of the following: altered mental status, agitation, myoclonus, hyperreflexia, diaphoresis, shivering, tremor, diarrhea, poor coordination, and fever (1). Radomski and colleagues have confirmed the validity of Sternbach’s criteria (2). Mills reviewed 127 SS cases and reported neuromuscular features including myoclonus (57%), hyper- reflexia (50%), tremor (49%), restlessness (42%), and ataxia (38%) (3). Prolonged dysphagia was not prominent in any of these cases (K Mills, personal communication, March 13, 2003). Dysphagia is not included in SS diagnostic criteria, nor is it commonly cited in case descriptions. Conversely, dysphagia is commonly seen in neuro- leptic malignant syndrome (NMS), a potentially fatal psychotropic toxidrome involving dopaminergic hyperactivity. Dysphagia in SS may lead to its confusion with NMS, an important distinction recently reviewed by Birmes and colleagues (4). We report a case of SS associated with prolonged dysphagia, and we discuss a potential mechanism.
Case Report
Our patient was a 74-year-old white woman with a history of major depressive disorder. Her medical history included ulcerative colitis with total colectomy– ileostomy at age 25 years and aortic valve replacement at age 72 years. She presented with an acute onset of agitation, tremor, hyperreflexia, myoclonus, ataxia, mutism, and swallowing difficulties evolving 48 hours after trazodone was increased from 50 to 100 mg daily. Her other medications were citalopram 40 mg and clonazepam 4 mg, each taken daily during the previous 6 months for treatment of a major depressive recurrence. Comprehensive laboratory investigations were noncontributory. Cranial CT scan revealed diffuse age-related cortical atrophy but no acute vascular changes, confirmed by follow-up CT scan after 48 hours. In consultation with neurology and internal medicine, we diagnosed SS, stopped the medications, and instituted supportive treatment. We started lorazepam to prevent benzodiazepine withdrawal symptoms. A feeding trial resulted in severe coughing with poorly coordinated orolingual movements that impaired swallowing and speech. We continued intravenous hydration and nasogastric feeding. Six days after admission, the neurological symptoms were resolving, except for dysphagia. A bedside swallowing assessment revealed lingual tremor, poor tongue extrusion, mild reflex trigger delay, and mouth breathing during swallow. Coughing and distress during a feeding trial of thick liquids resulted in a regression of diet to gels only. Marked dysphagia persisted 25 days after admission, despite the resolution of all other neurological symptoms. A modified barium swallow revealed normal anatomy, with poorly coordinated tongue action and pharyngeal leakage coating the underside of the epiglottis without frank aspiration. The patient was eventually able to protect her own airway and tolerated gradual dietary advancement.
SS involves excessive stimulation of postsynaptic brainstem and spinal cord 5-HT1A receptors (1). In this patient, we observed SS with the combination of trazodone, citalopram, and clonazepam, all of which have serotonergic properties and no major mutual pharmacokinetic interactions (5). The brainstem swallowing centre is localized at the nucleus tractus solitarius (NTS) (6). In animal studies, microinjections of serotonin into the NTS inhibit the swallowing reflex (7). In patients with SS, serotonergic hyperactivity at the NTS may thus inhibit the swallowing reflex. We hope to inform clinicians of the potential for dysphagia in SS and we encourage monitoring for complications such as aspiration pneumonia during the recovery phase.
References
1. Sternbach H. The serotonin syndrome. Am J Psychiatry 1991;148:705–13.
2. Radomski JW, Dursun SM, Reveley MA, Kutcher SP. An exploratory approach to the serotonin syndrome: an update of clinical phenomenology and revised diagnostic criteria. Med Hypotheses 2000;55:218–24.
3. Mills KC. Serotonin syndrome-a clinical update. Crit Care Clin 1997;13:763–83.
4. Birmes P, Coppin D, Schmitt L, Lauque D.
Serotonin syndrome: a brief review. CMAJ 2003;168:1439–42.
5. Ballenger JC, Garlow SJ, Kelsey JE, Nemeroff CB. In: Sadock BJ, Sadock VA, editors. Kaplan and Sadock’s comprehensive textbook of psychiatry. 7th ed. Philadelphia: Lippincott, Williams and Wilkins; 2000. p 2319, 2435, 2483.
6. Clouse RE, Diamant NE. Esophageal motor and sensory function and motor disorders of the esophagus. In: Feldman M, editor. Sleisenger and Fordtran’s gastrointestinal and liver disease. 7th ed. Philadelphia: Elsevier Science; 2002. p 563.
7. Kessler JP, Jean A. Inhibition of the swallowing reflex by local application of serotonergic agents into the nucleus of the solitary tract. Eur J Pharmacol 1985;118(1–2):77–85.
Michael J Passmore, BSc, MD, FRCPC
S Devarajan, MD, FRCPC, MRCPsych
K Ghatavi, MD, FRCPC
DM Gardner, PharmD
SP Kutcher, MD, FRCPC
Halifax, Nova Scotia
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