AI Article Synopsis

  • Serotonin syndrome and Parkinson's disease have overlapping symptoms, making accurate diagnosis critical for appropriate treatment, as misdiagnosis can lead to severe complications.
  • A case study of a 75-year-old woman revealed serotonin syndrome triggered by escitalopram, initially mistaken for worsened Parkinson's symptoms, highlighting the importance of therapeutic drug monitoring.
  • The findings emphasize the need for healthcare providers to distinguish between serotonin syndrome and Parkinson's manifestations to ensure proper treatment and management, particularly in patients with psychiatric conditions linked to Parkinson's disease.

Article Abstract

Background: Serotonin syndrome and Parkinson's disease (PD) are two diseases whose symptoms partially overlap; this poses challenges in distinguishing them in clinical practice. Early manifestations such as tremor, akathisia, diaphoresis, hypertonia and hyperreflexia are common in mild-to-moderate serotonin syndrome and can also occur in PD. Without prompt recognition and treatment, serotonin syndrome can rapidly progress, potentially leading to severe complications such as multiple organ failure within hours. Given their disparate treatment strategies, accurate clinical distinction is crucial for effective treatment. This case study explores a patient with serotonin syndrome triggered by escitalopram in the context of PD psychosis (PDP), providing insights into diagnosis and treatment planning.

Case Presentation: A 75-year-old Asian woman with a one-year history of PD, a two-month history of PDP, and a six-year history of depression presented with symptoms including hyperreflexia, tremor, hypertonia, impaired level of consciousness, and inappropriate behavior following a recent one-month adjustment in medication. Initially suspected of being drug-induced parkinsonism or worsening PD, therapeutic drug monitoring revealed warning levels of escitalopram. Subsequent diagnoses confirmed serotonin syndrome. This syndrome may result from increased cortical serotonin activity at the serotonin2A receptor due to dopamine and serotonin imbalances in PDP, compounded by increased dopamine-mediated serotonin release. Additionally, being an intermediate metabolizer of cytochrome P450 enzyme 2C19, the patient experienced excessive escitalopram accumulation, exacerbating her condition.

Conclusions: This case underscores the critical need to differentiate between symptoms of serotonin syndrome and PD, particularly in manifestations like tremor and hypertonia. Careful consideration of receptor profiles in patients with PDP is essential when selecting antidepressants to mitigate the risk of serotonin syndrome.

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Source
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC11409801PMC
http://dx.doi.org/10.1186/s12877-024-05371-wDOI Listing

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