Antidepressant-Induced Adverse Reactions in a Patient with Hemorrhagic Stroke

Bogdanović, Zoran; Nalamati, J.; Kilcullen, J; Dhuper, Sunil

doi:10.1345/aph.1g169

Cited by 4 publications

(2 citation statements)

References 17 publications

(12 reference statements)

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“…2006). A number of cases have been reported in which treatments for depression have lead to the onset of serotonin syndrome (Bogdanovic et al. 2005; Gnanadesigan et al.…”

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confidence: 99%

Serotonin catabolism in the central and enteric nervous systems of rats upon induction of serotonin syndrome

Squires

Talbot

Rubakhin

et al. 2007

Journal of Neurochemistry

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Serotonin, a well-known neurotransmitter in mammals, has been linked to a number of neurological and gastrointestinal disorders. One of these disorders, serotonin syndrome, is a potentially deadly condition caused by increased levels of serotonin in the extracellular space. Information on the neurochemical effects of serotonin syndrome on serotonin catabolism is lacking, particularly in relation to the enteric system of the gastrointestinal tract. Here the catabolism of serotonin is monitored in rats with pharmacologically induced serotonin syndrome, with the catabolites characterized using a specialized capillary electrophoresis system with laser-induced native fluorescence detection. Animals induced with serotonin syndrome demonstrate striking increases in the levels of serotonin and its metabolites. In the brain, levels of serotonin increased 2-to 3-fold in animals induced with serotonin syndrome. A major serotonin metabolite, 5-hydroxyindole acetic acid, increased 10-to 100-fold in experimental animals. Similar results were observed in the gastrointestinal tissues; in the small intestines, serotonin levels increased 4-to 5-fold. Concentrations of 5-hydroxyindole acetic acid increased 32-to 100-fold in the intestinal tissues of experimental animals. Serotonin sulfate showed surprisingly large increases, marking what may be the first time the compound has been reported in rat intestinal tissues. Keywords: capillary electrophoresis system with laserinduced native fluorescence detection, enteric nervous system, serotonin, serotonin metabolism, serotonin sulfate, serotonin syndrome. Serotonin (5-HT) is well known as a neurotransmitter in the CNS of mammals where it plays an important role in learning and memory (Martin et al. 1997;Buhot et al. 2000) and in various stages of development (Gaspar et al. 2003). Imbalances in levels of 5-HT have been observed in a number of neurological disorders including: Parkinson, Huntington, Alzheimer, Alzheimer-like dementia, anxiety, and depression (Osborne and Hamon 1988). Although the majority of research aimed at understanding 5-HT function, release, uptake, and metabolism has focused on the CNS, an estimated 95% of the 5-HT in the human body is located in the PNS of the gastrointestinal tract, the enteric nervous system (ENS) (Kim and Camilleri 2000). 5-HT fulfills all criteria necessary for classification as a neurotransmitter in the ENS (Gershon 2004) and has been linked to a number of gastrointestinal disorders including irritable bowel syndrome, functional dyspepsia, non-cardiac chest pain, and gastric ulcer formation (Orlicz-Szczesna et al. 1989;Dhasmana et al. 1993). Thus, it is important to consider 5-HT metabolism in both the ENS and CNS. Understanding the catabolic pathways, the enzymes involved and the products of these conversions is particularly important because catabolism is vital to the regulation of 5-HT levels. Elucidating 5-HT catabolic pathways (Fig. 1) may provide novel approaches for the regulation of this compound and thus, improved targets for...

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“…2006). A number of cases have been reported in which treatments for depression have lead to the onset of serotonin syndrome (Bogdanovic et al. 2005; Gnanadesigan et al.…”

mentioning

confidence: 99%

Serotonin catabolism in the central and enteric nervous systems of rats upon induction of serotonin syndrome

Squires

Talbot

Rubakhin

et al. 2007

Journal of Neurochemistry

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“…Stages I to V are derived from the report by Woodbury and Woodbury [81]. Quetiapine (50-750 mg) 26 36 Olanzapine ( rone in combination with other concurrently prescribed serotonergic agents (SSRIs in most cases) has been reported [98][99][100][101][102][103][104][105][106][107][108]. There are also at least two case reports published demonstrating serotonin toxicity developed in association with tandospirone, alone [109] or in combination with trazodone [110].…”

Section: Some Atypical Antipsychotics Are 5-ht 1a Receptor Agonistsmentioning

confidence: 99%

Atypical Neuroleptic Malignant Syndrome or Serotonin Toxicity Associated with Atypical Antipsychotics?

Odagaki

2009

CDS

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Atypical antipsychotics and selective serotonin reuptake inhibitors (SSRIs) have been prescribed extensively, often in combination with each other. When toxic encephalopathy develops with neuromuscular and autonomic symptoms in a patient taking medication including atypical antipsychotics, it has tended to be diagnosed as neuroleptic malignant syndrome (NMS). However, there have recently been several case reports where the diagnosis of serotonin syndrome is given or raised as a likely differential diagnosis to such cases. In the present review, the author addressed himself to the issues surrounding the neurotoxic reaction to the treatment regimen containing atypical antipsychotics, focusing on the "atypical" forms of NMS and pathophysiological as well as clinical features of serotonin toxicity. Although NMS is idiosyncratic in nature, it appears practically useful to comprehend this syndrome as a spectrum-based concept. Likewise, serotonin toxicity is a broad spectrum of clinical syndromes in close connection with serotomimetic drug use, including varied severity. Some of atypical antipsychotics, i.e., perospirone, aripiprazole, ziprasidone, clozapine, and quetiapine, have been shown to behave as partial agonists at 5-HT1A receptors, providing direct evidence that these atypical antipsychotics are serotomimetic per se. The reciprocal interaction between the dopaminergic and serotonergic systems disturbed by either dopaminergic blockers or serotonergic enhancers leads to the disruption of homeostasis, with typical forms of NMS and serotonin syndrome representing the ends of the common pathophysiological background. The practical and flexible way to consider and manage such cases with updated knowledge derived from basic research should be warranted to be beneficial to our patients.

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Current awareness: Pharmacoepidemiology and drug safety

2006

Pharmacoepidemiology and Drug

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In order to keep subscribers up‐to‐date with the latest developments in their field, John Wiley & Sons are providing a current awareness service in each issue of the journal. The bibliography contains newly published material in the field of pharmacoepidemiology and drug safety. Each bibliography is divided into 20 sections: 1 Books, Reviews & Symposia; 2 General; 3 Anti‐infective Agents; 4 Cardiovascular System Agents; 5 CNS Depressive Agents; 6 Non‐steroidal Anti‐inflammatory Agents; 7 CNS Agents; 8 Anti‐neoplastic Agents; 9 Haematological Agents; 10 Neuroregulator‐Blocking Agents; 11 Dermatological Agents; 12 Immunosuppressive Agents; 13 Autonomic Agents; 14 Respiratory System Agents; 15 Neuromuscular Agents; 16 Reproductive System Agents; 17 Gastrointestinal System Agents; 18 Anti‐inflammatory Agents ‐ Steroidal; 19 Teratogens/fetal exposure; 20 Others. Within each section, articles are listed in alphabetical order with respect to author. If, in the preceding period, no publications are located relevant to any one of these headings, that section will be omitted.

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Antidepressant-Induced Adverse Reactions in a Patient with Hemorrhagic Stroke

Cited by 4 publications

References 17 publications

Serotonin catabolism in the central and enteric nervous systems of rats upon induction of serotonin syndrome

Serotonin catabolism in the central and enteric nervous systems of rats upon induction of serotonin syndrome

Atypical Neuroleptic Malignant Syndrome or Serotonin Toxicity Associated with Atypical Antipsychotics?

Current awareness: Pharmacoepidemiology and drug safety

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