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Heewon Bae,Ji Hyun Lee,Sungsuk Je,Seung-Hoon Lee,Hayun Choi 대한신경정신의학회 2024 PSYCHIATRY INVESTIGATION Vol.21 No.2
Objective Second-generation antipsychotics (SGAs) have revolutionized the treatment of psychiatric disorders, but are associated with significant metabolic risks, including diabetes and hyperglycemic crises. This review explores the complex interplay between antipsychotics, diabetes, and hyperglycemic crises, highlighting the mechanisms underlying SGA-induced diabetes.Methods We present the case of a patient with schizophrenia who was taking antipsychotic medication and was admitted to the emergency room due to the sudden onset of diabetic ketoacidosis (DKA) without any history of diabetes. We extensively searched databases, including Elsevier, PubMed, IEEE, SpringerLink, and Google Scholar, for papers on the effects of antipsychotic drugs on DKA from 2002 to 2021. We focused on DKA, hyperglycemia, and atypical antipsychotics, and retrieved 117 papers. After full-text review, 32 papers were included in this comprehensive review.Results DKA was significantly more frequent in patients taking SGAs. Antipsychotics can induce insulin resistance either directly or through the onset of obesity. Antipsychotics can reduce insulin secretion from pancreatic β-cells, which is associated with absolute insulin deficiency.Conclusion As the use of antipsychotics continues to increase, understanding their risks and mechanisms is crucial for clinicians to enable informed treatment decisions and prevent potentially life-threatening complications.
Central Post-Stroke Pain: A Review Focusing on Pathophysiology
Heewon Bae,Min Ju Kang,Sang-Won Ha 대한통증연구학회 2020 International Journal of Pain Vol.11 No.1
Central post-stroke pain (CPSP) is one of the complication of ischemic stroke that can occur in 1-12% of patients. CPSP is related with both neuropathic and nociceptive pain. Pain is characterised by sudden, brief pain and presented as dysaethesia, allodynia and hyperalgesia. The area of pain corresponds to the body parts that corresponds to the brain lesion. Various mechanisms are presented as hypothesis, but there are no clearly defined. Commonly, It is known to be caused by the hyperexcitability of pain conduction pathway, as well as disinhibition of central inhibitory pathway. While pharmacological and non-pharmachological treatments are being tried, clinically, they are mainly prescribed amitriptyline. It would be find effective treatment if more clear mechanism are identified through prospective research.