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Dextromethorphan is a distant derivative of morphine, used as an antitussive agent indicated in standard care for various infections and respiratory conditions ranging from the common cold (rhinoviruses) to severe acute respiratory illness (SARI). Being a derivative of morphine, a natural central nervous system (CNS) depressant, dextromethorphan produces little to no action on CNS when ingested in the prescription dosage. We present a case of a 64-year-old female patient, a known case of ischemic heart disease post angioplasty and stenting to the left anterior descending artery (LAD), with heart failure with reduced ejection fraction (HFrEF), diabetes, hypertension, chronic kidney disease, and hypothyroidism who developed extrapyramidal symptoms post dextromethorphan administration.

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Glioblastoma multiforme is the most common malignant primary brain tumor in adults. Despite new treatments developed including immunomodulation using vaccines and cell therapies, mortality remains high due to the resistance mechanisms presented by these tumor cells and the function of the blood-brain barrier that prevents the entry of most drugs. In this context of searching for new glioblastoma therapies, the study of the existing drugs to treat neurological disorder is gaining great relevance.

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The anticonvulsant and adverse effects of dextromethorphan, a non-opioid antitussive, and its metabolite dextrorphan were examined in amygdala-kindled rats. Both drugs have repeatedly been proposed to be functional non-competitive N-methyl-D-aspartate (NMDA) receptor antagonists, but they also exert effects distinct from antagonism at NMDA receptors, such as blockade of voltage-gated calcium channels and sigma-site mediated actions. Since recent data have demonstrated that kindled rats are more susceptible to the adverse effects of NMDA receptor antagonists than non-kindled rats, the time course, characteristics and severity of adverse effects of dextromethorphan and dextrorphan were also determined in non-kindled animals.

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