Bupropion is an atypical antidepressant that inhibits norepinephrine and dopamine reuptake. Poison control data demonstrate toxic effects at doses as low as 600 mg. Common adverse effects of overdose include tachycardia, seizures, and cardiac arrhythmias. Gastrointestinal complications are rarely described. Our case shows an 18-year-old male presented to the emergency department after witnessed seizure-like activity. Family reported ingestion of approximately thirty 300-mg sustained-release bupropion tablets 4-5 hours prior to presentation. On arrival, he required endotracheal intubation for airway protection. Sedation was initiated with propofol and fentanyl; fentanyl was rapidly discontinued. Given delayed presentation and sustained-release ingestion, whole bowel irrigation was initiated with nasogastric administration of 50 g activated charcoal followed by 6 L polyethylene glycol-electrolyte solution. Subcutaneous methylnaltrexone (12 mg) was administered to reverse potential opioid-related ileus without effect. Worsening abdominal distension prompted contrast-enhanced computed tomography of the abdomen and pelvis, which demonstrated diffuse fluid-filled colonic distension with distal small bowel dilation and no evidence of mechanical obstruction or pill bezoar. Gastroenterology performed colonoscopic decompression with rectal tube placement. This resulted in successful decompression. The patient was extubated the following day with return of bowel function on post-decompression day two. In supratherapeutic states, bupropion exhibits anticholinergic properties through poorly understood mechanisms, which may impair intestinal motility. Colonic complications remain rare, with only isolated reports describing colonic ischemia or pseudo-obstruction associated with bupropion toxicity. Clinicians should consider severe gastrointestinal dysmotility when managing sustained-release bupropion toxicity.

We report a case of a previously healthy 3-year-old girl who developed acute altered consciousness, agitation, and visual hallucinations consistent with an anticholinergic toxidrome. Initial examinations were unremarkable, and urine immunoassay screening (SIGNIFY™ ER) was negative. Serum analysis by liquid chromatography-quadrupole time-of-flight mass spectrometry identified chlorpheniramine and scopolamine, while excluding other agents. Concentrations were 370 ng/mL for chlorpheniramine and 1 ng/mL for scopolamine, both near reported toxic ranges. An empty blister pack of 22 pediatric motion sickness tablets was found at the patient's home, confirming accidental overdose of an over-the-counter (OTC) anti-motion sickness medication. This case demonstrates the diagnostic utility of high-resolution mass spectrometry in pediatric poisoning, particularly for drugs not detected by routine screening. It represents a rare report documenting quantitative confirmation of both chlorpheniramine and scopolamine in a child, with correlation between serum concentrations and clinical presentation. Scopolamine is highly toxic even at low concentrations, and pediatric cases with measured blood levels are exceedingly rare. Our findings highlight the need to consider additive or synergistic toxicity in OTC formulations containing multiple anticholinergic agents and emphasize the importance of caregiver education regarding the potential risks of OTC medications often perceived as safe.

Hyoscyamus niger (henbane) is a toxic plant containing tropane alkaloids that can cause anticholinergic toxicity. Pediatric presentations may differ from adults and may include atypical behavioral manifestations such as hyperactivity and euphoria without agitation. An 11-year-old previously healthy boy presented with sudden behavioral changes, hyperactivity, and unexplained euphoria. Approximately four hours earlier, he had ingested about one tablespoon of fresh Hyoscyamus niger seeds. Physical examination revealed minimal mydriasis and mild flushing. The patient was cooperative but disoriented, with visual hallucinations. Laboratory tests were normal, and electrocardiography showed sinus tachycardia. Findings were consistent with anticholinergic toxicity. Activated charcoal and physostigmine were not administered due to delayed presentation and absence of severe or life-threatening symptoms. Symptoms resolved completely within 24 hours with supportive care. In conclusion, Hyoscyamus niger intoxication may present predominantly with hyperactivity and euphoria without agitation, representing an atypical behavioral phenotype in pediatric patients. Plant-derived toxicities should be considered when acute behavioral changes occur, especially in rural settings.

Curare's implementation into anesthesia care by Dr. Harold Griffith was facilitated by the availability of medical-grade curare, the demonstration that it could provide safe muscle relaxation in psychiatric patients undergoing "shock therapy," and the foresight of a Squibb scientist who realized its potential in the operating room. Griffith's demonstration that curare safely provided muscle relaxation in surgical patients eliminated the need for dangerously high doses of anesthetic gases. This helped pave the way to "balanced anesthesia," whereby small doses of selectively acting drugs are given to achieve specific ends.Curare's initial reception by anesthesiologists, particularly in the UK, was frosty owing to its lingering reputation as a lethal poison associated with witchcraft. We recently unearthed a scathing review of Griffith's work housed in the Wellcome Collection (London, UK). That review, requested by Sir Robert Macintosh, Oxford University's inaugural Nuffield Professor of Anesthesia, was authored by his colleague, Dr. Stuart L. Cowan. In hindsight, this disparaging assessment is especially fascinating: Why was this review so negative when curare would have such a remarkable positive impact on medicine? In the present Special Article, we present the above British response to curare's introduction to anesthesia and trace curare's remarkable journey through the contributions of explorers, scientists, and clinicians preceding the review to help put it in perspective.

The Solanaceae family comprises numerous species of economic and pharmacological importance, including the toxic deadly nightshade (Atropa belladonna), bittersweet nightshade (Solanum dulcamara), and black nightshade (Solanum nigrum). These plants are native to Europe, North Africa, and Western Asia, and have been used since ancient times in both ritual practices and medicine. A. belladonna contains potent tropane alkaloids (atropine, hyoscyamine, and scopolamine) and is widely utilized in modern pharmacology, although accidental poisonings still occur, often due to confusion with edible plants or the misuse of herbal and homeopathic preparations. In contrast, S. dulcamara contains glycoalkaloids such as solanine, solasodine, and β-solamarine, while S. nigrum contains solanine, solamargine, and solasonine. Both species have a history of traditional use as narcotics, diuretics, and treatments for skin, rheumatic, and respiratory conditions, as well as for pain, inflammation, fever, and other disorders; however, they also pose significant toxicological risks to humans and animals. Although poisonings from these two species are less common than those caused by A. belladonna, they still occur. A review of the literature identified 41 studies reporting poisoning cases associated with these plants, primarily resulting from berry ingestion. Poisoning typically produces anticholinergic syndrome, underscoring the importance of accurate identification and prompt treatment.

The α7 nicotinic acetylcholine receptor (α7 nAChR) is implicated in organophosphate (OP) poisoning, but the scarcity of potent and subtype-selective small-molecule antagonists has hindered the development of related therapeutic strategies. Based on previous structure-activity relationship (SAR) studies, 43 novel piperidine-spirooxadiazole derivatives were designed, synthesized and evaluated using patch-clamp electrophysiology. Two optimized compounds, Y9 and YZ4, exhibited submicromolar inhibition of α7 nAChR and demonstrated high subtype-selectivity for α7 over other nAChR and muscarinic acetylcholine receptor (mAChR) subtypes. They showed robust neuroprotective effects against paraoxon (POX)-induced cytotoxicity in vitro. Notably, YZ4 displayed favorable pharmacokinetic (PK) profiles, including high oral bioavailability and excellent brain penetration. In a POX-intoxicated mouse model, YZ4 significantly improved survival rates, alleviated seizure severity and mitigated multiorgan injury. These findings demonstrate YZ4 as a promising molecular tool for probing α7 nAChR pathophysiology and a potential therapeutic candidate for OP poisoning.

Cyclizine is a first-generation H1 antihistamine widely used for the treatment of nausea and motion sickness. In addition to its antiemetic properties, it has anticholinergic and central nervous system effects that may confer psychoactive potential. Although generally regarded as a low-risk medication, increasing evidence suggests a potential for misuse, particularly among adolescents and individuals with mental health disorders or substance-use vulnerabilities. Published data on cyclizine toxicity are limited, and paediatric reports of intentional overdose remain scarce. We report a case of intentional cyclizine overdose in a 14-year-old girl with underlying mental health disorders, highlighting the clinical presentation, management considerations, including serial electrocardiographic assessment, and safeguarding implications. This case underscores the need for increased clinician awareness of cyclizine misuse and its potential harms in the paediatric population.

In a patient with belladonna poisoning, symptom recurrence was accompanied by a rebound in drug concentration. This suggests reabsorption of residual alkaloids during impaired intestinal peristalsis. The case emphasizes the importance of carefully monitoring bowel motility in the management of belladonna poisoning to prevent delayed or recurrent toxic manifestations.

OBJECTIVE: Hepatotoxicity is a significant adverse effect associated with long-term methotrexate (MTX) treatment, limiting its clinical utility. This study aimed to comprehensively evaluate the potential hepatoprotective effects of Otilonium Bromide (OB) against MTX-induced liver injury in an experimental rat model by integrating biochemical, molecular, and histopathological assessments. RESULTS: MTX administration resulted in significant structural and functional liver damage, as evidenced by elevated biochemical markers, alanine aminotransferase (ALT), transforming growth factor-beta (TGF-β), NOD-like receptor family pyrin domain-containing 3 (NLRP3), platelet-derived growth factor (PDGF), malondialdehyde (MDA) and worsened histopathological scores, including increased hepatocyte necrosis, fibrosis, and cellular infiltration. Treatment with OB significantly reduced these biochemical markers and improved histopathological changes compared to the MTX + saline group. Otilonium Bromide demonstrated hepatoprotective effects in the rat model of MTX-induced liver injury, likely through its anti-inflammatory and antifibrotic properties. These effects may be mediated by modulation of oxidative stress and the intestinal microbiome. Further studies are needed to explore its clinical applicability.