Individuals with severe mental illness face a substantially higher risk of suicide compared with the general population, with drug overdose representing one of the most common and potentially lethal methods. This narrative review explores toxidromes frequently encountered in psychiatric populations, such as opioid, anticholinergic, and serotonergic toxicity, highlighting the clinical presentation in intentional overdose. Emphasis is placed on clinical recognition, antidote-based treatment, and systems-level strategies for the prevention of lethal overdose. We conducted a comprehensive literature search of PubMed, Google Scholar, and Web of Science for English-language articles using combinations of the following keywords: mental disorders; persons with psychiatric disorders; drug overdose; poisoning; serotonin syndrome; neuroleptic malignant syndrome; anticholinergic agents/poisoning; cholinergic antagonists/poisoning; psychotropic drugs/adverse effects; substance-related disorders; drug-related side effects and adverse reactions; polypharmacy; suicide, attempted; emergency service, hospital. By embedding toxidrome awareness into routine emergency and psychiatric practice, we aim to expedite treatment and improve patient outcomes.

Agitated patients may present with life-threatening emergency. Differential diagnoses span a wide range, conveniently remembered by the acronym VITAMINS (Vascular, Infections, Toxins/Trauma, Auto-immune/-inflammatory, Metabolic, Iatrogenic, Neoplastic, and pSychiatric aetiology). Common toxidromes include anticholinergic syndrome, serotonin toxicity, sympathomimetic toxicity, neuroleptic malignant syndrome, and withdrawal from alcohol or sedative-hypnotics. Diagnosis is primarily clinical, based on exposure history and characteristic signs. A focused physical examination is often sufficient when history is unclear. Unlike routine medical evaluations that begin with a full history and examination, management starts with rapid behavioural control and stabilization of vital signs, followed by focused examination and targeted investigations. Specific antidote therapy is seldom required in the initial management.

Organophosphate (OP) poisoning is a frequent toxicological emergency worldwide, particularly in low- and middle-income countries. Because the characteristic cholinergic toxidrome involves multiple systems, the absence of a clear history of exposure and clinical suspicion may lead to a disastrous misdiagnosis. We report a previously healthy male who presented with acute dyspnoea, chest pain, and diaphoresis, whose signs were suggestive of non-ST elevation acute coronary syndrome and pneumonia. Despite standard treatment, he deteriorated, necessitating intubation. However, the characteristic odour of OP prompted atropine treatment, leading to significant clinical improvement. Serum acetylcholinesterase activity was markedly reduced, confirming OP poisoning as the underlying cause.

A toxicologic syndrome, or toxidrome, is a distinct pattern of effects of poisoning. Well-defined toxidromes are the opioid, anticholinergic, cholinergic and sympathomimetic, and an additional described toxidrome is GABAergic. These toxidromes are named for the receptor effects causing their specific clinical findings, and knowledge of toxidromes allows rapid pattern recognition of specific poisonings. In this review, toxidromes and the initial assessment and general approach to management of acute poisoning are discussed. This article details the receptor-level effects of the poisoning, key clinical signs and symptoms and the role antidotes play in treatment. Clinical resources such as Toxbase and others exist to provide detailed guidance on clinical management of poisoning.

Dextromethorphan toxicity in young children (especially those 4 years of age or younger) can have an extremely poor prognosis if untreated. However, if timely recognized and optimally managed, it can have a good clinical outcome despite a profound initial insult. We present 3 pediatric cases (younger than 5 years of age) with sudden unresponsiveness following ingestion of cough medications containing dextromethorphan. All these children showed cytotoxic edema in the cerebellar hemispheres on MR of the brain, with diffusion-restricting foci in the supratentorial white matter in 2 patients. These features resemble the recently described acute opioid toxidrome in children, pediatric opioid use-associated neurotoxicity with cerebellar edema (POUNCE). Hence, we named this entity dextromethorphan-associated neurotoxicity with cerebellar edema (DANCE) to increase the awareness of dextromethorphan toxicity in young children and the need to promptly recognize it to initiate optimal management.

In this article, we will discuss the history, pharmacodynamics, and neurotoxicity of psychostimulants and hallucinogens. The drugs discussed are widely used and have characteristic toxidromes and potential for neurological injuries with which the practicing clinician should be familiar. Psychostimulants are a class of drugs that includes cocaine, methamphetamine/amphetamines, and cathinones, among others, which produce a crescendoing euphoric high. Seizures, ischemic and hemorrhagic strokes, rhabdomyolysis, and a variety of movement disorders are commonly encountered in this class. Hallucinogens encompass a broad class of drugs, in which the user experiences hallucinations, altered sensorium, distorted perception, and cognitive dysfunction. The experience can be unpredictable and dysphoric, creating a profound sense of anxiety and panic in some cases. Recognizing the associated neurotoxicities and understanding the appropriate management is critical in caring for these patient populations. Several of these agents are not detectable by standard clinical laboratory analysis, making identification and diagnosis an even greater challenge.

Methamidophos is a highly hazardous organophosphate and is known to cause an acute cholinergic toxidrome. Methamidophos use is not allowed in South Africa and therefore local data pertaining to methamidophos poisoning is very limited, with no paediatric clinical cases described. Methamidophos is an active metabolite of acephate, a commonly used organophosphate, registered for agricultural use in South Africa. We present a paediatric case of methamidophos poisoning with prolonged clinical effects. The patient experienced a prolonged cholinergic toxidrome lasting 10 days, with a period of near-full recovery during this time. We discuss the biological plausibility of the detected methamidophos being a byproduct of acephate. In addition, we highlight the importance of closer monitoring of patients with organophosphate poisoning in areas where acephate is commonly used.

Most patients exposed to organophosphates come into contact with insecticides. The first organophosphate insecticide was created in the mid-1800s but was not widely used until after World War II. Organophosphates are used as medications, insecticides, and nerve agents as a weapon. Symptoms include increased saliva and tear production, diarrhea, nausea, vomiting, small pupils, sweating, muscle tremors, and confusion. The onset of symptoms is often within minutes, and it can take weeks to disappear.[1][2][3][4][5] Today, the majority of organophosphate toxicity occurs in farmers and people who work in agriculture, since these agents are heavily used in this industry.

According to the EU Early Warning System (EWS), synthetic cathinones (SCs) are the second largest new psychoactive substances (NPS) class, with 162 synthetic cathinones monitored by the EU EWS. They have a similar structure to cathinone, principally found in Catha Edulis; they have a phenethylamine related structure but also exhibit amphetamine-like stimulant effects. Illegal laboratories regularly develop new substances and place them on the market. For this reason, during the last decade this class of substances has presented a great challenge for public health and forensic toxicologists. Acting on different systems and with various mechanisms of action, the spectrum of side effects caused by the intake of these drugs of abuse is very broad. To date, most studies have focused on the substances' cardiac effects, and very few on their associated neurotoxicity. Specifically, synthetic cathinones appear to be involved in different neurological events, including increased alertness, mild agitation, severe psychosis, hyperthermia and death. A systematic literature search in PubMed and Scopus databases according to PRISMA guidelines was performed. A total of 515 studies published from 2005 to 2022 (350 articles from PubMed and 165 from Scopus) were initially screened for eligibility. The papers excluded, according to the criteria described in the Method Section (n = 401) and after full text analyses (n = 82), were 483 in total. The remaining 76 were included in the present review, as they met fully the inclusion criteria. The present work provides a comprehensive review on neurotoxic mechanisms of synthetic cathinones highlighting intoxication cases and fatalities in humans, as well as the toxic effects on animals (in particular rats, mice and zebrafish larvae). The reviewed studies showed brain-related adverse effects, including encephalopathy, coma and convulsions, and sympathomimetic and hallucinogenic toxidromes, together with the risk of developing excited/agitated delirium syndrome and serotonin syndrome.

Kratom is a mixture of compounds that are present in the leaves of the tropical tree Mitragyna speciosa. It is used as a psychoactive agent with both opiate and stimulant-like effects. In this case series we describe the signs, symptoms, and the management of kratom overdose in the prehospital setting and in intensive care. We retrospectively searched for cases in the Czech Republic. Over 36 months we found 10 cases of kratom poisoning, which healthcare records were analyzed and reported as per CARE guidelines. The dominant symptoms in our series were neurological and included quantitative (n = 9) or qualitative (n = 4) disorder of consciousness. Signs and symptoms of vegetative instability [hypertension (n = 3) and tachycardia (n = 3) vs. bradycardia/cardiac arrest (n = 2), mydriasis (n = 2) vs. miosis (n = 3)] were noticed. Prompt response to naloxone in two cases and lack of response in one patient were observed. All patients survived and the effect of intoxication wore off within two days. Kratom overdose toxidrome is variable and, in keeping with its receptor physiology, consists of signs and symptoms of opioid-like overdose, sympathetic overactivation and serotonin-like syndrome. Naloxone can help to avoid intubation in some cases.