The muscarinic (M) receptors, located in various tissues (the heart, salivary glands, blood vessels, the brain, gastrointestinal tract, etc) are the sites where acetylcholine, the principal neurotransmitter in the peripheral, but also the central nervous system (CNS), exerts its effects [1]. These receptors are also a target of both cholinergic and anticholinergic drugs, and the term anticholinergic toxicity (widely described in the literature as an anticholinergic syndrome) denotes the development of symptoms as a result of profound anticholinergic effects [1] [2] [3] [4]. This clinical entity can be seen after ingestion (either accidental or intentional) of large concentrations of various drugs - atropine and scopolamine (true anticholinergic agents), but also antihistamines (diphenhydramine), tricyclic antidepressants, loperamide, and certain antipsychotics, all possessing anticholinergic effects in addition to their primary roles [3] [4] [5]. Furthermore, ingestion of Atropa belladonna (known as deadly nightshade), a plant that contains an abundant amount of alkaloid compounds that constitute atropine and scopolamine (particularly in the ripe fruit and leaves), is also an important cause of anticholinergic toxicity [6]. In fact, numerous herbal products made from this alkaloid plant exist and have been reported in the literature as agents of anticholinergic toxicity [1] [2]. Regardless of the underlying cause, signs, and symptoms appear due to the same pathophysiological mechanism, and the clinical presentation may encompass numerous systems. Tachycardia, hyperthermia, flushing, urinary retention, reduced gastrointestinal motility, pupillary dilation (mydriasis), reduced light reactivity, dry skin and mouth, as well as reduced salivary gland secretion are notable signs stemming from the inhibition of peripheral muscarinic receptors [1] [4] [5] [6] [7]. On the other hand, psychosis, agitation, confusion, hallucinations, seizures, altered consciousness, and coma in later stages are hallmarks of CNS toxicity [1] [4] [5] [7] [8].

Clinical criteria supported by findings obtained during history taking are essential in making the diagnosis of anticholinergic toxicity. Physicians must obtain a complete personal history that will determine if the patient is taking (or has intentionally taken) drugs or herbal products containing Atropa belladonna that possess anticholinergic effects, as both intentional and accidental cases are described in the literature [2] [4] [5] [7] [8]. It is not uncommon for patients to be in a state that is not suitable for communication (altered consciousness, psychosis, etc.), thus a heterogeneous anamnesis (from parents, friends or relatives) might be highly useful for obtaining additional information [7]. A thorough physical examination of all systems should follow, which will confirm the presence of anticholinergic signs and thus lead the physician to raise valid clinical suspicion. Laboratory investigations are of limited use in anticholinergic toxicity, as reports show no significant abnormalities except sporadic leukocytosis and hyperglycemia [7] [8]. Some authors, however, further solidify the diagnosis by performing qualitative and quantitative screening for detecting drugs in urine through procedures such as mass spectrometry (MS) [4] [8].

The primary goal of treatment is to stabilize the patient and reverse the effects of the toxicity:

• Supportive Care: Monitoring vital signs and providing intravenous fluids.
• Activated Charcoal: Administered if the ingestion was recent, to prevent further absorption of the toxin.
• Antidote: Physostigmine, a drug that can reverse central and peripheral anticholinergic effects, may be used in severe cases.
• Symptomatic Treatment: Managing symptoms such as seizures or agitation with appropriate medications.

The prognosis for anticholinergic toxicity is generally good if recognized and treated promptly. Most patients recover fully with appropriate medical intervention. However, severe cases can lead to complications such as seizures, coma, or even death if not managed in a timely manner.

Anticholinergic toxicity is primarily caused by the ingestion of substances that block acetylcholine. Common culprits include:

• Medications: Antihistamines, tricyclic antidepressants, antipsychotics, and certain muscle relaxants.
• Plants: Some plants, like deadly nightshade (Atropa belladonna), contain natural anticholinergic compounds.
• Overdose: Intentional or accidental overdose of medications with anticholinergic properties.

Anticholinergic toxicity can affect individuals of all ages, but certain populations are at higher risk:

• Elderly: More susceptible due to polypharmacy and age-related changes in drug metabolism.
• Children: Accidental ingestion of medications is a common cause.
• Individuals with Mental Health Disorders: May be at risk due to the use of psychiatric medications with anticholinergic effects.

Anticholinergic toxicity results from the inhibition of acetylcholine, a neurotransmitter essential for communication between nerve cells. This inhibition affects both the central nervous system (brain and spinal cord) and the peripheral nervous system (nerves outside the brain and spinal cord), leading to the wide range of symptoms observed in this condition.

Preventing anticholinergic toxicity involves:

• Medication Management: Careful monitoring of drug use, especially in the elderly and those on multiple medications.
• Education: Informing patients and caregivers about the potential risks of medications with anticholinergic properties.
• Safe Storage: Keeping medications out of reach of children to prevent accidental ingestion.

Anticholinergic toxicity is a potentially serious condition caused by the excessive blockade of acetylcholine. It presents with a range of symptoms affecting the nervous system and other bodily functions. Prompt recognition and treatment are crucial for a favorable outcome. Understanding the causes, symptoms, and management strategies is essential for healthcare providers and patients alike.

If you or someone you know is experiencing symptoms such as confusion, dry mouth, dilated pupils, or rapid heart rate after taking medication, it may be due to anticholinergic toxicity. This condition occurs when certain drugs block the action of a chemical in the body called acetylcholine. It's important to seek medical attention promptly, as treatment can help reverse the effects and prevent complications. Always follow your doctor's instructions regarding medication use and keep medicines out of reach of children.

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2. Centers for Disease Control and Prevention (CDC). Anticholinergic poisoning associated with an herbal tea--New York City, 1994.
3. Walker A, Delle Donne A, Douglas E, Spicer K, Pluim T. Novel Use of Dexmedetomidine for the Treatment of Anticholinergic Toxidrome. J Med Toxicol. 2014;10(4):406-410.
4. Verheijden NA, Koch BC, Brkic Z, Alsma J, Klein Nagelvoort-Schuit SC. A 45-year-old woman with an anticholinergic toxidrome. Neth J Med. 2016;74(3):133-135.
5. Lee AC, So KT. Acute anticholinergic poisoning in children. Hong Kong Med J. 2005;11(6):520-523.
6. Joshi P, Wicks A, Munshi S. Recurrent autumnal psychosis. Postgrad Med J. 2003;79(930):239-240.
7. Demirhan A, Tekelioğlu ÜY, Yıldız İ, et al. Anticholinergic Toxic Syndrome Caused by Atropa Belladonna Fruit (Deadly Nightshade): A Case Report. Turk J Anaesthesiol Reanim. 2013;41(6):226-228.
8. Heindl S, Binder C, Desel H, Matthies U, Lojewski I, Bandelow B, et al. [Etiology of initially unexplained confusion of excitability in deadly nightshade poisoning with suicidal intent. Symptoms, differential diagnosis, toxicology and physostigmine therapy of anticholinergic syndrome]. Dtsch Med Wochenschr. 2000;125:1361–1365.