Anticholinergics generally have antisialagogue effects (decreasing saliva production), and most produce some level of sedation, both being advantageous in surgical procedures.[8][9]
Until the beginning of the 20th century, anticholinergic drugs were widely used to treat psychiatric disorders.[10]
Clinically the most significant feature is delirium, particularly in the elderly, who are most likely to be affected by the toxidrome.[3]
Side effects
Long-term use may increase the risk of both cognitive and physical decline.[14][15] It is unclear whether they affect the risk of death generally.[14] However, in older adults they do appear to increase the risk of death.[16]
Hallucinated presence of people not actually there (e.g. shadow people)
Rarely: seizures, coma, and death
Orthostatic hypotension (severe drop in systolic blood pressure when standing up suddenly) and significantly increased risk of falls in the elderly population[20]
Older patients are at a higher risk of experiencing CNS side effects.[citation needed] The link possible between anticholinergic medication use and cognitive decline/dementia has been noted in weaker observational studies.[21] Although there is no strong evidence from randomized controlled trials to suggest that these medications should be avoided, clinical guidelines suggest that a consideration be made to decrease the use of these medications if safe to do so and the use of these medications be carefully considered to reduce any possible adverse effects including cognitive decline.[21]
Toxicity
An acute anticholinergic syndrome is reversible and subsides once all of the causative agents have been excreted. Reversible acetylcholinesterase inhibitor agents such as physostigmine can be used as an antidote in life-threatening cases. Wider use is discouraged due to the significant side effects related to cholinergic excess including seizures, muscle weakness, bradycardia, bronchoconstriction, lacrimation, salivation, bronchorrhea, vomiting, and diarrhea. Even in documented cases of anticholinergic toxicity, seizures have been reported after the rapid administration of physostigmine. Asystole has occurred after physostigmine administration for tricyclic antidepressant overdose, so a conduction delay (QRS > 0.10 second) or suggestion of tricyclic antidepressant ingestion is generally considered a contraindication to physostigmine administration.[22]
Dementia
A recent study carried out by experts from the University of Nottingham and funded by the National Institute for Health Research (NIHR) has shown there to be an increased risk of up to 50% of patients developing Dementia due to some of these medications and cautions have been advised with their use. The study findings showed increased risks of dementia for anticholinergic drugs overall and specifically for the anticholinergic antidepressants, antipsychotic drugs, antiparkinsons drugs, bladder drugs and epilepsy drugs after accounting for other risk factors for dementia.
Physostigmine is one of only a few drugs that can be used as an antidote for anticholinergic poisoning. Nicotine also counteracts anticholinergics by activating nicotinic acetylcholine receptors. Caffeine (although an adenosinereceptor antagonist) can counteract the anticholinergic symptoms by reducing sedation and increasing acetylcholine activity, thereby causing alertness and arousal.
Psychoactive uses
When a significant amount of an anticholinergic is taken into the body, a toxic reaction known as acute anticholinergic syndrome may result. This may happen accidentally or intentionally as a consequence of either recreational or entheogenic drug use, though many users find the side effects to be exceedingly unpleasant and not worth the recreational effects they experience. In the context of recreational use, anticholinergics are often called deliriants.[24]
^"Anticholinergics", Anticholinergic Agents, Bethesda (MD): National Institute of Diabetes and Digestive and Kidney Diseases, 2012, PMID31643610, retrieved 2020-03-23, Anticholinergics have antisecretory activities and decrease nasal and bronchial secretions, salivation, lacrimation, sweating and gastric acid production, and can be used to decrease secretions in allergic and inflammatory diseases. Anticholinergics relax smooth muscle in the gastrointestinal tract, bladder and lung and can be used for gastrointestinal, urological or respiratory conditions associated with spasm and dysmotility.
^Clinical Pharmacology [database online]. Tampa, FL: Gold Standard, Inc.; 2009. Drugs with Anticholinergic Activity. Prescriber's Letter 2011; 18 (12):271233.
^ abcdeMigirov, A; Datta, AR (2020), "article-17683", Physiology, Anticholinergic Reaction, This book is distributed under the terms of the Creative Commons Attribution 4.0 International License, which permits use, duplication, adaptation, distribution, and reproduction in any medium or format, as long as you give appropriate credit to the original author(s) and the source, a link is provided to the Creative Commons license, and any changes made are indicated., Treasure Island (FL): StatPearls Publishing, PMID31536197, retrieved 2020-03-24
^Sharee A. Wiggins; Tomas Griebling. "Urinary Incontinence". Landon Center on Aging. Archived from the original on 2011-09-27. Retrieved 2011-07-09.
^Su, Mark; Goldman, Matthew. Traub, Stephen J.; Burns, Michele M.; Grayzel, Jonathan (eds.). "Anticholinergic poisoning". UpToDate. Retrieved 2020-03-24.
^Page 592 in: Cahalan, Michael D.; Barash, Paul G.; Cullen, Bruce F.; Stoelting, Robert K. (2009). Clinical Anesthesia. Hagerstwon, MD: Lippincott Williams & Wilkins. ISBN978-0-7817-8763-5.
^Andre, L; Gallini, A; Montastruc, F; Montastruc, JL; Piau, A; Lapeyre-Mestre, M; Gardette, V (29 August 2019). "Association between anticholinergic (atropinic) drug exposure and cognitive function in longitudinal studies among individuals over 50 years old: a systematic review". European Journal of Clinical Pharmacology. 75 (12): 1631–1644. doi:10.1007/s00228-019-02744-8. PMID31468067. S2CID201675824.
^Rosen, Peter, John A. Marx, Robert S. Hockberger, and Ron M. Walls. Rosen's Emergency Medicine: Concepts and Clinical Practice. 8th ed. Philadelphia, PA: Mosby Elsevier, 2014.
^ abBersani, F. S.; Corazza, O.; Simonato, P.; Mylokosta, A.; Levari, E.; Lovaste, R.; Schifano, F. (2013). "Drops of madness? Recreational misuse of tropicamide collyrium; early warning alerts from Russia and Italy". General Hospital Psychiatry. 35 (5): 571–3. doi:10.1016/j.genhosppsych.2013.04.013. PMID23706777.
^Carroll FI, Blough BE, Mascarella SW, Navarro HA, Lukas RJ, Damaj MI (2014). "Bupropion and Bupropion Analogs as Treatments for CNS Disorders". Emerging Targets & Therapeutics in the Treatment of Psychostimulant Abuse. Advances in Pharmacology. Vol. 69. pp. 177–216. doi:10.1016/B978-0-12-420118-7.00005-6. ISBN9780124201187. PMID24484978.
^Tasman, Allan; Kay, Jerald; Lieberman, Jeffrey A.; First, Michael B.; Maj, Mario (11 October 2011). Psychiatry. John Wiley & Sons. ISBN978-1-119-96540-4. Archived from the original on 20 March 2017.
^Damaj, M. I.; Flood, P; Ho, K. K.; May, E. L.; Martin, B. R. (2004). "Effect of Dextrometorphan and Dextrorphan on Nicotine and Neuronal Nicotinic Receptors: In Vitro and in Vivo Selectivity". Journal of Pharmacology and Experimental Therapeutics. 312 (2): 780–5. doi:10.1124/jpet.104.075093. PMID15356218. S2CID149958.
^Lee, Jun-Ho; Shin, Eun-Joo; Jeong, Sang Min; Kim, Jong-Hoon; Lee, Byung-Hwan; Yoon, In-Soo; Lee, Joon-Hee; Choi, Sun-Hye; Lee, Sang-Mok; Lee, Phil Ho; Kim, Hyoung-Chun; Nah, Seung-Yeol (2006). "Effects of dextrorotatory morphinans on α3β4 nicotinic acetylcholine receptors expressed in Xenopus oocytes". European Journal of Pharmacology. 536 (1–2): 85–92. doi:10.1016/j.ejphar.2006.02.034. PMID16563374.
^Zacny, James P. (2003). "Characterizing the subjective, psychomotor, and physiological effects of a hydrocodone combination product (Hycodan) in non-drug-abusing volunteers". Psychopharmacology. 165 (2): 146–156. doi:10.1007/s00213-002-1245-5. PMID12404072. S2CID7835794.
