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Treatment Of Alzheimer’s Disease
Published in Zaven S. Khachaturian, Teresa S. Radebaugh, Alzheimer’s Disease, 2019
Lina Shihabuddin, Kenneth L. Davis
Physostigmine is a natural alkaloid that is absorbed in the gastrointestinal tract, subcutaneous tissue, and mucous membrane. It readily crosses the blood-brain barrier and reaches maximal levels in short time; it is hydrolyzed and inactivated within 2 hours. Most studies using parenteral administration of physostigmine have documented transient cognitive improvement in at least a subgroup of patients with AD (Mohs and Davis, 1987). Oral administration of the drug has shown to have some efficacy as well (Mohs et al., 1985). It has been speculated that long-term treatment with physostigmine, or any cholimemetic, may delay deterioration in Alzheimer’s disease: four out of five patients who received the drug over a 3-year period did not significantly deteriorate in their performances on the Buschke selective reminding task (Beller, 1988). Two out of six patients treated with oral physostigmine for 29 months also did not show deterioration, whereas all six drug free subjects did (Jenike, 1990). However, these observations are little more than intriguing anecdotes. Oral physostigmine administration is associated with problems. For example, the blood, and therefore CNS, levels achieved with a given dose are quite variable and necessitate individual titration of medication. Blood levels required to achieve CNS concentrations necessary for cognitive enhancement may be associated with significant adverse effects. Physostigmine short half-life is also a problem further intensifying fluctuations in drug levels and necessitating the frequent administration.
Anticholinergic and Neuroleptic Drugs
Published in Frank A. Barile, Barile’s Clinical Toxicology, 2019
Pharmacological cholinergic intervention is warranted when signs and symptoms result from moderate to severe anticholinergic toxicity. Although controversial, intravenous (I.V.) physostigmine (Antilirium®), a reversible cholinesterase inhibitor, is warranted only if conventional therapy fails to control seizures, agitation, and unstable dysrhythmia, coma with respiratory depression, malignant hypertension, or hypotension. Through its action at both central and peripheral cholinergic receptors, physostigmine reverses anticholinergic activity and ameliorates the coma, delirium, and seizures that accompany severe toxicity.* As discussed later, however, physostigmine is not recommended in reversing the anticholinergic actions of TCA and phenothiazine derivatives due to potential induction of fatal asystoles. Physostigmine administration is contraindicated in patients with cardiovascular or peripheral vascular disease, bronchospasm, intestinal obstruction, heart block, or bladder obstruction.
Psychopharmacology EMIs
Published in Michael Reilly, Bangaru Raju, Extended Matching Items for the MRCPsych Part 1, 2018
Choline.Donepezil.Galanthamine.Ginkgo biloba.Lecithin.Nicotinic acid.Physostigmine.Rivastigmine.Tacrine.Tyrosine.
Adverse events associated with diphenhydramine in children, 2008–2015
Published in Clinical Toxicology, 2020
Robert B. Palmer, Kate M. Reynolds, William Banner, G. Randall Bond, Ralph E. Kauffman, Ian M. Paul, Jody L. Green, Richard C. Dart
In the present study, despite the prevalence of reported anticholinergic effects, it was very rare for physostigmine to be used as a treatment, even when the report documented that physostigmine was recommended. This could be due to a lack of practitioner familiarity with physostigmine, challenges with diagnosing anticholinergic delirium in preverbal children or toddlers with limited verbal skills, or due to the belief that the anticholinergic effects observed were mild and antidotal treatment was unnecessary. Scharman et al. concluded that physostigmine may have benefit, but the finding that phsyostigmine was used relatively infrequently is consistent with our finding. Future research regarding physician knowledge of physotigmine, reluctance to physostigmine use, or side effects associated with physostigmine may improve the proper use of this antidote to DPH toxicity [17].
Datura and Brugmansia plants related antimuscarinic toxicity: an analysis of poisoning cases reported to the Taiwan poison control center
Published in Clinical Toxicology, 2019
Uyen Vy Doan, Ming-Ling Wu, Dong-Haur Phua, Bomar Mendez Rojas, Chen-Chang Yang
Physostigmine can be used to reverse antimuscarinic toxicity and has been shown to be effective and safe [34–39]. Physostigmine reversed delirium in 87% of patients and controlled agitation in 96% of patients. Burns et al. [40] reported that the mean response time of anticholinergic poisoned patients to physostigmine was 10.9 ± 5.3 min. In some cases, relapse did occur with a mean time of 100 ± 42 min. However, asystole has been reported in two severe cases of antidepressant toxicity when physostigmine was given [41]. Since then, physicians are reluctant to treat anticholinergic poisoned patients with physostigmine. In a survey of clinical toxicologists (2012–2014), only 12.4% of patients manifesting antimuscarinic syndrome had received physostigmine as a monotherapy [42].
Safety and effectiveness of physostigmine: a 10-year retrospective review*
Published in Clinical Toxicology, 2018
Ann M. Arens, Krishna Shah, Suad Al-Abri, Kent R. Olson, Tom Kearney
Physostigmine is a tertiary carbamate and reversible acetylcholinesterase inhibitor that can provide rapid reversal of anticholinergic toxicity [1]. Its rapid reversal anticholinergic delirium makes physostigmine a useful diagnostic and therapeutic tool [2–6]. Reversal of agitated delirium secondary to anticholinergic toxicity may prevent complications such as agitation, rhabdomyolysis, and hyperthermia [1,7]. Concern for cholinergic excess including seizure, bradycardia, emesis, and asystole in the setting of tricyclic overdose have been reported and often limits use [2–6,8–10], however, previous studies have shown that adverse reactions are infrequent [3,6].