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Physostigmine as treatment for severe CNS anticholinergic toxicity
  1. R Teoh,
  2. A-V Page,
  3. R Hardern
  1. Acute Medical Assessment Area, The General Infirmary, Leeds LS1 3EX, UK
  1. Correspondence to: Dr Hardern (rhardern{at}

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Editor,—We report the successful use of physostigmine to treat central anticholinergic toxicity: a use described before but rarely seen.1 We treated a patient admitted after an overdose of amisulpride and procyclidine (not his own medication). He became extremely agitated and was treated with intravenous benzodiazepines (total quantity in 26 hours equivalent to 125 mg diazepam) but remained agitated. Because of the risks of serious injury if his agitation was untreated and of further benzodiazepine use outside a critical care area (the ward to which he was admitted has a patient:nurse ratio of 8:1), he was treated with 1 mg of physostigmine. This was immediately and dramatically followed by a period of complete lucidity lasting 90 minutes. He did not become agitated again and his confusion resolved fully after a further 16 hours. Referral to an ITU was considered but it was felt that the risks of paralysis, intubation and ventilation (and the possible need for interhospital transfer) outweighed those associated with physostigmine treatment. This latter option had the advantage of therapeutic and diagnostic potential.

Procyclidine is an antimuscarinic drug with a half life of 8 to 16 hours. When taken in overdose the features of anticholinergic toxicity may be delayed.2 His agitation was unlikely to be attributable to amisulpride as this is a D2/D3 receptor antagonist but the patient had no signs of extrapyramidal side effects.2 Physostigmine is a tertiary ammonium compound that reverses anticholinergic effect via acetylcholinesterase inhibition. Uniquely, for this class, it crosses the blood-brain barrier. It has a rapid onset of effect and duration of action of one to two hours.3

We do not propose that physostigmine be routinely used to treat changed mental status after poisoning. We do, believe, however, that it has a very specific role in the treatment of patients with persisting central anticholinergic toxicity despite sedation with benzodiazepines.


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