Delirium anticholinergic-induced

Tune LE, BylsmaFW (1991) Benzodiazepine-induced and anticholinergic-induced delirium in the elderly. Int Psychogeriatr 3 397-408... 

Other sleep-inducing benzodiazepines should be avoided. They are more difficult to metabolize and can accumulate in elderly, demented patients. Sedating, low potency antipsychotics should also be avoided. Their strong anticholinergic (acetylcholine-blocking) effects can worsen dementia or cause delirium. 

Although diazepam does not have anticholinergic properties, it is possible to reverse diazepam-induced delirium by the use of cholinesterase inhibitors, such as physostig-mine however, physostigmine can on occasion induce severe arterial hypertension, especially if the dose exceeds 2 mg intravenously. In healthy volunteers sedated with diazepam, an increase in awareness was established with the use of physostigmine, but there was also a reduction in ventilatory drive (SEDA-10, 119). 

Itil, T., Fink, M. (1966). Anticholinergic drug-induced delirium experimental modification, quantitative EEG and behavioral correlations. J. Nerv. Ment. Dis. 143 492-507. 

Heiser JF, Gillin JC. The reversal of anticholinergic drug-induced delirium and coma with physostigmine. Amer /Psychiatry. 1971 127 1050. 

Relative history of seizure disorder, bipolar disorder (may induce mania), urinary retention, narrow-angle glaucoma, delirium, hyperthyroidism, bradycardia (or drugs that cause bradycardia), or electrolyte disturbance (esp. K+ or Mg ). Use caution in conjunction with other antidepressants (including MAOIs and SSRIs), other anticholinergic medications, drugs that increase plasma levels (phenothiazines, haloperidol, cimetidine), or drugs that lower seizure threshold (esp. tramadol). Use caution in elderly, children/adolescents. 

Cases cf Neurotoxicity Toxicity at therapeutic or subtherapeutic levels was reported in three cases. In two of these cases, the role of lithium is questionable. In one case of a rapidly fatal presentation of neuroleptic malignant syndrome (NMS) in a 72-year-old woman whose lithium level was 1.5 mM, the authors report a lithium-induced fatal NMS because she was not prescribed an antipsychotic [84 ]. However, her presentation is also consistent with fatal catatonia, sepsis, or unknown consumption of an antipsychotic, none of which were ruled out, and all of which are more likely than lithium-induced NMS. A second case in which a delirium with dyspraxia, but not ataxia in a 57-year-old man with a lithium level of 0.44 mM, that resolved after discontinuation of botii lithium and tricyclic antidepressant medication, was felt to be an interaction between the lithium and the antidepressant [85 ]. Lithium may have played a role, but he had been on lithium for years, and had developed anticholinergic problems with quetiapine previously, suggesting that the anticholinei c effects of the tricyclic antidepressant were more important in the delirium than the lithium. The third case of a 65-year-old man with multisystem atrophy becoming considerably worse with lithium at a level of 1.1 mM, is much more likely to represent lithium-related neurotoxicity at therapeutic levels [86 ]. 

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