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PubMed · 11368397

Fatal benztropine toxicity.

M J Lynch·A Kotsos
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Abstract

Benztropine is an anticholinergic agent used in the treatment of Parkinson's disease and drug induced extrapyramidal disorders. We report a case of fatal benztropine toxicity. This drug is regarded as relatively safe and reports of isolated toxicity are scarce. In ascribing a particular death to fatal drug toxicity the forensic pathologist must take into account the circumstances surrounding the death, the presence and significance of any co-existent natural disease and the potential contribution of any other detected therapeutic or illicit agents. This interpretation will occur in the knowledge that certain drugs will not be detected and that with respect to quantification of postmortem drug levels, the notion of postmortem redistribution should always be considered.

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Antiparkinson AgentsAutopsyBenztropineDrug OverdoseFemaleHumansMiddle AgedMuscarinic AntagonistsCase ReportsJournal Article

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BibTeXRIS

M J Lynch, A Kotsos. 2001. Fatal benztropine toxicity.. https://doi.org/10.1177/002580240104100212

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PubMed2001

Ten-year follow-up of three different initial treatments in de-novo PD: a randomized trial.

BACKGROUND: The long-term effectiveness of three different initial drug regimes in patients with early, mild PD was evaluated by the PD Research Group of the United Kingdom (PDRGUK). In 1995, the selegiline arm of the trial was terminated following an interim analysis. METHOD: This was an open, randomized trial. Between 1985 and 1990, 782 patients with de-novo PD were recruited and randomized to one of three treatment arms: levodopa plus dopa decarboxylase inhibitor; levodopa plus decarboxylase inhibitor and selegiline; or bromocriptine. The main endpoints were mortality, disability, and adverse events. Intention-to-treat analysis was used. RESULTS: There was no significant difference in mortality between the bromocriptine and the levodopa arms (hazard ratio 1.15 [95% CI 0.90, 1.47]). Patients initially randomized to bromocriptine had slightly worse disability scores throughout follow-up. This difference was significant during the first years. Patients in the bromocriptine arm returned to pretreatment disability levels one year earlier than those in the levodopa arm. Patients randomized to bromocriptine had a significantly lower incidence of dyskinesias than those randomized to levodopa (rate ratio 0.73 [95% CI 0.57, 0.93]). However, this difference was not significant when only moderate to severe dyskinesias were considered. Patients in the bromocriptine arm had slightly lower rates of dystonias and on-off fluctuations, but moderate and severe forms were equally frequent in both arms. CONCLUSION: Starting treatment with the dopamine agonist bromocriptine does not reduce mortality in PD. A slightly lower incidence of motor complications is achieved at the expense of significantly worse disability scores throughout the first years of therapy.

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