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Information |
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Drug Groups
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approved |
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Description
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Benzotropine is a centrally-acting, antimuscarinic agent used as an adjunct in the treatment of Parkinson’s disease. It may also be used to treat extrapyramidal reactions, such as dystonia and Parkinsonism, caused by antipsychotics (e.g. phenothiazines). Symptoms of Parkinson’s disease and extrapyramidal reactions arise from decreases in dopaminergic activity which creates an imbalance between dopaminergic and cholinergic activity. Anticholinergic therapy is thought to aid in restoring this balance leading to relief of symptoms. In addition to its anticholinergic effects, benztropine also inhibits the reuptake of dopamine at nerve terminals via the dopamine transporter. Benzotropine also produces antagonistic effects at the histamine H1 receptor. |
| Indication |
For use as an adjunct in the therapy of all forms of parkinsonism and also for use in the control of extrapyramidal disorders due to neuroleptic drugs. |
| Pharmacology |
Benztropine is an anticholinergic used in the symptomatic treatment of all etiologic groups of parkinsonism and drug-induced extrapyramidal reactions (except tardive dyskinesia). Benztropine possesses both anticholinergic and antihistaminic effects, although only the former has been established as therapeutically significant in the management of parkinsonism. Benztropine's anticholinergic activity is about equal to that of atropine. Benztropine also inhibits dopamine reuptake via the dopamine transporter at nerve terminals. |
| Toxicity |
Signs of overdose include confusion, nervousness, listlessness, hallucinations, dizziness; muscle weakness, ataxia, dry mouth, mydriasis, blurred vision, palpitations, tachycardia, elevated blood pressure, nausea, vomiting, dysuria, numbness of fingers, headache, delirium, coma, shock, convulsions, respiratory arrest, anhidrosis, hyperthermia, glaucoma, and constipation. |
| Affected Organisms |
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Humans and other mammals |
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| Absorption |
Onset of action is 1-2 hours following oral administration. The onset of action is within minutes when administered by IM or IV injection. |
| Protein Binding |
~95% to serum proteins |
| References |
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Wszola BA, Newell KM, Sprague RL: Risk factors for tardive dyskinesia in a large population of youths and adults. Exp Clin Psychopharmacol. 2001 Aug;9(3):285-96.
[Pubmed]
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van Harten PN, Hoek HW, Matroos GE, Koeter M, Kahn RS: Intermittent neuroleptic treatment and risk for tardive dyskinesia: Curacao Extrapyramidal Syndromes Study III. Am J Psychiatry. 1998 Apr;155(4):565-7.
[Pubmed]
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