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Use of drugs with anticholinergic effect and impact on cognition in Parkinson’s disease: A cohort study
  1. Uwe Ehrt (uweehrt{at}gmail.com)
  1. The Norwegian Centre for Movement Disorders, Stavanger University Hospital, Norway
    1. Karl Broich (k.broich{at}bfarm.de)
    1. Federal Institute for Drugs and Medical Devices (BfArM), Bonn, Germany
      1. Jan Petter| Larsen (jpl{at}sus.no)
      1. The Norwegian Centre for Movement Disorders, Stavanger University Hospital, Norway
        1. Clive Ballard (clive.ballard{at}kcl.ac.uk)
        1. Wolfson Center for Age-Related Diseases, Kings College, London, United Kingdom
          1. Dag Aarsland (daarsland{at}gmail.com)
          1. The Norwegian CentrWolfson Center for Age-Related Diseases, Kings College, London, Norway

            Abstract

            Background: Cognitive decline is common in Parkinson’s disease (PD). Although some of the etiological factors are known, it is not yet known whether drugs with anticholinergic activity (AA) contribute to this cognitive decline. Such knowledge would provide opportunities to prevent acceleration of cognitive decline in PD.

            Objective: To study whether the use of agents with anticholinergic properties is an independent risk factor for cognitive decline in patients with PD.

            Methods: A community-based cohort of patients with PD (n=235) were included and assessed at baseline. They were re-assessed four and 8 years later. Cognition was assessed using the Mini-Mental State Examination (MMSE). A detailed assessment of the AA of all drugs prescribed was made, and AA was classified according to a standardised scale. Relationships between cognitive decline and AA load and duration of treatment were assessed using bivariate and multivariate statistical analyses.

            Results: More than 40% used drugs with AA at baseline. During the 8-year follow-up, the cognitive decline was higher in those who had been taking AA drugs (median decline on MMSE 6.5 points) compared to those who had not taken such drugs (median decline 1 point; p=0.025). In linear regression analyses adjusting for age, baseline cognition and depression, significant associations with decline on MMSE were found for total AA load (standardised Beta=0.229, p=0.04) as well as duration of using AA drugs (standardized beta 0.231, p=0.032).

            Conclusion: Our findings suggest that there is an association between the use of drugs with anticholinergic properties and cognitive decline in PD. This may provide an important opportunity for clinicians to avoid increasing progression of cognitive decline by avoiding such drugs if possible. Increased awareness by clinicians is required about the classes of drugs that have anticholinergic properties.

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