Background: Clinical decision support software (CDSS) solutions can automatically identify drug interactions and thereby aim to improve drug safety. However, data on the comparative performance of different CDSS to detect and appropriately classify interactions in real-life prescription datasets is limited.
Objective: The aim of this study was to compare the results from two different CDSS analysing the pharmacotherapy of a large population of psychiatric inpatients for drug interactions.
Purpose: The comparative evaluation of clinical decision support software (CDSS) programs regarding their sensitivity and positive predictive value for the identification of clinically relevant drug interactions.
Methods: In this research, we used a cross-sectional study that identified potential drug interactions using the CDSS MediQ and the ID PHARMA CHECK in 484 neurological inpatients. Interactions were reclassified according to the Zurich Interaction System, a multidimensional classification that incorporates the Operational Classification of Drug Interactions.
Purpose: The current study aimed at identifying and quantifying critical drug interactions in neurological inpatients using clinical decision support software (CDSS). Reclassification of interactions with a focus on clinical management aimed to support the development of CDSS with higher efficacy to reduce overalerting and improve medication safety in clinical practice.
Methods: We conducted a cross-sectional study in consecutive patients admitted to the neurology ward of a tertiary care hospital.
The recently discovered trace amine associated receptors (TAARs) represent attractive potential mediators of certain aspects of movement control. The TAAR that is best characterized, TAAR1, is particularly interesting because it can be activated by a variety of monoaminergic compounds including trace amines, amphetamines and dopamine metabolites. By using an experimental paradigm developed in our laboratory that involves a novel model of acute dopamine deficiency (DDD mice), and mice lacking TAAR1 (TAAR1 knockout mice), we explored the role of TAAR1 in movement control and actions of antiparkinsonian drugs.
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