Clinical Study The Interactive Relationship between Pain, Psychosis, and Agitation in People with Dementia: Results from a Cluster-Randomised Clinical Trial Torstein F. Habiger, 1 Elisabeth Flo, 1 Wilco P. Achterberg, 2 and Bettina S. Husebo 1,3 1 Department of Global Public Health and Primary Care, Centre for Elderly and Nursing Home Medicine, University of Bergen, 5018 Bergen, Norway 2 Department of Public Health and Primary Care, Leiden University Medical Center, 2300 RC Leiden, Netherlands 3 Municipality of Bergen, 5020 Bergen, Norway Correspondence should be addressed to Torstein F. Habiger; torstein.habiger@igs.uib.no Received 8 January 2016; Accepted 29 March 2016 Academic Editor: Marina De Tommaso Copyright © 2016 Torstein F. Habiger et al. Tis is an open access article distributed under the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited. Background. Neuropsychiatric symptoms are common in people with dementia, and pain is thought to be an important underlying factor. Pain has previously been associated with agitation, and pain treatment has been shown to ameliorate agitated behaviour. So far, the association between pain and psychosis and the efect of pain treatment on psychotic symptoms is unclear. Furthermore, the impact of opioid treatment on psychosis is not established. Aim. To investigate the efcacy of a stepwise protocol for treating pain (SPTP) on psychosis and agitation measured with the Neuropsychiatric Inventory, Nursing Home version, and to explore the impact of opioid analgesics on psychosis. Method. Secondary analyses are from a cluster-randomised controlled trial including 352 patients with advanced dementia and agitation from 18 nursing homes in Western Norway. Te intervention group received pain treatment according to SPTP. Results. Pain was associated with disinhibition (adjusted OR: 1.21, 95% CI: 1.10–1.34) and irritability (adjusted OR: 1.10, 95% CI: 1.01–1.21) at baseline. Pain treatment reduced agitation (p < 0.001, df = 1; 300) and aberrant motor behaviour (p = 0.017, df = 1; 300). Psychosis was reduced in people with at least one symptom at baseline (p = 0.034, df = 1; 135). Te use of opioid analgesics did not increase psychotic symptoms. Study Registration. Tis trial is registered with ClinicalTrials.gov (NCT01021696), Norwegian Medicines Agency, EudraCT (EudraCTnr: 2008-007490-20). 1. Introduction Neuropsychiatric symptoms (NPS) are a feature in many neurodegenerative diseases, among other dementia, where over 90% of patients sufer from at least one NPS during the course of their disease [1]. NPS can be distressing for both patients and family alike and is ofen the main reason for admission to a nursing home (NH) [2]. NPS can be clustered in diferent ways. Tese clusters are most commonly defned by symptoms that present concurrently, like mood symptoms such as depression and anxiety, agitation symptoms such as aggression and irritability, and psychosis symptoms such as delusion and hallucination [3–6]. Te aetiology of NPS is largely unknown, but factors like neuropathological changes in the brain, unmet psychosocial needs, and pain are thought to play a role [7]. Despite the multiple potential underlying factors, NPS are ofen treated with antipsychotic drugs with potential harmful side efects [8]. Tis highlights the importance of investigating the relationship between NPS and possible underlying treatable causes, such as pain, to avoid unnecessary antipsychotic drug use [9–11]. People in the later stages of dementia ofen reside in NHs and frequently experience pain, with 30–60% sufering daily from pain [12–14]. Te cognitive decline with a subsequent loss of communicative abilities puts people with dementia at an increased risk of sufering from untreated pain [15, 16]. Research demonstrates that pain in people with dementia can act as a trigger for NPS such as agitation and mood symptoms [17, 18]. However, the relationship between pain Hindawi Publishing Corporation Behavioural Neurology Volume 2016, Article ID 7036415, 8 pages http://dx.doi.org/10.1155/2016/7036415