Background: Agitation and aggression are common in patients with Alzheimer’s disease and related dementias and pose a significant burden on patients, caregivers, and the healthcare systems. Guidelines recommend personalized behavioral interventions as the first-line treatment; however, these interventions are often underutilized. The Standardizing Care for Neuropsychiatric Symptoms and Quality of Life in Dementia (StaN) study (ClinicalTrials.gov Identifier # NCT0367220) is a multisite randomized controlled trial comparing an Integrated Care Pathway, that includes a sequential pharmacological algorithm and structured behavioral interventions, with treatment-as-usual to treat agitation in dementia in long-term care and inpatient settings. Objective: To describe the rationale and design of structured behavioral interventions in the StaN study. Methods: Structured behavioral interventions are designed and implemented based on the following considerations: 1) personalization, 2) evidence base, 3) dose and duration, 4) measurement-based care, and 5) environmental factors and feasibility. Results: The process to design behavioral interventions for each individual starts with a comprehensive assessment, followed by personalized, evidence-based interventions delivered in a standardized manner with ongoing monitoring of global clinical status. Measurement-based care is used to tailor the interventions and to integrate them with pharmacotherapy. Conclusion: Individualized behavioral interventions in patients with dementia may be challenging to design and implement. Here we describe a process to design and implement individualized and structured behavioral interventions in the context of a multisite trial in long-term care and inpatient settings. This process can inform the design of behavioral interventions in future trials and in clinical settings for the treatment of agitation in dementia.
Two studies report statistically significant differences in dermatoglyphic patterns between individuals with childhood psychosis and randomly selected controls. Such differences could constitute fairly strong evidence that some factors, genetic or environmental, disrupted the development of these children in utero. In an attempt to confirm these reports, we studied a group of psychotic children using their parents and normal siblings as controls. Our results indicate no differences between the affected children and their relatives. Our ability to detect subtle differences was precluded by the small sample available for analysis.
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