Factors Associated With Residents' Responsive Behaviors Toward Staff in Long-Term Care Homes: A Systematic Review.

BACKGROUND AND OBJECTIVES: When staff experience responsive behaviors from residents, this can lead to decreased quality of work life and lower quality of care in long-term care homes. We synthesized research on factors associated with resident responsive behaviors directed toward care staff and characteristics of interventions to reduce the behaviors. RESEARCH DESIGN AND METHODS: We conducted a mixed-methods systematic review with quantitative and qualitative research. We searched 12 bibliographic databases and "gray" literature, using 2 keywords (long-term care, responsive behaviors) and their synonyms. Pairs of reviewers independently completed screening, data extraction, and risk of bias assessment. We developed a coding scheme using the ecological model as an organizing structure and prepared narrative summaries for each factor. RESULTS: From 86 included studies (57 quantitative, 28 qualitative, 1 mixed methods), multiple factors emerged, such as staff training background (individual level), staff approaches to care (interpersonal level), leadership and staffing resources (institutional level), and racism and patriarchy (societal level). Quantitative and qualitative results each provided key insights, such as qualitative results pertaining to leadership responses to reports of behaviors, and quantitative findings on the impact of staff approaches to care on behaviors. Effects of interventions (n = 14) to reduce the behaviors were inconclusive. DISCUSSION AND IMPLICATIONS: We identified the need for an enhanced understanding of the interrelationships among factors associated with resident responsive behaviors toward staff and processes leading to the behaviors. To address these gaps and to inform theory-based effective interventions for preventing or mitigating responsive behaviors, we suggest intervention studies with systematic process evaluations.

Sex differences in the inflammatory response of the mouse DRG and its connection to pain in experimental autoimmune encephalomyelitis.

Multiple Sclerosis (MS) is an autoimmune disease with notable sex differences. Women are not only more likely to develop MS but are also more likely than men to experience neuropathic pain in the disease. It has been postulated that neuropathic pain in MS can originate in the peripheral nervous system at the level of the dorsal root ganglia (DRG), which houses primary pain sensing neurons (nociceptors). These nociceptors become hyperexcitable in response to inflammation, leading to peripheral sensitization and eventually central sensitization, which maintains pain long-term. The mouse model experimental autoimmune encephalomyelitis (EAE) is a good model for human MS as it replicates classic MS symptoms including pain. Using EAE mice as well as naïve primary mouse DRG neurons cultured in vitro, we sought to characterize sex differences, specifically in peripheral sensory neurons. We found sex differences in the inflammatory profile of the EAE DRG, and in the TNFα downstream signaling pathways activated intracellularly in cultured nociceptors. We also found increased cell death with TNFα treatment. Given that TNFα signaling has been shown to initiate intrinsic apoptosis through mitochondrial disruption, this led us to investigate sex differences in the mitochondria's response to TNFα. Our results demonstrate that male sensory neurons are more sensitive to mitochondrial stress, making them prone to neuronal injury. In contrast, female sensory neurons appear to be more resistant to mitochondrial stress and exhibit an inflammatory and regenerative phenotype that may underlie greater nociceptor hyperexcitability and pain. Understanding these sex differences at the level of the primary sensory neuron is an important first step in our eventual goal of developing sex-specific treatments to halt pain development in the periphery before central sensitization is established.