State Regulation of Community Paramedicine Programs: A National Analysis.

BACKGROUND: Community Paramedicine (CP) is a rapidly evolving field within prehospital care where paramedics step outside of their traditional roles of treating acute conditions to provide elements of primary and preventive care. It is unclear if current state oversight regarding the scope of practice (SOP) for paramedics provides clear guidance on the novel functions provided and skills performed by CP programs. OBJECTIVE: To determine the process and authority, as currently defined by state laws and regulations in the United States, to expand paramedic SOP in order to perform CP roles and to assess state EMS agencies' interpretation of paramedic SOP as it applies to CP. METHODS: We conducted a systematic review of laws, regulations, and policies from the 50 U.S. states in effect between February and June 2016 that define or apply to paramedic SOP. We determined whether each state's SOP included 21 potential skills applicable to CP within the following categories: assessment, treatment & intervention, referrals, and prevention & public health. Laws were also queried for mechanisms for expanding SOP, alternate destinations, and community paramedicine for each state. Additionally, we surveyed representatives from U.S. State Emergency Medical Services (EMS) agencies and asked which of these skills were a part of their current SOP. All data was coded into Excel™ and analyzed using descriptive statistics. RESULTS: All 50 U.S. states have laws relating to EMS. Forty-one states have a statewide SOP (82%), and 3 states have statewide protocols from which the SOP has been inferred for purposed of this study, but may not legally constitute SOP in this jurisdiction (6%). 20 states (40%) had a clearly defined mechanism for expanding SOP. Sixteen states (32%) had laws specific to CP. Seven states (14%) allowed for patients to be transported to alternate destinations. Of the 21 skills surveyed, on average there were 8.63 (6.41-10.85) fewer skills for paramedics found in state SOP laws and regulations than were reported as being a part of a state's paramedic SOP. All skills demonstrated variability between the legal review and survey results with 13.04-96.15% concordance. CONCLUSION: There is a lack of guidance and consistency regarding CP programs and scope of practice. Further studies are needed to understand best practices around regulation and oversight of CP.

Chronic stress enhanced fear memories are associated with increased amygdala zif268 mRNA expression and are resistant to reconsolidation.

The chronically stressed brain may present a vulnerability to develop maladaptive fear-related behaviors in response to a traumatic event. In rodents, chronic stress leads to amygdala hyperresponsivity and dendritic hypertrophy and produces a post traumatic stress disorder (PTSD)-like phenotype that includes exaggerated fear learning following Pavlovian fear conditioning and resistance to extinction. It is unknown whether chronic stress-induced enhanced fear memories are vulnerable to disruption via reconsolidation blockade, as a novel therapeutic approach for attenuating exaggerated fear memories. We used a chronic stress procedure in a rat model (wire mesh restraint for 6h/d/21d) to create a vulnerable brain that leads to a PTSD-like phenotype. We then examined freezing behavior during acquisition, reactivation and after post-reactivation rapamycin administration (i.p., 40mg/kg) in a Pavlovian fear conditioning paradigm to determine its effects on reconsolidation as well as the subsequent functional activation of limbic structures using zif268 mRNA. Chronic stress increased amygdala zif268 mRNA during fear memory retrieval at reactivation. Moreover, these enhanced fear memories were unaffected by post reactivation rapamycin to disrupt long-term fear memory. Also, post-reactivation long term memory processing was also associated with increased amygdala (LA and BA), and decreased hippocampal CA1 zif268 mRNA expression. These results suggest potential challenges for reconsolidation blockade as an effective approach in treating exaggerated fear memories, as in PTSD. Our findings also support chronic stress manipulations combined with fear conditioning as a useful preclinical approach to study a PTSD-like phenotype.

Discordance in Perceptions of Barriers to Breast Cancer Treatment Between Hispanic Women and Their Providers.

Despite comparable screening and incidence rates that are 26% below that of non-Hispanic Whites, Hispanic women present with breast cancer at more advanced stages of disease, representing a continuing and troubling health disparity for this population. Reducing these disparities warrant more innovative research approaches to better understand perspectives of Hispanic patients regarding barriers to treatment and how these perspectives compare to those of their providers. A pilot qualitative study was conducted at a major urban cancer center in Arizona that measured both patient and provider perspectives regarding barriers to treatment. Through a multimethod qualitative analysis, researchers surveyed patients and providers to identify perceived barriers and discordance in shared understanding. Data collection and analysis consisted of surveying patients and providers, then performing inductive qualitative analysis. Results indicated the highest concordance, or shared understanding, between patients and providers was in recognizing barriers within delivery of care, such as cost of care and insurance coverage. The greatest discordance, or gaps in shared understanding, existed in upstream barriers of the health care system, such as emotional support and trust in systems. These results underscore the gap in shared understanding between patients and providers regarding upstream barriers to care as well as the nonclinical social determinants of health Hispanic patients face in accessing breast cancer treatment. More research is warranted using this approach as a tool to reduce health disparities.

BDNF and TrkB Mediate the Improvement from Chronic Stress-induced Spatial Memory Deficits and CA3 Dendritic Retraction.

The brain is capable of improving from a chronically stressed state. The hippocampus in particular appears to "recover" from chronic stress-induced morphological and functional deficits following a post-stress rest period of several weeks. We previously found that hippocampal brain-derived neurotrophic factor (BDNF) was necessary for spatial ability to improve following a post-stress rest period. The following studies are the first to investigate the involvement of BDNF and its TrkB receptor on the recovery process following the end of chronic stress, as it pertains to hippocampal dendritic retraction and spatial memory deficits. In the first study, hippocampal BDNF was downregulated via RNA interference and then hippocampal CA3 and CA1 dendritic complexity were evaluated following chronic stress and a post-stress rest period in male Sprague-Dawley rats. Downregulating hippocampal BDNF prevented the enhancement of CA3 apical dendritic complexity following the rest period. Moreover, chronic stress and downregulated BDNF in the post-stress rest group led to regionally specific enhancements in CA1 dendritic complexity. In the second study, we tested whether the TrkB receptor was involved by administering daily systemic injections of ANA-12, a TrkB receptor antagonist, during the three-week post-stress rest period. ANA-12 prevented the improvement in spatial ability and CA3 apical dendritic complexity following the post-stress rest period. These data demonstrate that hippocampal BDNF acting via its TrkB receptor is necessary during the post-stress rest period in order to improve the impaired hippocampal structural and cognitive outcomes that occur in response to chronic stress.

Early and Persistent Dendritic Hypertrophy in the Basolateral Amygdala following Experimental Diffuse Traumatic Brain Injury.

In the pathophysiology of traumatic brain injury (TBI), the amygdala remains understudied, despite involvement in processing emotional and stressful stimuli associated with anxiety disorders, such as post-traumatic stress disorder (PTSD). Because the basolateral amygdala (BLA) integrates inputs from sensory and other limbic structures coordinating emotional learning and memory, injury-induced changes in circuitry may contribute to psychiatric sequelae of TBI. This study quantified temporal changes in dendritic complexity of BLA neurons after experimental diffuse TBI, modeled by midline fluid percussion injury. At post-injury days (PIDs) 1, 7, and 28, brain tissue from sham and brain-injured adult, male rats was processed for Golgi, glial fibrillary acidic protein (GFAP), or silver stain and analyzed to quantify BLA dendritic branch intersections, activated astrocytes, and regional neuropathology, respectively. Compared to sham, brain-injured rats at all PIDs showed enhanced dendritic branch intersections in both pyramidal and stellate BLA neuronal types, as evidenced by Sholl analysis. GFAP staining in the BLA was significantly increased at PID1 and 7 in comparison to sham. However, the BLA was relatively spared from neuropathology, demonstrated by an absence of argyrophilic accumulation over time, in contrast to other brain regions. These data suggest an early and persistent enhancement of dendritic complexity within the BLA after a single diffuse TBI. Increased dendritic complexity would alter information processing into and through the amygdala, contributing to emotional symptoms post-TBI, including PTSD.