Faculty Bibliography

Psychotherapy has undergone a widespread change recently, with many interventions now available as wireless device apps or online courses. The current study compared the efficacy of an online program with a personal group treatment intervention. The in-person group (n = 37) attended a 6-day workshop called Tapping Deep Intimacy that focused on the development of interpersonal skills. The online group (n = 37) consumed to the same information in the form of a 12-week online course. The content of both courses was drawn from the curriculum for Whole Energy Lifestyle, which trains participants in 12 evidence-based interpersonal and stress-reduction skills designed to reduce emotional triggering and promote health. These include mindfulness, breathwork, meditation (EcoMeditation), heart coherence, Clinical Emotional Freedom Techniques, active listening, and qigong. In both groups, depression, anxiety, and relationship satisfaction were assessed pre, post, and at 1-year follow-up. Anxiety reduced in the in-person but not the online group. Significant improvements in depression (p < 0.001) were found in both groups, although sharper symptom declines were found in the in-person group. A 29% improvement in relationship satisfaction was found in both groups (p < 0.003), and both maintained their gains over time. Anxiety and depression symptoms were much higher in the in-person group pretest despite similar demographic characteristics, suggesting differences in the population that uses online courses. These preliminary findings suggest that while online programs may play a role in the development of stress-reduction and interpersonal skills, it cannot be assumed that they mirror the therapeutic efficacy of in-person treatment in every dimension.

BACKGROUND:High prevalence rates of posttraumatic stress disorder (PTSD) in active military and veterans present a treatment challenge. Many PTSD studies have demonstrated the efficacy and safety of Emotional Freedom Techniques (EFT). OBJECTIVES:To develop clinical best practice guidelines for the use of EFT to treat PTSD, on the basis of the published literature, practitioner experience, and typical case histories. METHODS:We surveyed 448 EFT practitioners to gather information on their experiences with PTSD treatment. This included their demographic profiles, prior training, professional settings, use of assessments, and PTSD treatment practices. We used their responses, with the research evidence base, to formulate clinical guidelines applying the "stepped care" treatment model used by the United Kingdom's National Institute for Health and Clinical Excellence. RESULTS:Most practitioners (63%) reported that even complex PTSD can be remediated in 10 or fewer EFT sessions. Some 65% of practitioners found that more than 60% of PTSD clients are fully rehabilitated, and 89% stated that less than 10% of clients make little or no progress. Practitioners combined EFT with a wide variety of other approaches, especially cognitive therapy. Practitioner responses, evidence from the literature, and the results of a meta-analysis were aggregated into a proposed clinical guideline. CONCLUSION:We recommend a stepped care model, with 5 EFT therapy sessions for subclinical PTSD and 10 sessions for clinical PTSD, in addition to group therapy, online self-help resources, and social support. Clients who fail to respond should be referred for appropriate further care.

Prior research indicates elevated but subclinical posttraumatic stress disorder (PTSD) symptoms as a risk factor for a later diagnosis of PTSD. This study examined the progression of symptoms in 21 subclinical veterans. Participants were randomized into a treatment as usual (TAU) wait-list group and an experimental group, which received TAU plus six sessions of clinical emotional freedom techniques (EFT). Symptoms were assessed using the PCL-M (Posttraumatic Checklist-Military) on which a score of 35 or higher indicates increased risk for PTSD. The mean pretreatment score of participants was 39 ± 8.7, with no significant difference between groups. No change was found in the TAU group during the wait period. Afterward, the TAU group received an identical clinical EFT protocol. Posttreatment groups were combined for analysis. Scores declined to a mean of 25 (-64%, P < .0001). Participants maintained their gains, with mean three-month and six-month follow-up PCL-M scores of 27 (P < .0001). Similar reductions were noted in the depth and breadth of psychological conditions such as anxiety. A Cohen's d = 1.99 indicates a large treatment effect. Reductions in traumatic brain injury symptoms (P = .045) and insomnia (P = .004) were also noted. Symptom improvements were similar to those assessed in studies of PTSD-positive veterans. EFT may thus be protective against an increase in symptoms and a later PTSD diagnosis. As a simple and quickly learned self-help method, EFT may be a clinically useful element of a resiliency program for veterans and active-duty warriors.

Emotional Freedom Technique (EFT) combines elements of exposure and cognitive therapies with acupressure for the treatment of psychological distress. Randomized controlled trials retrieved by literature search were assessed for quality using the criteria developed by the American Psychological Association's Division 12 Task Force on Empirically Validated Treatments. As of December 2015, 14 studies (n = 658) met inclusion criteria. Results were analyzed using an inverse variance weighted meta-analysis. The pre-post effect size for the EFT treatment group was 1.23 (95% confidence interval, 0.82-1.64; p < 0.001), whereas the effect size for combined controls was 0.41 (95% confidence interval, 0.17-0.67; p = 0.001). Emotional freedom technique treatment demonstrated a significant decrease in anxiety scores, even when accounting for the effect size of control treatment. However, there were too few data available comparing EFT to standard-of-care treatments such as cognitive behavioral therapy, and further research is needed to establish the relative efficacy of EFT to established protocols.

Biofilms are colonies of bacteria or fungi that adhere to a surface, protected by an extracellular polymer matrix composed of polysaccharides and extracellular DNA. They are highly complex and dynamic multicellular structures that resist traditional means of killing planktonic bacteria. Recent developments in nanotechnology provide novel approaches to preventing and dispersing biofilm infections, which are a leading cause of morbidity and mortality. Medical device infections are responsible for approximately 60% of hospital acquired infections. In the United States, the estimated cost of caring for healthcare-associated infections is approximately between $28 billion and $45 billion per year. In this review, we will discuss our current understanding of biofilm formation and degradation, its relevance to challenges in clinical practice, and new technological developments in nanotechnology that are designed to address these challenges.

BACKGROUND: Little focus is on health care disparities in the elderly, a population largely covered by public insurance. We characterized insurance type and race in elderly trauma patients to determine if lack of insurance or minority status predict increased mortality. METHODS: The National Trauma Data Bank (version 7.0) was queried for all adult blunt trauma patients. We divided patients into two cohorts (15-64 or >/= 65 years) based on age for universal Medicare eligibility. Our primary outcome measure was in-hospital mortality. Multiple logistic regression was used to control for confounding variables. RESULTS: A total of 541,471 patients met inclusion criteria. Among younger patients, the most common insurance type was private (41.0%), with 26.9% uninsured. In contrast, the most common insurance type among older patients was Medicare (64.6%), with 6.0% uninsured. Within the younger cohort, private insurance (adjusted odds ratio [AOR], 0.6; p < 0.01) and other insurance (AOR, 0.8; p < 0.01) predicted reduced mortality, while Medicare predicted similar mortality (AOR, 1.1; p = 0.18) compared with no insurance. Black race (AOR, 1.4; p < 0.01) and Hispanic ethnicity (AOR, 1.4; p < 0.01) predicted higher mortality compared with white race. Within the older cohort, no insurance predicted similar mortality as Medicare (AOR, 1.0; p = 0.43), private insurance (AOR, 1.0; p = 0.51), and other insurance (AOR, 1.0; p = 0.71). Hispanic ethnicity predicted increased mortality (AOR, 1.4; p < 0.01), while Asian race was protective (AOR, 0.7; p = 0.01) compared with white race. CONCLUSION: Elderly trauma patients present primarily with Medicare, while younger trauma patients are mostly privately insured; elderly patients are four times more likely to be insured. Disparities caused by lack of insurance and minority race are reduced in elderly trauma patients. LEVEL OF EVIDENCE: Epidemiologic/prognostic study, level III.

Traumatic brain injury (TBI) is an enormous public health problem, with 1.7 million new cases of TBI recorded annually by the Centers for Disease Control. However, TBI has proven to be an extremely challenging condition to treat. Here, we apply a nanoprodrug strategy in a mouse model of TBI. The novel nanoprodrug contains a derivative of the nonsteroidal anti-inflammatory drug (NSAID) ibuprofen in an emulsion with the antioxidant α-tocopherol. The ibuprofen derivative, Ibu2TEG, contains a tetra ethylene glycol (TEG) spacer consisting of biodegradable ester bonds. The biodegradable ester bonds ensure that the prodrug molecules break down hydrolytically or enzymatically. The drug is labeled with the fluorescent reporter Cy5.5 using nonbiodegradable bonds to 1-octadecanethiol, allowing us to reliably track its accumulation in the brain after TBI. We delivered a moderate injury using a highly reproducible mouse model of closed-skull controlled cortical impact to the parietal region of the cortex, followed by an injection of the nanoprodrug at a dose of 0.2 mg per mouse. The blood brain barrier is known to exhibit increased permeability at the site of injury. We tested for accumulation of the fluorescent drug particles at the site of injury using confocal and bioluminescence imaging of whole brains and brain slices 36 hours after administration. We demonstrated that the drug does accumulate preferentially in the region of injured tissue, likely due to an enhanced permeability and retention (EPR) phenomenon. The use of a nanoprodrug approach to deliver therapeutics in TBI represents a promising potential therapeutic modality.

BACKGROUND: We undertook the current study to determine the impact of elevated admission systolic blood pressure (SBP) on trauma patients without severe brain injury. MATERIALS AND METHODS: We conducted a retrospective review of the Los Angeles County Trauma System database to identify all patients with moderate to severe injuries (injury severity score >9) admitted between 2003 and 2008. Patients with head abbreviated injury score >3 were excluded. We divided the remaining patients into three age cohorts and conducted multivariate regression modeling at increasing SBP thresholds to identify independent predictors of mortality. RESULTS: A total of 23,931 patients met inclusion criteria. Overall mortality was 8.6% and it increased with age across the three groups. The admission SBP thresholds associated with significantly increased mortality in the young and middle-aged were >190 mm Hg (AOR 1.5, P = 0.04) and >180 mm Hg (AOR 1.5, P = 0.01), respectively. In the elderly, no admission SBP threshold was associated with significantly increased mortality. Interestingly, several elevated admission SBP thresholds were associated with significantly reduced mortality in the elderly (>150 mm Hg AOR 0.6, P < 0.01; >160 mm Hg AOR 0.6, P < 0.01; and >170 mm Hg AOR 0.7, P = 0.02). CONCLUSIONS: The admission SBP thresholds that predicted higher mortality for the young and middle-aged were >190 mm Hg and >180 mm Hg, respectively. Elderly trauma patients tolerated higher admission SBP than their younger counterparts and multiple elevated SBP thresholds were associated with significantly reduced mortality in the elderly.

BACKGROUND: Increasing evidence suggests that the spleen harbors stem cells that act as precursors to insulin-producing pancreas cells. Additionally, small studies with short-term follow-up associate splenectomy with increased rates of diabetes mellitus. The purpose of this study was to analyze the long-term effect of trauma splenectomy on blood glucose. MATERIALS AND METHODS: Patients were included if a blood glucose level was measured more than 5 y after trauma splenectomy or laparotomy with bowel repair. Mean blood glucose level was then compared between the two groups. RESULTS: During the 10-y study period 61 patients underwent trauma splenectomy and 50 survived until discharge. In comparison, 229 patients underwent trauma laparotomy and bowel repair and 207 survived until discharge. Nine splenectomy patients compared with 12 control patients had, blood glucose measured at least 5 y after initial trauma. Mean follow-up period was not significantly different between groups (splenectomy 82.8 +/- 17.6 mo versus control 96.0 +/- 44.3 mo, P = 0.41). In the splenectomy cohort mean glucose level was significantly higher compared with the control (114 +/- 34 mg/dL versus 90 +/- 13 mg/dL, P = 0.04), as was the number of patients with recorded blood glucose level greater than 130 mg/dL (4 patient versus 0 patients P = 0.02). One new diagnosis of diabetes mellitus was noted only in the trauma splenectomy cohort. CONCLUSIONS: This small study suggests that trauma splenectomy may be associated with hyperglycemia at long-term follow-up.

BACKGROUND: The purpose of this study was to evaluate how beta-adrenergic receptor inhibition after traumatic brain injury (TBI) alters changes in early cerebral glucose metabolism and motor performance, as well as cerebral cytokine and heat shock protein (HSP) expression. METHODS: Mouse cerebral glucose metabolism was measured by microPET fluorodeoxyglucose uptake and converted into standardized uptake values (SUV). Four groups of C57/Bl6 mice (wild type [WT]) were initially evaluated: sham or TBI, followed by tail vein injection of either saline or a nonselective beta-adrenergic receptor inhibitor (propranolol, 4 mg/kg). Then motor performance, cerebral cytokine, and HSP70 expression were studied at 12 hours and 24 hours after sham injury or TBI in WT mice treated with saline or propranolol and in beta1-adrenergic/beta2-adrenergic receptor knockout (BARKO) mice treated with saline. RESULTS: Cerebral glucose metabolism was significantly reduced after TBI (mean SUV TBI, 1.63 vs. sham 1.97, p < 0.01) and propranolol attenuated this reduction (mean SUV propranolol, 1.89 vs. saline 1.63, p < 0.01). Both propranolol and BARKO reduced motor deficits at 24 hours after injury, but only BARKO had an effect at 12 hours after injury. TBI WT mice treated with saline performed worse than propranolol mice at 24 hours after injury on rotarod (23 vs. 44 seconds, p < 0.01) and rearing (130 vs. 338 events, p = 0.01) results. At 24 hours after injury, sham BARKO and TBI BARKO mice were similar on rotarod (21 vs. 19 seconds, p = 0.53), ambulatory testing (2,891 vs. 2,274 events, p = 0.14), and rearing (129 vs. 64 events, p = 0.09) results. Interleukin 1beta expression was affected by BARKO and propranolol after TBI; attenuation of interleukin 6 and increased HSP70 expression were noted only with BARKO. CONCLUSION: beta-adrenergic receptor inhibition affects cerebral glucose metabolism, motor performance, as well as cerebral cytokine and HSP expression after TBI.