The Current State of Physical Therapy Pain Curricula in the United States: A Faculty Survey

Insufficient pain education is problematic across the health care spectrum. Recent educational advancements have been made to combat the deficits in pain education to ensure that health care professionals are proficient in assessing and managing pain. The purpose of this survey was to determine the extent of pain education in current Doctorate of Physical Therapy schools in the United States, including how pain is incorporated into the curriculum, the amount of time spent teaching about pain, and the resources used to teach about pain. The survey consisted of 10 questions in the following subject areas: basic science mechanisms and concepts about pain, pain assessment, pain management, and adequacy of pain curriculum. The overall response was 77% (167/216) for the first series of responses of the survey (Question 1), whereas 62% completed the entire survey (Questions 2–10). The average contact hours teaching about pain was 31 ± 1.8 (mean ± standard error of the mean) with a range of 5 to 115 hours. The majority of schools that responded covered the science of pain, assessment, and management. Less than 50% of respondents were aware of the Institute of Medicine report on pain or the International Association for the Study of Pain guidelines for physical therapy pain education. Only 61% of respondents believed that their students received adequate education in pain management. Thus, this survey demonstrated how pain education is incorporated into physical therapy schools and highlighted areas for improvement such as awareness of recent educational advancements. Perspective This article demonstrates how pain education is incorporated into physical therapy curricula within accredited programs. Understanding the current structure of pain education in health professional curriculum can serve as a basis to determine if recent publications of guidelines and competencies impact education

Co-Localization of p-CREB and p-NR1 in Spinothalamic Neurons in a Chronic Muscle Pain Model

Activation of the cAMP pathway is an important mediator of chronic muscle pain. This study examined phosphorylation of the transcription factor cAMP-response-element-binding protein (p-CREB) and the NR1 subunit of the NMDA receptor (p-NR1) in the spinal cord. Bilateral mechanical hyperalgesia of the paw was induced by administering two injections of acidic saline, 5 days apart, into the gastrocnemius muscle of male Sprague–Dawley rats. The proportion of spinothalamic neurons that expressed p-NR1 or p-CREB did not change in the dorsal horn 24 h after the second intramuscular acid injection compared with animals that received pH 7.2 injections. This lack of change in spinothalamic neurons in the dorsal horn may be due to increases in individual spinothalamic neurons or increases in non-spinothalamic neurons. There was an increase in the proportion of spinothalamic neurons expressing p-NR1 in lamina X. These findings suggest that there are region-specific changes in spinothalamic neurons that express p-NR1 and lamina X may play an important role in the modulation of chronic muscle pain

Concentric zones of active RhoA and Cdc42 around single cell wounds

Rho GTPases control many cytoskeleton-dependent processes, but how they regulate spatially distinct features of cytoskeletal function within a single cell is poorly understood. Here, we studied active RhoA and Cdc42 in wounded Xenopus oocytes, which assemble and close a dynamic ring of actin filaments (F-actin) and myosin-2 around wound sites. RhoA and Cdc42 are rapidly activated around wound sites in a calcium-dependent manner and segregate into distinct, concentric zones around the wound, with active Cdc42 in the approximate middle of the F-actin array and active RhoA on the interior of the array. These zones form before F-actin accumulation, and then move in concert with the closing array. Microtubules and F-actin are required for normal zone organization and dynamics, as is crosstalk between RhoA and Cdc42. Each of the zones makes distinct contributions to the organization and function of the actomyosin wound array. We propose that similar rho activity zones control related processes such as cytokinesis

Contraction and polymerization cooperate to assemble and close actomyosin rings around Xenopus oocyte wounds

Xenopus oocytes assemble an array of F-actin and myosin 2 around plasma membrane wounds. We analyzed this process in living oocytes using confocal time-lapse (four-dimensional) microscopy. Closure of wounds requires assembly and contraction of a classic “contractile ring” composed of F-actin and myosin 2. However, this ring works in concert with a 5–10-μm wide “zone” of localized actin and myosin 2 assembly. The zone forms before the ring and can be uncoupled from the ring by inhibition of cortical flow and contractility. However, contractility and the contractile ring are required for the stability and forward movement of the zone, as revealed by changes in zone dynamics after disruption of contractility and flow, or experimentally induced breakage of the contractile ring. We conclude that wound-induced contractile arrays are provided with their characteristic flexibility, speed, and strength by the combined input of two distinct components: a highly dynamic zone in which myosin 2 and actin preferentially assemble, and a stable contractile actomyosin ring

Sex Differences in Arm Muscle Fatigability With Cognitive Demand in Older Adults

Background Muscle fatigability can increase when a stressful, cognitively demanding task is imposed during a low-force fatiguing contraction with the arm muscles, especially in women. Whether this occurs among older adults (\u3e 60 years) is currently unknown. Questions/purposes We aimed to determine if higher cognitive demands, stratified by sex, increased fatigability in older adults (\u3e 60 years). Secondarily, we assessed if varying cognitive demand resulted in decreased steadiness and was explained by anxiety or cortisol levels. Methods Seventeen older women (70 ± 6 years) and 13 older men (71 ± 5 years) performed a sustained, isometric, fatiguing contraction at 20% of maximal voluntary contraction until task failure during three sessions: high cognitive demand (high CD = mental subtraction by 13); low cognitive demand (low CD = mental subtraction by 1); and control (no subtraction). Results Fatigability was greater when high and low CD were performed during the fatiguing contraction for the women but not for the men. In women, time to failure with high CD was 16 ± 8 minutes and with low CD was 17 ± 4 minutes, both of which were shorter than time to failure in control contractions (21 ± 7 minutes; high CD mean difference: 5 minutes [95% confidence interval {CI}, 0.78–9.89], p = 0.02; low CD mean difference: 4 minutes [95% CI, 0.57–7.31], p = 0.03). However, in men, no differences were detected in time to failure with cognitive demand (control: 13 ± 5 minutes; high CD mean difference: −0.09 minutes [95% CI, −2.8 to 2.7], p = 1.00; low CD mean difference: 0.75 minutes [95% CI, −1.1 to 2.6], p = 0.85). Steadiness decreased (force fluctuations increased) more during high CD than control. Elevated anxiety, mean arterial pressure, and salivary cortisol levels in both men and women did not explain the greater fatigability during high CD. Conclusions Older women but not men showed marked increases in fatigability when low or high CD was imposed during sustained static contractions with the elbow flexor muscles and contrasts with previous findings for the lower limb. Steadiness decreased in both sexes when high CD was imposed. Clinical Relevance Older women are susceptible to greater fatigability of the upper limb with heightened mental activity during sustained postural contractions, which are the foundation of many work-related tasks

An Interprofessional Consensus of Core Competencies for Prelicensure Education in Pain Management: Curriculum Application for Physical Therapy

Core competencies in pain management for prelicensure health professional education were recently established. These competencies represent the expectation of minimal capabilities for graduating health care students for pain management and include 4 domains: multidimensional nature of pain, pain assessment and measurement, management of pain, and context of pain (Appendix 1). The purpose of this article is to advocate for and identify how core competencies for pain can be applied to the professional (entry-level) physical therapist curriculum. By ensuring that core competencies in pain management are embedded within the foundation of physical therapist education, physical therapists will have the core knowledge necessary for offering best care for patients, and the profession of physical therapy will continue to stand with all health professions engaged in comprehensive pain management

Bring the pain: wounding reveals a transition from cortical excitability to epithelial excitability in Xenopus embryos

The cell cortex plays many critical roles, including interpreting and responding to internal and external signals. One behavior which supports a cell’s ability to respond to both internal and externally-derived signaling is cortical excitability, wherein coupled positive and negative feedback loops generate waves of actin polymerization and depolymerization at the cortex. Cortical excitability is a highly conserved behavior, having been demonstrated in many cell types and organisms. One system well-suited to studying cortical excitability is Xenopus laevis, in which cortical excitability is easily monitored for many hours after fertilization. Indeed, recent investigations using X. laevis have furthered our understanding of the circuitry underlying cortical excitability and how it contributes to cytokinesis. Here, we describe the impact of wounding, which represents both a chemical and a physical signal, on cortical excitability. In early embryos (zygotes to early blastulae), we find that wounding results in a transient cessation (“freezing”) of wave propagation followed by transport of frozen waves toward the wound site. We also find that wounding near cell-cell junctions results in the formation of an F-actin (actin filament)-based structure that pulls the junction toward the wound; at least part of this structure is based on frozen waves. In later embryos (late blastulae to gastrulae), we find that cortical excitability diminishes and is progressively replaced by epithelial excitability, a process in which wounded cells communicate with other cells via wave-like increases of calcium and apical F-actin. While the F-actin waves closely follow the calcium waves in space and time, under some conditions the actin wave can be uncoupled from the calcium wave, suggesting that they may be independently regulated by a common upstream signal. We conclude that as cortical excitability disappears from the level of the individual cell within the embryo, it is replaced by excitability at the level of the embryonic epithelium itself