Impact of Educational Format on Learner Commitment to Change and Satisfaction.

INTRODUCTION: The value proposition of CME lies in its ability to elicit change in learners so new knowledge and skills are used to improve patient outcomes. In this study, we test the hypothesis that, in contrast to passive learning, education with an active engagement component has a greater impact on the motivation of learners to make changes in their practice. METHODS: We analyzed nine educational formats produced by the American Academy of Family Physicians. CME program between 2015 and 2017. Postactivity learner evaluations were used to measure both satisfaction and "commitment to change"-the percentage of learners who committed in making a change in their practice as a result of their participation. RESULTS: We found education that was interactive and leveraged elements of social learning theory produced the greatest commitment to change the score. Lower scores were obtained for more passive education formats. By contrast, satisfaction scores were not significantly different between formats. DISCUSSION: Our data demonstrate differences between commitment to change and educational format that could inform how format types might be better used to promote a behavior change. We also demonstrate that learner satisfaction has little or no value as a measure of educational efficacy.

Effect of a performance improvement CME activity on management of patients with diabetes.

INTRODUCTION: Primary care in the United States faces unprecedented challenges from an aging population and the accompanying prevalence of chronic disease. In response, continuing medical education (CME) initiatives have begun to adopt the principles of performance improvement (PI) into their design, although currently there is a dearth of evidence from national initiatives supporting the effectiveness of this methodology. The specific aim of this study was to demonstrate the value of a national PI-CME activity to improve the performance of physicians treating patients with diabetes. METHODS: We analyzed data from the American Academy of Family Physicians' METRIC® PI-CME activity in a cohort of family physician learners. The study utilized the 3-stage design standard approved for PI-CME. Baseline and follow-up performance data across a range of clinical and systems-based measures were compared in aggregate. RESULTS: Data were assessed for 509 learners who completed the activity. Statistically significant changes occurred both for self-assessment of a range of practice aspects and for diabetes care measures. Learners recognized that the organization of their practices had improved, and mechanisms were in place for better staff feedback, as well as aspects of patient self-management. Based on the clinical data obtained from 11 538 patient charts, 6 out of 8 diabetes measures were significantly improved. DISCUSSION: The activity appears to have had a positive, measurable impact on the medical practice of learners and suggests that, when appropriately designed and executed, PI-CME on a national scale can be a useful vehicle to influence performance change in physicians and to inform future CME activities.

Results of a survey assessing provider beliefs of adherence barriers to antiplatelet medications.

The guidelines published by the American College of Cardiology Foundation/American Heart Association provide an evidence-based rationale and continuum of care for patients with unstable angina/non-ST-segment elevation acute coronary syndromes (UA/NSTE-ACS) from acute through to chronic management. Antiplatelet therapy forms an integral part of the care regimen, and a wealth of evidence supports appropriate dual or triple antiplatelet therapy in significantly reducing the frequency of potentially fatal secondary ischemic events. However, as is often the case with long-term therapies, adherence issues become apparent that limit this potential. In this article, we report on the results of a national survey of health care providers involved in the care of UA/NSTE-ACS patients on chronic (posthospital discharge) antiplatelet therapy. Our data reveal that the participants believe costs, lack of patient understanding of their condition or medication, and perception of the value of their therapy are important patient factors that promote nonadherence. Participants indicated that nonadherence occurs more frequently among minority and elderly patients, and less frequently when a caregiver is involved. We also show that deficits of knowledge, competence, and confidence exist in providers who treat patients with UA/NSTE-ACS. These deficits were generally greater in primary/family care providers compared with internal medicine and cardiologists, and for nurse practitioners/physician assistants compared with physicians (MDs/DOs). In addition, providers of all types frequently did not use adherence-improving tools or resources with their staff or patients. Our data suggest that because of its potential impact on patient outcomes, there is a pressing need to improve provider antiplatelet therapy adherence management in UA/NSTE-ACS.

Pain-related synaptic plasticity in spinal dorsal horn neurons: role of CGRP.

BACKGROUND: The synaptic and cellular mechanisms of pain-related central sensitization in the spinal cord are not fully understood yet. Calcitonin gene-related peptide (CGRP) has been identified as an important molecule in spinal nociceptive processing and ensuing behavioral responses, but its contribution to synaptic plasticity, cellular mechanisms and site of action in the spinal cord remain to be determined. Here we address the role of CGRP in synaptic plasticity in the spinal dorsal horn in a model of arthritic pain. RESULTS: Whole-cell current- and voltage-clamp recordings were made from substantia gelatinosa (SG) neurons in spinal cord slices from control rats and arthritic rats (> 6 h postinjection of kaolin/carrageenan into the knee). Monosynaptic excitatory postsynaptic currents (EPSCs) were evoked by electrical stimulation of afferents in the dorsal root near the dorsal root entry zone. Neurons in slices from arthritic rats showed increased synaptic transmission and excitability compared to controls. A selective CGRP1 receptor antagonist (CGRP8-37) reversed synaptic plasticity in neurons from arthritic rats but had no significant effect on normal transmission. CGRP facilitated synaptic transmission in the arthritis pain model more strongly than under normal conditions where both facilitatory and inhibitory effects were observed. CGRP also increased neuronal excitability. Miniature EPSC analysis suggested a post- rather than pre-synaptic mechanism of CGRP action. CONCLUSION: This study is the first to show synaptic plasticity in the spinal dorsal horn in a model of arthritic pain that involves a postsynaptic action of CGRP on SG neurons.

Enhanced group II mGluR-mediated inhibition of pain-related synaptic plasticity in the amygdala.

BACKGROUND: The latero-capsular part of the central nucleus of the amygdala (CeLC) is the target of the spino-parabrachio-amygdaloid pain pathway. Our previous studies showed that CeLC neurons develop synaptic plasticity and increased neuronal excitability in the kaolin/carrageenan model of arthritic pain. These pain-related changes involve presynaptic group I metabotropic glutamate receptors (mGluRs) and postsynaptic NMDA and calcitonin gene-related peptide (CGRP1) receptors. Here we address the role of group II mGluRs. RESULTS: Whole-cell current- and voltage-clamp recordings were made from CeLC neurons in brain slices from control rats and arthritic rats (>6 h postinjection of kaolin/carrageenan into the knee). Monosynaptic excitatory postsynaptic currents (EPSCs) were evoked by electrical stimulation of afferents from the pontine parabrachial (PB) area. A selective group II mGluR agonist (LY354740) decreased the amplitude of EPSCs more potently in CeLC neurons from arthritic rats (IC50 = 0.59 nM) than in control animals (IC50 = 15.0 nM). The inhibitory effect of LY354740 was reversed by a group II mGluR antagonist (EGLU) but not a GABAA receptor antagonist (bicuculline). LY354740 decreased frequency, but not amplitude, of miniature EPSCs in the presence of TTX. No significant changes of neuronal excitability measures (membrane slope conductance and action potential firing rate) were detected. CONCLUSION: Our data suggest that group II mGluRs act presynaptically to modulate synaptic plasticity in the amygdala in a model of arthritic pain.

Protein kinase A-dependent enhanced NMDA receptor function in pain-related synaptic plasticity in rat amygdala neurones.

Mechanisms of pain-related plasticity in the amygdala, a key player in emotionality, were studied at the cellular and molecular levels in a model of arthritic pain. The influence of the arthritis pain state induced in vivo on synaptic transmission and N-methyl-d-aspartate (NMDA) receptor function was examined in vitro using whole-cell voltage-clamp recordings of neurones in the latero-capsular part of the central nucleus of the amygdala (CeA), which is now defined as the 'nociceptive amygdala'. Synaptic transmission was evoked by electrical stimulation of afferents from the pontine parabrachial area (part of the spino-parabrachio-amygdaloid pain pathway) in brain slices from control rats and from arthritic rats. This study shows that pain-related synaptic plasticity is accompanied by protein kinase A (PKA)-mediated enhanced NMDA-receptor function and increased phosphorylation of NMDA-receptor 1 (NR1) subunits. Synaptic plasticity in the arthritis pain model, but not normal synaptic transmission in control neurones, was inhibited by a selective NMDA receptor antagonist. Accordingly, an NMDA receptor-mediated synaptic component was recorded in neurones from arthritic animals, but not in control neurones, and was blocked by inhibition of PKA but not protein kinase C (PKC). Exogenous NMDA evoked a larger inward current in neurones from arthritic animals than in control neurones, indicating a postsynaptic effect. Paired-pulse facilitation, a measure of presynaptic mechanisms, was not affected by an NMDA-receptor antagonist. Increased levels of phosphorylated NR1 protein, but not of total NR1, were measured in the CeA of arthritic rats compared to controls. Our results suggest that pain-related synaptic plasticity in the amygdala involves a critical switch of postsynaptic NMDA receptor function through PKA-dependent NR1 phosphorylation.

Computerized analysis of audible and ultrasonic vocalizations of rats as a standardized measure of pain-related behavior.

The behavioral assessment of experimental pain is essential for the analysis of pain mechanisms and the validation of therapeutic targets. Arthritic pain, in particular, is significantly associated with negative affective states and disorders. Here we present a standardized method for the quantitative analysis of audible and ultrasonic (25 +/- 4 kHz) vocalizations in awake rats as a measure of higher integrated behavior in a model of arthritic pain. A bat detector and a condenser microphone were used to record ultrasonic and audible vocalizations, respectively, in response to innocuous and noxious mechanical stimulation of the knee before and after induction of acute arthritis in one knee. A computerized system was used to analyze number and duration of the filtered signals. For the behavioral tests, the animal was placed in a customized recording chamber to ensure consistent stimulus application and stable recordings and to eliminate any movement-induced noise. Noxious stimuli produced stronger vocalizations than innocuous stimuli. Both audible and ultrasonic vocalizations to innocuous (allodynia) and noxious (hyperalgesia) stimuli increased after the induction of acute arthritis. These changes were accompanied by increased knee joint circumference, lowered hind limb withdrawal thresholds and reduced exploratory behavior in the same animals. The computerized analysis of audible and ultrasonic vocalizations is a valid, quantitative, reliable and convenient method to measure pain-related behavior.

The amygdala and persistent pain.

A reciprocal relationship exists between persistent pain and negative affective states such as fear, anxiety, and depression. Accumulating evidence points to the amygdala as an important site of such interaction. Whereas a key role of the amygdala in the neuronal mechanisms of emotionality and affective disorders has been well established, the concept of the amygdala as an important contributor to pain and its emotional component is still emerging. This article will review and discuss evidence from anatomical, neuroimaging, behavioral, electrophysiological, pharmacological, and biochemical data that implicate the amygdala in pain modulation and emotional responses to pain. The latero-capsular division of the central nucleus of the amygdala is now defined as the "nociceptive amygdala" and integrates nociceptive information with poly-modal information about the internal and external bodily environment. Dependent on environmental conditions and affective states, the amygdala appears to play a dual facilitatory and inhibitory role in the modulation of pain behavior and nociceptive processing at different levels of the pain neuraxis. Only recently, electrophysiological, pharmacological, and biochemical neuroplastic changes were shown in the nociceptive amygdala in persistent pain. It is conceivable, however, that amygdala plasticity plays an important role in emotional pain behavior and its modulation by affective state.

Enhanced group III mGluR-mediated inhibition of pain-related synaptic plasticity in the amygdala.

Pain has a strong emotional component. A key player in emotionality, the amygdala is also involved in pain processing. Our previous studies showed synaptic plasticity in the central nucleus of the amygdala (CeA) in a model of arthritic pain. Here, we address the role of group III metabotropic glutamate receptors (mGluRs) in the regulation of synaptic transmission in CeA neurons. Whole-cell current- and voltage-clamp recordings were made from neurons in the latero-capsular part of the CeA in brain slices from control rats and arthritic rats (>6 h postinduction). The latero-capsular part of the CeA is the target of the spino-parabrachio-amygdaloid pain pathway and is now designated as the "nociceptive amygdala". Monosynaptic excitatory postsynaptic currents (EPSCs) were evoked by electrical stimulation of afferents from the pontine parabrachial (PB) area. LAP4 decreased the amplitude of EPSCs more potently in CeA neurons from arthritic rats (EC(50)=1.2 nM) than in control animals (EC(50)=11.5 nM). The inhibitory effect of LAP4 was reversed by a selective group III mGluR antagonist (UBP1112). During the application of LAP4, paired-pulse facilitation was increased, while no significant changes in slope conductance and action potential firing rate of CeA neurons were observed. These data suggest that presynaptic group III mGluRs are involved in the regulation of synaptic plasticity in the amygdala in an arthritis pain model.

Synaptic plasticity in the amygdala in a model of arthritic pain: differential roles of metabotropic glutamate receptors 1 and 5.

Pain has a strong emotional-affective dimension, and the amygdala plays a key role in emotionality. Mechanisms of pain-related changes in the amygdala were studied at the cellular and molecular levels in a model of arthritis pain. The influence of the arthritic condition induced in vivo on synaptic transmission and group I metabotropic glutamate receptor (mGluR1 and mGluR5) function was examined in vitro using whole-cell voltage-clamp recordings of neurons in the central nucleus of the amygdala (CeA). G-protein-coupled mGluRs are implicated in various forms of neuroplasticity as well as in neurological and psychiatric disorders. Synaptic transmission was evoked by electrical stimulation of afferents from the basolateral amygdala (BLA) and the pontine parabrachial (PB) area in brain slices from control (untreated or saline-injected) rats and from arthritic rats. This study shows enhanced synaptic transmission of nociceptive-specific inputs (PB-->CeA synapse) and polymodal sensory inputs (BLA-->CeA synapse) in the arthritis model. CeA neurons from arthritic rats also developed increased excitability compared with control CeA neurons. Synaptic plasticity in the CeA was accompanied by increased presynaptic mGluR1 function and upregulation of mGluR1 and mGluR5. A selective mGluR1 antagonist reduced transmission in CeA neurons from arthritic animals but not in control neurons, and increased levels of mGluR1 and mGluR5 protein were measured in the CeA of arthritic rats compared with controls. Our results show that plastic changes in the amygdala in an arthritis model that produces prolonged pain involve a critical switch of presynaptic mGluR1 expression and function.