Articles: function.
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People with chronic pain are frequently exposed to stigma, which is typically distressing and may lead to internal stigmatizing thoughts. The thought content associated with stigma has similarities to pain catastrophizing, although these concepts differ in that stigma is arguably more social in origin. Stigma can be measured by the Stigma Scale for Chronic Illness - 8-item version (SSCI-8). In this study, we first demonstrate the validity of this measure in Swedish. We then examine the role of stigma in the health and functioning of people with chronic pain, particularly beyond the role played by pain catastrophizing. ⋯ This study points to the importance of a social perspective on pain-related outcomes. We may need to more fully appreciate the way that people with chronic pain are treated by both health care providers and others can have an impact on their well-being. Potential negative impacts of stigmatizing responses to people with chronic pain are highlighted by the current results.
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Current guidelines recommend initial monotherapy for pulmonary arterial hypertension (PAH) with cardiopulmonary comorbidities, despite limited available evidence to guide management. ⋯ In a real-world cohort, patients with PAH with LHD risk factors were less likely to be exposed to initial combination therapy. Nevertheless, selected patients with PAH with LHD risk factors who were treated with initial combination therapy derived similar functional response compared with the reference group. Further studies are needed to phenotype patients with PAH with cardiopulmonary comorbidities who may benefit from initial combination therapy.
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In 2010, the Office of the US Army Surgeon General recommended the Veterans Administration (VA) assess pain using the Defense and Veterans Pain Rating Scale (DVPRS). One item in the DVPRS is for measuring pain intensity. This item contains a combination of five response metrics: categories, faces, colors, numbers, and functional descriptors. A few studies have supported patients' and health care providers' preferences for the DVPRS and its psychometric properties. However, they also left uncertainties about its usability and validity. ⋯ Results from this study inform the nursing community about the DVPRS' pain intensity item, which combines multiple response metrics. The results support the need for nursing units to generate and standardize procedures for using the item to measure multi-site pain and for interpreting and documenting patients' non-numeric responses. The effects of such procedures on the measure's usability and psychometric properties warrants additional investigation.
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Volatile anesthetics induce hyperpolarizing potassium currents in spinal cord neurons that may contribute to their mechanism of action. They are induced at lower concentrations of isoflurane in noncholinergic neurons from mice carrying a loss-of-function mutation of the Ndufs4 gene, required for mitochondrial complex I function. The yeast NADH dehydrogenase enzyme, NDi1, can restore mitochondrial function in the absence of normal complex I activity, and gain-of-function Ndi1 transgenic mice are resistant to volatile anesthetics. The authors tested whether NDi1 would reduce the hyperpolarization caused by isoflurane in neurons from Ndufs4 and wild-type mice. Since volatile anesthetic behavioral hypersensitivity in Ndufs4 is transduced uniquely by glutamatergic neurons, it was also tested whether these currents were also unique to glutamatergic neurons in the Ndufs4 spinal cord. ⋯ Bypassing complex I by overexpression of NDi1 eliminates increases in potassium currents induced by isoflurane in the spinal cord. The isoflurane-induced potassium currents in glutamatergic neurons represent a potential downstream mechanism of complex I inhibition in determining minimum alveolar concentration.
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The voltage-gated sodium channel Na V 1.7 is an essential component of human pain signaling. Changes in Na V 1.7 trafficking are considered critical in the development of neuropathic pain. SUMOylation of collapsin response mediator protein 2 (CRMP2) regulates the membrane trafficking and function of Na V 1.7. ⋯ Moreover, enhancing SENP1 expression did not affect the activity of TRPV1 channels or voltage-gated calcium and potassium channels. Intrathecal injection of CRISPRa SENP1 lentivirus reversed mechanical allodynia in male and female rats with spinal nerve injury. These results provide evidence that the pain-regulating effects of SENP1 overexpression involve, in part, the modulation of Na V 1.7 channels through the indirect mechanism of CRMP2 deSUMOylation.