I am a
Home I AM A Search Login

Accepted

Share this

Cognitive profile and mild cognitive impairment in people with chronic lower back pain.

A growing body of evidence suggests Chronic Lower Back Pain (CLBP) is associated with cognitive dysfunction. Little is known, however, about the extent of cognitive impairment in CLBP. The present study explored the cognitive profile of people with CLBP and sought to determine the extent of Mild Cognitive Impairment (MCI) according to the DSM-V and the Movement Disorders Society criteria for MCI. Thirty-one participants with CLBP and 27 age and gender matched healthy controls completed a full neuropsychological battery, consisting of two tasks for each of the five cognitive domains (Executive Function, Attention/Working Memory, Memory, Language, and Visuospatial). Participants with CLBP performed worse, compared to controls, on measures of Attention/Working Memory, Memory, Language, and Visuospatial performance. Cognitive performance in CLBP was also compared to equivalent normative data to determine cognitive impairment. Sixteen CLBP participants were impaired on at least one cognitive measure, with 5 participants meeting criteria for MCI. MCI was not associated with pain-related experience, or psychological health. The present study supports and extends previous findings that CLBP is associated with cognitive dysfunction and some people with CLBP meet criteria for MCI. These findings support that rehabilitation in people with CLBP requires a multidisciplinary approach.

Learn More >

Low Back Pain in Adolescent and Geriatric Populations.

Spinal pain is the most common form of musculoskeletal pain. Chronic low back pain may contain nociceptive, neuropathic, and central components. Children are at risk of developing spinal pain. An increasing proportion of children develop low back pain as they become adolescents. In most adolescents, no specific diagnosis is identified. Psychological factors play a role in adolescents with back pain. Lumbar spinal stenosis causes neurogenic claudication in older patients. Magnetic resonance imaging is the best radiographic technique to detect nerve compression. Surgical decompression with or without fusion may offer greater short-term benefit but may not be significantly better than medical therapy.

Learn More >

Crystal structures of the σ2 receptor template large-library docking for selective chemotypes active in vivo.

Learn More >

Neural dynamics between anterior insular cortex and right supramarginal gyrus dissociate genuine affect sharing from automatic responses to pretended pain.

Learn More >

Long-term sensitization of rat spinal neurons induced by adolescent psychophysical stress is further enhanced by a mild-nociceptive lumbar input.

Learn More >

Differential Risk Factor Profiles in the Prediction of General and Pain-Specific Functional Limitations 12 Months after Major Pediatric Surgery.

Pediatric chronic post-surgical pain is a surgical complication associated with various levels of functional limitation. Two commonly used measures of functional limitations in youth are the Functional Disability Inventory (FDI) and the PROMIS Pediatric Pain Interference Scale (PPIS), where the former is general, and the latter, pain specific. The aim of the present study was to prospectively compare pre-surgical youth and parent risk factors for youth functional limitations, assessed by the FDI and PPIS, 12 months after major pediatric surgery. Risk factors for the FDI and PPIS were compared in 79 dyads consisting of youth (58% female, = 14.56 years; SD = 2.31) undergoing major surgery and one of their parents. The FDI and PPIS were highly correlated prior to surgery ( = 0.698, < 0.001) and even more so 12 months after surgery ( = 0.807, < 0.001). Parent pre-surgical anxiety sensitivity and youth pre-surgical functional disability significantly predicted 12-month FDI ((6,56) = 4.443, = 0.001, Adjusted R = 0.25), whereas parent pre-surgical anxiety sensitivity, trait anxiety, pain anxiety, as well as youth pain-related anxiety and worry significantly predicted 12-month PPIS ((6,45) = 4.104, = 0.002, Adjusted R = 0.27). Risk factors for 12-month general and pain-specific functional limitations differ by dyad member and type. Functional limitations in youth after surgery are predicted by youth and parent factors, however the risk factors differ between the FDI and the PPIS.

Learn More >

β2 adrenergic receptor mediates noradrenergic action to induce CREB phosphorylation in satellite glial cells of dorsal root ganglia to regulate visceral hypersensitivity.

Sympathoneuronal outflow into dorsal root ganglia (DRG) is suggested to be involved in sympathetically maintained chronic pain, which is mediated by norepinephrine (NE) action on DRG cells. The present study combined in vitro and in vivo approaches to identify the cell types of DRG that received NE action and examined cell-type specific expression of adrenergic receptors (ARs) in DRG. Using DRG explants, we identified that NE acted on satellite glial cells (SGCs) to induce the phosphorylation of cAMP response element-binding (CREB). Using primarily cultured SGCs, we identified that beta (β)2AR but not alpha (α)AR nor other βAR isoforms mediated NE-induced CREB phosphorylation and CRE-promoted luciferase transcriptional activity. Using fluorescence in situ hybridization and affinity purification of mRNA from specific cell types, we identified that β2AR was expressed by SGCs but not DRG neurons. We further examined β2AR expression and CREB phosphorylation in vivo in a model of colitis in which sympathetic nerve sprouting in DRG was observed. We found that β2AR expression and CREB phosphorylation were increased in SGCs of thoracolumbar DRG on day 7 following colitis induction. Inhibition but not augmentation of β2AR reduced colitis- induced calcitonin gene-related peptide (CGRP) release into the spinal cord dorsal horn and colonic pain responses to colorectal distention. Prolonged activation of β2AR in naïve DRG increased CGRP expression in DRG neurons. These findings provide molecular basis of sympathetic modulation of sensory activity and chronic pain that involves β2AR-mediated signaling in SGCs of DRG.

Learn More >

Sympathectomy decreases pain behaviors and nerve regeneration by downregulating monocyte chemokine CCL2 in dorsal root ganglia in the rat tibial nerve crush model.

Peripheral nerve regeneration is associated with pain in several preclinical models of neuropathic pain. Some neuropathic pain conditions and preclinical neuropathic pain behaviors are improved by sympathetic blockade. In this study we examined the effect of a localized "microsympathectomy," i.e., cutting the gray rami containing sympathetic postganglionic axons where they enter the L4 and L5 spinal nerves, which is more analogous to clinically used sympathetic blockade compared to chemical or surgical sympathectomy. We also examined manipulations of CCL2 (monocyte chemoattractant protein 1; MCP-1), a key player in both regeneration and pain. We used rat tibial nerve crush as a neuropathic pain model in which peripheral nerve regeneration can occur successfully. CCL2 in the sensory ganglia was increased by tibial nerve crush and reduced by microsympathectomy. Microsympathectomy and localized siRNA-mediated knockdown of CCL2 in the lumbar DRG had very similar effects: partial improvement of mechanical hypersensitivity and guarding behavior; reduction of regeneration markers growth-associated protein 43 (GAP43) and activating transcription factor 3 (ATF3); and reduction of macrophage density in the sensory ganglia and regenerating nerve. Microsympathectomy reduced functional regeneration as measured by myelinated action potential propagation through the injury site and denervation-induced atrophy of the tibial-innervated gastrocnemius muscle at day 10. Microsympathectomy plus CCL2 knockdown had behavioral effects similar to microsympathectomy alone. The results show that local sympathetic effects on neuropathic pain may be mediated in large part by the effects on expression of CCL2, which in turn regulates the regeneration process.

Learn More >

Virtual Reality Augments Movement during Physical Therapy: A Pragmatic Randomized Trial.

Virtual reality (VR) facilitates physical therapy (PT) via improved engagement. While shown to benefit specific patient populations, such as stroke patients, it is less established in otherwise healthy adults and children receiving outpatient PT. The primary objective was to compare total PT-guided Movement supplemented with VR (PTMVR) to PT guided Movement alone, without VR (PTM).

Learn More >

Neuropathic corneal pain and dry eye: a continuum of nociception.

Throughout the body, damage to peripheral nerves normally involved in nociception may produce a constellation of symptoms-including irritation, itchiness and pain. The neurobiological processes involved in corneal symptoms of dry eye (DE) and neuropathic corneal pain (NCP) have not been clearly considered in terms of nociceptive processing. The conventional underlying presumption is that a labelled line principle is responsible; that these distinct perceptions are hard coded by primary afferent inputs to the central nervous system. This presumption oversimplifies the neurobiological mechanisms underlying somatosensory perception. The labelled line perspective that DE represents a chronic pain condition does not make intuitive sense: how can an eye condition that is not painful in most cases be considered a pain condition? Does not chronic pain by definition require pain to be present? On the other hand, NCP, a term that clearly denotes a painful condition, has historically seemed to resonate with clinical significance. Both DE and NCP can share similar features, yet their differentiation is not always clear. As is often the case, clinical terms arise from different disciplines, with DE evolving from ophthalmological findings and NCP inspired by pain neurophysiology. This review evaluates the current definition of these terms, the rationale for their overlap and how the neurophysiology of itch impacts our understanding of these conditions as a continuum of the same disease. Despite the complexity of nociceptive physiology, an understanding of these mechanisms will allow us a more precise therapeutic approach.

Learn More >

Search