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Fibromyalgia (FM) is a chronic pain syndrome, and alexithymia, which is a condition that is characterised by deficits in emotional self-awareness, is highly prevalent among individuals with FM. Insecure attachment styles and inadequate parental care appear to play an important role in the onset and maintenance of both alexithymia and chronic pain. Therefore, the present study aimed to examine the associations between attachment styles, parental bonding, and alexithymia among patients with FM and healthy controls (HC).
Burning mouth syndrome (BMS) is classified into idiopathic orofacial pain conditions. Although central and peripheral neuropathic mechanisms are believed to be involved, the etiology remains to be fully elucidated. The present study examined temporal brain responses to an ongoing hot stimulus to investigate the pain modulating system in patients with BMS. The thermal stimulation sequence comprised baseline (32°C, 40 s) to warm (40°C, 32 s) to baseline (32°C, 40 s) to hot (49°C, 32 s), which was repeated four times using a Peltier thermode. These warm and hot stimuli were applied on the right palm and right lower lip in two separate sessions. Functional magnetic resonance imaging data were acquired by recording echo-planar images with a block design. Brain activity induced by purely hot stimulation (49°C vs. 40°C) applied to the palm was more pronounced than that induced by lip stimulation and in patients with BMS compared with controls. Comparison of brain activity between the first 16 s and second 16 s of the stimulus revealed pronounced time-dependent facilitation in patients with BMS during lip stimulation. These findings indicate that the pain modulating system in patients with BMS is dysregulated and that the brain in BMS is highly sensitized to pain information originating from the trigeminal system.
Chronic pain in later life is a worldwide problem. In younger patients, chronic pain affects life satisfaction negatively; however, it is unknown whether this outcome will extend into old age.
Cerebrospinal fluid (CSF) and brain tissue sodium levels increase during migraine. However, little is known regarding the underlying mechanisms of sodium homeostasis disturbance in the brain during the onset and propagation of migraine. Exploring the cause of sodium dysregulation in the brain is important, since correction of the altered sodium homeostasis could potentially treat migraine. Under the hypothesis that disturbances in sodium transport mechanisms at the blood-CSF barrier (BCSFB) and/or the blood-brain barrier (BBB) are the underlying cause of the elevated CSF and brain tissue sodium levels during migraines, we developed a mechanistic, differential equation model of a rat's brain to compare the significance of the BCSFB and the BBB in controlling CSF and brain tissue sodium levels. The model includes the ventricular system, subarachnoid space, brain tissue and blood. Sodium transport from blood to CSF across the BCSFB, and from blood to brain tissue across the BBB were modeled by influx permeability coefficients and , respectively, while sodium movement from CSF into blood across the BCSFB, and from brain tissue to blood across the BBB were modeled by efflux permeability coefficients and , respectively. We then performed a global sensitivity analysis to investigate the sensitivity of the ventricular CSF, subarachnoid CSF and brain tissue sodium concentrations to pathophysiological variations in , , and . Our results show that the ventricular CSF sodium concentration is highly influenced by perturbations of , and to a much lesser extent by perturbations of . Brain tissue and subarachnoid CSF sodium concentrations are more sensitive to pathophysiological variations of and than variations of and within 30 min of the onset of the perturbations. However, is the most sensitive model parameter, followed by and , in controlling brain tissue and subarachnoid CSF sodium levels within 3 h of the perturbation onset.
People with chronic neck pain have impaired proprioception (i.e., sense of neck position). It is unclear whether this impairment involves disruptions to the proprioceptive representation in the brain, peripheral factors, or both. Implicit motor imagery tasks, namely left/right judgements of body parts, assess the integrity of the proprioceptive represention. Previous studies evaluating left/right neck judgements in people with neck pain are conflicting. We conducted a large online study to comprehensively address whether people with neck pain have altered implicit motor imagery performance.
Pain can be both a cause and a consequence of sleep deficiency. This bidirectional relationship between sleep and pain has important implications for clinical management of patients, but also for chronic pain prevention and public health more broadly. The review that follows will provide an overview of the neurobiological evidence of mechanisms thought to be involved in the modulation of pain by sleep deficiency, including the opioid, monoaminergic, orexinergic, immune, melatonin, and endocannabinoid systems; the hypothalamus-pituitary-adrenal axis; and adenosine and nitric oxide signaling. In addition, it will provide a broad overview of pharmacological and non-pharmacological approaches for the management of chronic pain comorbid with sleep disturbances and for the management of postoperative pain, as well as discuss the effects of sleep-disturbing medications on pain amplification.
Recent research has highlighted a need for the psychometric evaluation of instruments targeting core domains of the pain experience in chronic pain populations. In this study, the measurement properties of SF-36, EQ-5D, and HADS were analyzed within the item response-theory framework based on data from 35,908 patients. To assess the structural validity of these instruments, the empirical representations of several conceptually substantiated latent structures were compared in a cross-validation procedure. The most structurally sound representations were selected from each questionnaire and their internal consistency reliability computed as a summary of their precision. Lastly, questionnaire scores were correlated to each other to evaluate their convergent and discriminant validity. Our results supported that SF-36 is an acceptable measure of two independent constructs of physical and mental health. In contrast, although the approach to summarize the HRQoL construct of EQ-5D as a unidimensional score was valid, its low reliability rendered practical model implementation of doubtful utility. Finally, rather than being separated into two subscales of anxiety and depression, HADS was a valid and reliable measure of overall emotional distress. In support of convergent and discriminant validity, correlations between questionnaires showed that theoretically similar traits were highly associated whereas unrelated traits were not. Our models can be applied to score SF-36 and HADS in chronic pain patients, but we recommend against using the EQ-5D model due to its low reliability. These results are useful for researchers and clinicians involved in chronic pain populations, as questionnaires' properties determine their discriminating ability in patient status assessment.
To investigate mental and physical health comorbidity with chronic back or neck pain in the Chinese population, and assess the level of disability associated with chronic back or neck pain.
Dissecting the organization of circuit pathways involved in pain affect is pivotal for understanding behavior associated with noxious sensory inputs. The central nucleus of amygdala (CeA) is comprised of distinct populations of inhibitory GABAergic neurons expressing a wide range of molecular markers. CeA circuits are associated with aversive learning and nociceptive responses. The CeA receives nociceptive signals directly from the parabrachial nuclei (PBn), contributing to the affective and emotional aspects of pain. While the CeA has emerged as an important node in pain processing, key questions remain regarding the specific targeting of PBn inputs to different CeA subregions and cell types. We used a multifaceted approach involving transgenic reporter mice, viral vector-mediated optogenetics, and brain slice electrophysiology to delineate cell-type-specific functional organization of the PBn-CeA pathway. Whole-cell patch clamp recordings of molecularly defined CeA neurons while optogenetically driving long-range inputs originating from PBn revealed the direct monosynaptic excitatory inputs from PBn neurons to three major subdivisions of the CeA: laterocapsular (CeC), lateral (CeL) and medial (CeM). Direct monosynaptic excitatory inputs from PBn targeted both somatostatin-expressing (SOM+) and corticotropin-releasing hormone expressing (CRH+) neurons in CeA. We find that monosynaptic PBn input is preferentially organized to molecularly specific neurons in distinct subdivisions of the CeA. The spared nerve injury model of neuropathic pain differentially altered PBn monosynaptic excitatory input to CeA neurons based on molecular identity and topographical location within the CeA. These results provide insight into the functional organization of affective pain pathways and how they are altered by chronic pain.
Opioid tapering is increasingly utilized by providers to decrease risks of chronic opioid therapy, but it is unknown whether tapering is associated with termination of care.