Discrepancy Between Reported and Calculated Pain Reduction in Patients With Spinal Cord Stimulation Therapy and Lack of Agreement Between Patient Satisfaction and Degree of Pain Relief.

OBJECTIVES: This study aimed to determine agreement between reported percentage pain reduction (RPPR) and calculated percentage pain reduction (CPPR) in patients with percutaneous spinal cord stimulation (SCS) implants, and to correlate RPPR and CPPR with patient satisfaction. We also sought to determine which patient-reported outcome measures are most improved in patients with SCS. MATERIALS AND METHODS: Fifty patients with percutaneous spinal cord stimulator implants with a mean follow-up of 51.1 months were interviewed and surveyed to assess their pain level, impression of degree of pain relief, satisfaction with the therapy, and desire to have the device again. Baseline pain level was obtained from their preimplant records. RESULTS: Overall, RPPR was found to be 53.3%, whereas CPPR was 44.4%. Of all patients, 21 reported <50% pain reduction; however, most of these (12/21, 57%) were satisfied with the outcome of therapy. In terms of individual improvement in outcomes, activities of daily life was the most improved measure at 82%, followed by mood, sleep, medication use, and health care utilization at 74%, 62%, 50%, and 48%, respectively. CONCLUSIONS: RPPR appears to be a complex outcome measure that may not agree with CPPR. Overall RPPR is greater than the CPPR. On the basis of our data, these independently valid measures should not be used interchangeably. A 50% pain reduction threshold is not a requisite for patient satisfaction and desire to have the device again. Activities of daily living was the most improved measure in this cohort, followed by mood, sleep, medication usage, and decrease in health care utilization.

The Influence of Sleep Disturbance on Chronic Pain.

PURPOSE OF REVIEW: The purpose of this review is to present an overview of common sleep disturbance pathologies and their impact on chronic pain, while examining various factors that are implicit in the relationship between sleep disturbance and chronic pain, including neurobiochemistry, anatomy, and systemic mediators, and reviewing recent and landmark literature. RECENT FINDINGS: Earlier literature reviews and studies have introduced the bidirectional relationship between sleep disturbance and chronic pain; that is, impaired sleep may worsen chronic pain, and chronic pain causes sleep disturbance. However, more recent reviews and studies seem to show a more associative, rather than causative relationship. There have been recent studies that attempt to determine mechanisms that link sleep disturbance and chronic pain; the results of these studies were more varied, ultimately concluding that there may be a separate, yet-to-be discovered mechanism that shows the causative relationship between sleep disturbance and pain. There are several neurotransmitters that are involved in the mediation of chronic pain and sleep disturbance as separate entities, and some studies have shown that there may be mechanisms that govern both chronic pain and sleep disturbance as a single unit. Other neuroendocrine substances also serve to mediate chronic pain and sleep disturbance. All these substances are found to be associated with various sleep disorders and are also associated with chronic pain symptoms as well. Inflammation plays a role in chronic pain and sleep disturbance, with an increase in inflammatory substances and mediators associated with an increase or worsening in chronic pain symptoms and sleep disorders. The HPA axis plays a role in chronic pain and sleep disorders, influencing pain and sleep pathways through stress response, inflammation, and maintenance of homeostasis. There are several variables that influence both chronic pain and sleep disturbance, and more research into these variables may further our understanding into the complex pathways governing the influence of sleep disturbance on pain, and ultimately to improve treatment for this issue.

The Impact of Smoking on the Development and Severity of Chronic Pain.

PURPOSE OF REVIEW: The purpose of this review is to examine the impact of smoking and its role on the development of chronic pain and provide a critical review of recent literature. RECENT FINDINGS: Recent studies demonstrate the bidirectional and dependent relationship between smoking and chronic pain. Those who are in pain have a more difficult time in the cessation of smoking as well as an increased sensitivity to pain during abstinence, lower confidence, and higher relapse rates. The fear of pain and the anxiety and depression that abstinence causes results in a grim outcome for long-term cessation. The dependent nature between chronic pain and smoking is affected by numerous variables. Providers should consider a multiprong approach to treating chronic pain and targeting smoking cessation treatment by providing motivational therapy, nicotine replacement, and medication therapies to prevent relapse, and providing those who are more likely to relapse with a higher level of care.

Cognitive and neural facets of dissociation in a traumatized population.

Dissociative phenomena are frequently experienced by psychologically traumatized people. However, little is known about the cognitive profiles of highly dissociative traumatized individuals, and corresponding patterns of neural connectivity when attentional networks are engaged in the context of emotion. One hundred seventeen traumatized women completed the multiscale dissociation inventory (MDI) and neuropsychological testing; MDI scores were used to classify high- and low-dissociative participants. Forty-six participants also underwent fMRI during performance of an attentional control task that incorporates emotionally distracting images (Affective Number Stroop; ANS). Compared to low-dissociative participants, high-dissociative participants demonstrated better performance on an executive functioning task (F1,111 = 4.64, p = .03), worse performance on a task of visual memory (F1,111 = 9.52, p = .003), and similar performance on all other neuropsychological measures. In addition, dissociative symptoms were negatively correlated with functional connectivity between the amygdala and right anterior insula in response to trauma-related ANS trials. These findings indicate that highly dissociative traumatized people experience difficulties with attentional control in the context of emotionally evocative stimuli, but in a neutral context, their overall cognitive profiles are similar to low-dissociative people. Highly dissociative participants also demonstrated weaker connectivity between the amygdala and insula in response to trauma-relevant images. Evocative, trauma-relevant stimuli appear to disrupt neutral networks involved with attention to salient cues and interoception in highly dissociative traumatized individuals. (PsycINFO Database Record (c) 2019 APA, all rights reserved).

Attentional control abnormalities in posttraumatic stress disorder: Functional, behavioral, and structural correlates.

BACKGROUND: Attentional disruptions are common in PTSD, but findings across neuropsychological and neuroimaging studies have been variable. Few PTSD studies have investigated abnormalities in attention networks using a multi-modal imaging approach and attentional tasks that include emotionally-salient images. This study combined a behavioral task that included these images (emotional Stroop) with functional and structural neuroimaging (fMRI and diffusion tensor imaging; DTI) methods to comprehensively investigate attentional control abnormalities in a highly-traumatized civilian sample. METHODS: 48 traumatized women with and without PTSD received clinical assessments, fMRI and DTI. During fMRI, the Affective Stroop (AS), an attentional control task that includes emotionally-salient distractor images (trauma-relevant, positive, neutral) and variable task demands, was administered. RESULTS: In response to more difficult AS trials, participants with PTSD demonstrated lower activation in the dorsal and rostral anterior cingulate cortex and greater activation in the insula. This group also showed comparatively poorer performance on positive AS distractor trials, even after adjusting for trauma exposure. Performance on these trials inversely correlated with structural integrity of the cingulum bundle and uncinate fasciculus. CONCLUSIONS: Even after adjusting for trauma exposure, participants with PTSD showed worse performance on an attentional control task in the context of emotional stimuli. They also showed relatively lower cognitive control network activation and greater salience network activation. Fronto-parietal and fronto-limbic white matter connectivity corresponded with AS performance. Our findings indicate that attentional control impairments in PTSD are most evident in the context of emotional cues, and are related to decrements in function and structure of cognitive control and salience networks.

Sickle cell disease activates peripheral blood mononuclear cells to induce cathepsins k and v activity in endothelial cells.

Sickle cell disease is a genetic disease that increases systemic inflammation as well as the risk of pediatric strokes, but links between sickle-induced inflammation and arterial remodeling are not clear. Cathepsins are powerful elastases and collagenases secreted by endothelial cells and monocyte-derived macrophages in atherosclerosis, but their involvement in sickle cell disease has not been studied. Here, we investigated how tumor necrosis alpha (TNFα) and circulating mononuclear cell adhesion to human aortic endothelial cells (ECs) increase active cathepsins K and V as a model of inflammation occurring in the arterial wall. ECs were stimulated with TNFα and cultured with peripheral blood mononuclear cells (PBMCs) from persons homozygous for sickle (SS) or normal (AA) hemoglobin. TNFα was necessary to induce cathepsin K activity, but either PBMC binding or TNFα increased cathepsin V activity. SS PBMCs were unique; they induced cathepsin K in ECs without exogenous TNFα (n = 4, P < 0.05). Inhibition of c-Jun N-terminal kinase (JNK) significantly reduced cathepsins K and V activation by 60% and 51%, respectively. Together, the inflammation and activated circulating mononuclear cells upregulate cathepsin activity through JNK signaling, identifying new pharmaceutical targets to block the accelerated pathology observed in arteries of children with sickle cell disease.