Search

ABSTRACT Purpose Pain is inherently salient and so draws our attention in addition to impacting performance on attention‐demanding tasks. Individual variability in pain–attention interactions can be assessed by two kinds of behavioral phenotypes that quantify how individuals prioritize pain versus attentional needs. The intrinsic attention to pain (IAP) measure quantifies the degree to which a person attends to pain (high‐IAP) or mind‐wanders away from pain (low‐IAP). The A/P categorization quantifies how pain impacts cognitive performance during an attention‐demanding task classifying individuals into P type (pain dominates, worse performance during pain in comparison to no pain) and A type (attention to task dominates, better performance during pain in comparison to no pain). Although previous MRI‐based studies have linked these phenotypes with the dynamic pain connectome (DPC), the underlying neural oscillations are not known. This paper aims to examine the brain–behavior relationship between alpha and theta oscillations within nodes of the DPC and pain–attention phenotypes. Method Fifty participants (27 F, 23 M) underwent resting‐state magnetoencephalography (MEG). Individual IAP scores were determined by assessing mind‐wandering during pain and A/P type was based on interference of pain with cognitive task performance. Finding The main findings were: (1) peak alpha frequency (PAF) power did not differ between low/high‐IAP individuals or A/P‐type individuals within the nodes of the DPC; (2) compared to high‐IAP individuals, those with low‐IAP have slower PAF in the left primary somatosensory cortex, posterior cingulate cortex and precuneus and higher theta power in the ascending nociceptive pathway and default mode network; (3) males with low‐IAP, compared to females, had higher PAF power throughout the DPC. Conclusion Alpha and theta oscillations within the DPC may underlie aspects of attentional focus and pain–attention interactions.

Background Pain is an individual and subjective experience that places a burden on individuals to convince others they have pain. Brain imaging technologies can potentially inform pain management but raise neuroethical questions.Aims We examined the degree of endorsement and concerns of adults in Canada with chronic pain regarding the use of brain imaging to detect and treat chronic pain in six areas: new brain imaging technologies, brain data privacy, stigma, treatment, objective representations of pain, and dismissing pain self-reports.Results An online survey was completed by 349 Canadian adults living with chronic pain. Most respondents were open to using brain imaging for diagnostics, prediction, and therapeutic decision making (>90%). More than half of respondents felt that a brain scan would give them more confidence in their diagnosis and treatment plans and that health care providers would be more likely to believe they had chronic pain. However, they worried that brain scans could be used to dismiss their pain self-report. Most respondents felt there were policies to protect their brain data, but 40% were concerned about privacy and brain scan use against them by their employers/insurers. Although most respondents felt that a brain scan could represent their pain and suffering, 80% disagreed that their pain is only real if seen in a brain scan.Conclusions People with chronic pain recognize the potential benefits of brain imaging but are concerned about data security and dismissal of their self-reported pain. Our data align with previous recommendations to use brain imaging as an adjunct to pain self-reports but not as a replacement for the same.

A comparative analysis on resting-state magnetoencephalography data from healthy controls and patients with chronic pain reveals spectral frequency-specific dysregulation and a temporal imbalance of brain microstates in chronic neuropathic pain.

Two behavioural phenotypes in healthy people have been delineated based on their intrinsic attention to pain (IAP) and whether their reaction times (RT) during a cognitively-demanding task are slower (P-type) or faster (A-type) during experimental pain. These behavioural phenotypes were not previously studied in chronic pain populations to avoid using experimental pain in a chronic pain context. Since pain rumination (PR) may serve as a supplement to IAP without needing noxious stimuli, we attempted to delineate A-P/IAP behavioural phenotypes in people with chronic pain and determined if PR can supplement IAP. Behavioural data acquired in 43 healthy controls (HCs) and 43 age-/sex-matched people with chronic pain associated with ankylosing spondylitis (AS) was retrospectively analyzed. A-P behavioural phenotypes were based on RT differences between pain and no-pain trials of a numeric interference task. IAP was quantified based on scores representing reported attention towards or mind-wandering away from experimental pain. PR was quantified using the pain catastrophizing scale, rumination subscale. The variability in RT was higher during no-pain trials in the AS group than HCs but was not significantly different in pain trials. There were no group differences in task RTs in no-pain and pain trials, IAP or PR scores. IAP and PR scores were marginally significantly positively correlated in the AS group. RT differences and variability were not significantly correlated with IAP or PR scores. Thus, we propose that experimental pain in the A-P/IAP protocols can confound testing in chronic pain populations, but that PR could be a supplement to IAP to quantify attention to pain.

Multiple concussions, particularly in contact sports, have been associated with cognitive deficits, psychiatric impairment and neurodegenerative diseases like chronic traumatic encephalopathy. We used volumetric and deformation-based morphometric analyses to test the hypothesis that repeated concussions may be associated with smaller regional brain volumes, poorer cognitive performance and behavioural symptoms among former professional football players compared to healthy controls. This study included fifty-three retired Canadian Football League players, 25 age- and education-matched healthy controls, and controls from the Cambridge Centre for Aging and Neuroscience database for validation. Volumetric analyses revealed greater hippocampal atrophy than expected for age in former athletes with multiple concussions than controls and smaller left hippocampal volume was associated with poorer verbal memory performance in the former athletes. Deformation-based morphometry confirmed smaller bilateral hippocampal volume that was associated with poorer verbal memory performance in athletes. Repeated concussions may lead to greater regional atrophy than expected for age. Keywords: Sport-related concussion, Mild traumatic brain injury, Deformation based morphometry, Aging

Classical trigeminal neuralgia (TN) is a chronic pain disorder that has been described as one ofthe most severe pains one can suffer. The most prevalent theory of TN etiology is that the trigeminal nerve is compressed at the root entry zone (REZ) by blood vessels. However, there is significant evidence showing a lack of neurovascular compression (NVC) for many cases of classical TN. Furthermore, a considerable number of patients who are asymptomatic have MR evidence of NVC. Since there is no validated animal model that reproduces the clinical features of TN, our understanding of TN pathology mainly comes from biopsy studies that have limitations. Sophisticated structural MRI techniques including diffusion tensor imaging provide new opportunities to assess the trigeminal nerves and CNS to provide insight into TN etiology and pathogenesis. Specifically, studies have used high-resolution structural MRI methods to visualize patterns of trigeminal nerve-vessel relationships and to detect subtle pathological features at the trigeminal REZ. Structural MRI has also identified CNS abnormalities in cortical and subcortical gray matter and white matter and demonstrated that effective neurosurgical treatment for TN is associated with a reversal of specific nerve and brain abnormalities. In conclusion, this review highlights the advanced structural neuroimaging methods that are valuable tools to assess the trigeminal system in TN and may inform our current understanding of TN pathology. These methods may in the future have clinical utility for the development of neuroimaging-based biomarkers of TN.

Thyroid hormone metabolic disarray has been identified as a risk factor for the progression of heart disease and the development of heart failure (HF). Both hyper- and hypothyroidism have been associated with a failing myocardium. Poor cardiac contractility and low cardiac output due to hyperthyroidism is a rare occurrence and is mostly seen in patients with preexisting heart disease. Referred to as a "rate related" phenomenon, hyperthyroid-induced sustained sinus tachycardia or atrial fibrillation may further reduce ventricular contractility. Increasingly, the hypothyroid state, and in particular a low triiodothyronine level, has been associated with a reduced cardiac performance and poor prognosis in HF, even in the presence of normal thyroid-stimulating hormone levels. Low thyroid hormone levels alter cardiac gene expression and increase systemic vascular resistance, both resulting in a reduction of cardiac contractility and cardiac output. This review summarizes current data on thyroid dysfunction and HF as well as the emerging implications of the "low triiodothyronine state."