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Much evidence from pain patients and animal models shows that chronic pain does not exist in a vacuum but has varied comorbidities and far-reaching consequences. Patients with long-term pain often develop anxiety and depression and can manifest changes in cognitive functioning, particularly with working memory. Longitudinal studies in rodent models also show the development of anxiety-like behavior and cognitive changes weeks to months after an injury causing long-term pain. Brain imaging studies in pain patients and rodent models find that chronic pain is associated with anatomical and functional alterations in the brain. Nevertheless, studies in humans reveal that lifestyle choices, such as the practice of meditation or yoga, can reduce pain perception and have the opposite effect on the brain as does chronic pain. In rodent models, studies show that physical activity and a socially enriched environment reduce pain behavior and normalize brain function. Together, these studies suggest that the burden of chronic pain can be reduced by nonpharmacological interventions. [ABSTRACT FROM AUTHOR]

Presents a study which investigated the role of different cortical areas in pain processing. Debate on the role of somatosensory cortex (S1) in pain perception; Cognitive modulation of S1 activity; Variability of S1 sulcal anatomy.

Humans have a distinguishing ability for fine motor control that is subserved by a highly evolved cortico-motor neuronal network. The acquisition of a particular motor skill involves a long series of practice movements, trial and error, adjustment and refinement. At the cortical level, this acquisition begins in the parieto-temporal sensory regions and is subsequently consolidated and stratified in the premotor-motor cortex. Task-specific dystonia can be viewed as a corruption or loss of motor control confined to a single motor skill. Using a multimodal experimental approach combining neuroimaging and non-invasive brain stimulation, we explored interactions between the principal nodes of the fine motor control network in patients with writer's cramp and healthy matched controls. Patients and healthy volunteers underwent clinical assessment, diffusion-weighted MRI for tractography, and functional MRI during a finger tapping task. Activation maps from the task-functional MRI scans were used for target selection and neuro-navigation of the transcranial magnetic stimulation. Single- and double-pulse TMS evaluation included measurement of the input-output recruitment curve, cortical silent period, and amplitude of the motor evoked potentials conditioned by cortico-cortical interactions between premotor ventral (PMv)-motor cortex (M1), anterior inferior parietal lobule (aIPL)-M1, and dorsal inferior parietal lobule (dIPL)-M1 before and after inducing a long term depression-like plastic change to dIPL node with continuous theta-burst transcranial magnetic stimulation in a randomized, sham-controlled design. Baseline dIPL-M1 and aIPL-M1 cortico-cortical interactions were facilitatory and inhibitory, respectively, in healthy volunteers, whereas the interactions were converse and significantly different in writer's cramp. Baseline PMv-M1 interactions were inhibitory and similar between the groups. The dIPL-PMv resting state functional connectivity was increased in patients compared to controls, but no differences in structural connectivity between the nodes were observed. Cortical silent period was significantly prolonged in writer's cramp. Making a long term depression-like plastic change to dIPL node transformed the aIPL-M1 interaction to inhibitory (similar to healthy volunteers) and cancelled the PMv-M1 inhibition only in the writer's cramp group. These findings suggest that the parietal multimodal sensory association region could have an aberrant downstream influence on the fine motor control network in writer's cramp, which could be artificially restored to its normal function. [ABSTRACT FROM AUTHOR]

Provoked vestibulodynia (PVD) is a common form of chronic vulvar pain with unknown aetiology. Central pain regulatory mechanisms have been suggested to be disrupted in PVD, and consequently, PVD may be associated with anatomical changes in pain modulatory brain areas. Here, we compared total gray matter volumes and regional gray matter densities between 14 medication-free young women with relatively short-standing PVD (1 to 9 yrs) and 14 control subjects using whole brain voxel-based morphometry (VBM). VBM revealed that PVD subjects had significantly higher gray matter densities in pain modulatory and stress-related areas, i.e. the parahippocampal gyrus/hippocampus and basal ganglia (globus pallidus, caudate nucleus, and substantia nigra). In several of these regions, gray matter was related to clinical symptoms, namely lowered pain thresholds and increased pain catastrophizing scores. No region showed decreased gray matter density in the PVD group. These results point at the morphological alterations in supra-spinal pain modulatory circuitry, which might contribute to the clinical symptoms of patients with PVD. Previous VBM studies in older subjects with a longstanding chronic pain condition have demonstrated gray matter decreases in similar areas. We therefore speculate that gray matter density might increase in young pain patients with short disease duration and decrease in older subjects with longstanding disease, similarly to some psychiatric conditions, in which bi-directional changes of gray matter have been observed. [ABSTRACT FROM AUTHOR]

Marginal elevations of troponin T among patients with chest pain are often considered to be insignificant. We sought to define the prognostic value of marginal troponin T elevations in patients presenting to the emergency department with suspected myocardial ischemia. Four hundred twenty-eight consecutive patients presenting to the emergency department with ongoing chest pain were evaluated, followed through their hospital course, and contacted for follow-up 4 months after discharge. Two hundred ninety-nine patients had undetectable troponin T levels (<0.01 μg/L), 76 had marginal troponin T elevations (0.01 to 0.09 μg/L), and 53 had frank troponin T elevations (≥0.1 μg/L). Patients with either marginally or frank elevated troponin levels were older and more likely to be men, but did not differ from patients with undetectable troponin levels with regard to the prevalence of coronary artery disease risk factors, history of coronary disease, or race. While in the hospital, the undetectable and marginal troponin groups were referred for cardiac testing in equal proportions (58% and 59%, respectively), whereas 87% of the elevated group underwent further testing. After adjustment for possible confounders, a significantly increased rate of death/myocardial infarction/revascularization was observed in the marginal troponin group compared with the undetectable troponin group (p = 0.004). Marginal elevations of troponin T identified a currently underevaluated high-risk subgroup of patients with suspected myocardial ischemia who are more likely to have adverse clinical outcomes than those with undetectable troponin levels. [Copyright &y& Elsevier]

Background: The belief that chest pain relief with nitroglycerin indicates the presence of active coronary artery disease is common. However, this hypothesis has not been tested. Objective: To define the diagnostic and prognostic value of chest pain relief with nitroglycerin. Design: Prospective observational cohort study. Setting: Urban community teaching hospital. Patients: 459 consecutive patients with chest pain admitted through the emergency department who received nitroglycerin from emergency services personnel or an emergency department nurse. Follow-up was obtained by telephone contact at 4 months. Measurements: Chest pain relief was defined as a decrease of at least 50% in patients’ self-reported pain within 5 minutes of the initial dose of sublingual or spray nitroglycerin. Active coronaryartery disease was defined as any elevated serum enzyme levels, coronary angiography demonstrating a 70% or greater stenosis, or a positive exercise test result. Results: Nitroglycerin relieved chest pain in 39% of patients 181 of 459). In patients with active coronary artery disease as the likely cause of their chest pain, 35% (49 of 141) had chest pain relief with nitroglycerin. In contrast, in patients without activecoronary artery disease, 41% (113 of 275) had chest pain relief P> 0.2). Four-month clinical outcomes were similar in patients with or without chest pain relief with nitroglycerin (P> 0.2). Conclusions: These data suggest that, in a general population admitted for chest pain, relief of pain after nitroglycerin treatmentdoes not predict active coronary artery disease and should not be used to guide diagnosis. [ABSTRACT FROM AUTHOR]