Measuring the neural response to continuous intramuscular infusion of hypertonic saline by perfusion MRI.
ABSTRACT To determine the extent to which arterial spin labeling (ASL), a functional magnetic resonance imaging technique that directly measures cerebral blood flow (CBF), is able to measure the neural activation associated with prolonged experimental muscle pain.
Hypertonic saline (HS) (5% NaCl) was infused into the brachioradialis muscle of 19 healthy volunteers for 15 min. The imaging volume extended from the dorsal side of the pons to the primary somatosensory cortices, covering most of the cortical and subcortical regions associated with pain perception.
Using a numerical scale from 0 to 10, ratings of pain intensity peaked at 5.9 ± 0.5 (mean ± SE). Group activation maps showed that the slow infusion of HS evoked CBF increases primarily in bilateral insula, with additional activation in right frontal regions. In the activated areas, CBF gradually increased at the onset of HS infusion and was maintained at relatively constant levels throughout the remainder of the infusion period. However, the level and extent of activation were smaller than observed in previous studies involving acute muscle pain.
This study demonstrates the ability of ASL to measure changes in CBF over extended periods of time and that the neural activation caused by muscle pain is paradigm specific.
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ABSTRACT: Neuroimaging studies have suggested the presence of alterations in the anatomo-functional properties of the brain of patients with chronic pain. However, investigation of the brain circuitry supporting the perception of clinical pain presents significant challenges, particularly when using traditional neuroimaging approaches. While potential neuroimaging markers for clinical pain have included resting brain connectivity, these cross-sectional studies have not examined sensitivity to within-subject exacerbation of pain. We used the dual regression probabilistic Independent Component Analysis approach to investigate resting-state connectivity on arterial spin labeling data. Brain connectivity was compared between patients with chronic low back pain (cLBP) and healthy controls, before and after the performance of maneuvers aimed at exacerbating clinical pain levels in the patients. Our analyses identified multiple resting state networks, including the default mode network (DMN). At baseline, patients demonstrated stronger DMN connectivity to the pregenual anterior cingulate cortex (pgACC), left inferior parietal lobule, and right insula (rINS). Patients' baseline clinical pain correlated positively with connectivity strength between the DMN and right insula (DMN-rINS). The performance of calibrated physical maneuvers induced changes in pain, which were paralleled by changes in DMN-rINS connectivity. Maneuvers also disrupted the DMN-pgACC connectivity, which at baseline was anticorrelated with pain. Finally, baseline DMN connectivity predicted maneuver-induced changes in both pain and DMN-rINS connectivity. Our results support the use of arterial spin labeling to evaluate clinical pain, and the use of resting DMN connectivity as a potential neuroimaging biomarker for chronic pain perception.Pain 10/2012; · 5.64 Impact Factor
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ABSTRACT: OBJECTIVE: Increasing evidence suggests a central nervous system (CNS) component underpinning persistent pain disease states. We aimed to determine regional cerebral blood flow (rCBF) changes representing ongoing pain experienced by patients with painful osteoarthritis (OA) of the carpometacarpal (CMC) joint. Our second aim was to examine rCBF variability across sessions. We used pulsed-continuous arterial spin-labelling (pCASL), a perfusion magnetic resonance imaging technique. METHODS: 16 CMC OA participants and 17 matched controls participated. Two pCASL scans and numerical rating scale (NRS) estimates of ongoing pain were acquired in two identical sessions. Voxelwise general linear model analyses were performed to determine: (i) rCBF differences between OA and control groups; (ii) rCBF differences between sessions within each group; (iii) whether session-wise rCBF differences related to variability in perceived ongoing pain. RESULTS: OA group rCBF increases representing ongoing pain were identified in primary and secondary somatosensory, insula and cingulate cortices, thalamus, amygdala, hippocampus and dorsal midbrain/pontine tegmentum, including periaqueductal grey/nucleus cuneiformis. Session-wise rCBF differences in the OA group in postcentral, rostral/subgenual cingulate, mid/anterior insula, prefrontal and premotor cortices related to changes in their perceived ongoing pain. No significant session-wise rCBF differences were observed in controls. CONCLUSION: This is the first quantitative endogenous perfusion MRI report of the cerebral representation of ongoing, persistent pain due to osteoarthritis. Observed rCBF changes potentially indicate dysregulated CNS appraisal and modulation of pain, most likely the maladaptive neuroplastic sequelae of living with painful OA. Understanding the neural basis of ongoing pain is likely to be important in developing novel treatment strategies. © 2012 American College of Rheumatology.Arthritis & Rheumatology 08/2012; · 7.48 Impact Factor