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News in brief

New research from Harvard Medical School (Boston, MA, USA) has demonstrated an association between neural activity and back pain in patients by using the technique arterial spin labeling. Owing to its varying nature, chronic pain is difficult to correlate with neural activity using conventional functional MRI. In addition, pain is a very personal experience, and therefore challenging for a patient to communicate accurately to a clinician. The aid of imaging technology in pain assessment has the potential to have an immense positive impact in this field. Arterial spin labeling is a perfusion-based method of functional MRI. This technique allows the absolute quantification of regional cerebral blood flow, which is the measure of neuronal activity. The resulting image is a ‘cerebral perfusion map’, which can be achieved without the administration of a contrast agent or ionizing radiation. This is because this technique uses magnetically labeled endogenous blood water as a freely diffusible tracer. So how do the changes detected by arterial spin labeling correlate with low back pain? Lead author of the study, Ajay Wasan explains: “we’ve found that when a patient has worsening of their usual pain there are changes in the activity of the brain. These changes occur in the network of areas in the brain that process pain and mood.” This study looked at participants with chronic low back and radicular pain and also healthy normal subjects. The participants partook in three sessions: a characterization and training session and two arterial spin labeling sessions. In the first imaging session, chronic pain was exacerbated using clinical maneuvers such as pelvic tilting or straight leg rising. In the second and third sessions, noxious heat was applied to the affected area of pain. Arterial spin labeling was used throughout to measure brain activity associated with their chronic pain. The results demonstrated that arterial spin labeling displayed significant changes in neuronal activity during the first activity and the other activities in subjects with low back pain. The healthy controls displayed no significant changes. These differences in neurological activity were not observed after administration of noxious heat to any of the patients, nor in any task involving the healthy subjects, suggesting that arterial spin labeling displayed neural processing that was specific to only chronic pain. The clinically significant worsening of ongoing chronic pain was associated with significant regional blood flow increases (6–10 mm/100 g of tissue/min; p < 0.01) within brain regions known to activate with experimental pain (somatosensory, prefrontal and insular cortices) and in other structures less frequently observed in experimental pain studies, such as the superior parietal lobule (part of the dorsal attention network). This effect is specific to changes in ongoing chronic pain as it is observed during worsening chronic pain but is not observed after thermal pain application, or in matched, pain-free healthy controls. Wasan speaks about future research directions: “While this study begins to uncover some of the basic physiology of the brain as it processes pain, more studies are needed to help us understand how the brain function may change over the course of treatment of pain and to examine the brain mechanisms by which pain improves.”