Cerebral Response To Actual And Anticipated Pain

Main Category: Pain / Anesthetics
Also Included In: Back Pain;  Neurology / Neuroscience
Article Date: 25 Aug 2005 - 14:00 PDT

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Researchers in Liverpool used fMRI mapping techniques to measure neural activity and cortical reorganisation in response to actual and anticipated pain. Three patient groups were included in the study: 17 healthy controls made up group C, and 20 chronic lower back pain patients that were subdivided into 8 patients in Group B who displayed maladaptive pain behaviour including Waddell signs (indicating a non-organic cause of their pain), and 12 patients made up group A where no such behaviour patterns were displayed.

Inside the MR scanner patients were subjected to three possible stimuli: thermal stimulation of the hand; electrical stimulation of the lower back (visual analogue score, VAS, of 7/10) or elevation of the leg to an uncomfortable position. Leg movement was accompanied by a visual cue: green signified certain pain, red accompanied no pain and yellow indicated an uncertain movement. During each stimulation or movement cortical activity was monitored and mapped.

Groups A and B (all back pain patients) both registered greater increase in activity than group C (healthy controls) in the left inferior parietal lobe (IPL) when stimulated by thermal pain in the right hand - as compared to activity at rest. Similarly, Groups A and B showed significantly more activation in response to the green light cue for imminent painful elevation of the leg than they did for the yellow light cue for an unpredictable movement - and this time in the right IPL, superior parietal lobe (SPL) and the primary sensorimotor cortex.

However, most significant was the overall comparison of response by Group A and group B (patients with non-organic pain and maladaptive behaviour). The former displayed significantly higher scores in catastrophising, disability and anxiety - suggesting that somato-sensory reorganisation increases with chronicity of back pain and that prolonged pain may directly generate cortical hyper-responsiveness.

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