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FUNCTIONAL MRI MEASUREMENT OF CORTICAL REORGANISATION IN CHRONIC LOW BACK PAIN



Abstract

The purpose of the study is to assess changes in cortical activity in chronic low back pain patients with and without illness behaviour.

Introduction: It is well recognised that patients with chronic low back pain (CLBP) may have major psychological factors which affect their level of disability. Abnormal patterns of illness behaviour have been described 1.

Methodology: 30 patients with CLBP of more than six months duration were recruited. Patients with radicular pain or previous surgery were excluded. Two groups were created dependant on the presence of Waddell signs. “Copers” (n=16) showed 0 or 1 Waddell signs. “Non-copers” (n=14) showed 4 or 5 Waddell signs.

After informed consent, all subjects underwent fMRI scanning. Experimental pain was induced by thermal stimulation of the right hand. Straight leg raising (SLR) was performed following visual clues indicating that a leg raise was either definitely, possibly or not going to occur. Finally, clinical LBP was simulated by direct vibrotactile stimulation of the lumbar spine to a VAS threshold of 7/10.

The individual fMRI scans were independently referenced to anatomical markers and corrected for motion. Inter group analysis was performed using cluster-corrected thresholds of p< 0.05.

Results: During experimental pain stimulation, Non-copers showed significantly increased cortical activity as compared to Copers. Similar findings were evident when SLR was anticipated. The areas of increased cortical activity were primarily regions known to be involved in affective pain interpretation suggesting heightened activity.

When clinical LBP was simulated, the outcome was strikingly different with the Copers showing increased cortical activity particularly in the dorsolateral prefron-tal cortex and regions associated with cognitive pain processing and inhibition of subcortical pain pathways.

Discussion: This study shows that in patients with CLBP and illness behaviour cortical pain processing is abnormal. The findings suggest that possibly the abnormal behaviour shown by such patients may be due to failure of cognitive inhibitory pain pathways. It is possible that these abnormalities might respond to either pharmacological or psychological treatment.

Correspondence should be addressed to: Sue Woodward, Secreteriat, Britspine, Vale Clinic, Hensol Park, Vale of Glamorgan, CF72 8JY Wales.

1 Waddell et al Spine1980:5;117–125. Google Scholar