Previous research has suggested that when subjected to painful lumbar stimulation, chronic low back pain (CLBP) patients with illness behaviour (IB) are unable to effectively engage a sensory modulation system utilised by patients without IB¹. Furthermore, reduced insular cortex volume in CLBP patients with IB, may compound this problem².

Pain Management Programs (PMP) has demonstrated reductions in IB and disability associated with chronic pain conditions. This current study aims to assess whether the pattern of cerebral response to pain in IB patients could be normalised by participation in a PMP.

12 patients with CLBP and IB (>4/5 Waddell signs present) were recruited prior to attending a 16-day PMP. FMRI scanning occurred prior to (PrePMP) and upon completion of the PMP (PostPMP). 8 healthy volunteers (HC) were scanned once.

As in previous research, painful stimuli consisted of intense electrical stimulation delivered bilaterally to the lower back. The presentation of 3 colours indicated the likelihood of receiving 10second stimulation to the lower back (Always, Never and Maybe).

IB scores were significantly reduced PostPMP (p <0.05). FMRI group activation maps for the Always condition revealed PostPMP patients increased activation in posterior regions, areas similarly activated by HC. For the Maybe condition, compared to PrePMP group, HC demonstrated greater activation in precuneus and middle and inferior frontal regions. Compared to their pre-treatment selves, PostPMP patients demonstrated increased activation in posterior and frontal regions.

The results demonstrate that completion of a 16-day PMP leads to alteration in the brain's response to painful low back stimulation in CLBP patients with IB. Increased activation is seen in regions associated with the top-down modulation of pain. The response is similar to that seen in HC, and greater than before PMP confirming that the PMP process facilitates the utilisation of more normal coping pathways in response to CLBP.

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.