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.
How much sway is significant for a traditional Romberg test has always been open to interpretation and debate. Prospective and detailed clinical examination of 50 consecutive patients of cervical myelopathy was performed. For the walking Romberg sign, patients were asked to walk five metres with their eyes open. This was repeated with their eyes closed. Swaying or inability to complete the walk with eyes closed was interpreted as a positive walking Romberg sign. This test was compared to common clinical signs to evaluate its relevance. Whilst the Hoffman’s reflex (79%) was the most prevalent sign, the walking Romberg sign was present in 74.5% of the cases. The proprioceptive deficit was evident by only using the walking Romberg in 21 out of 38 patients that had a positive Romberg sign. Though not statistically significant, the mean 30 metre walking times were slower in patients with standing Romberg test than in those with positive walking Romberg test and fastest in those with neither of these tests positive. The combination of either Hoffman’s reflex and/or Walking Romberg was positive in 96% of patients. The walking Romberg sign is more useful than the standing Romberg test as it shows evidence of a pro-prioceptive gait deficit in significantly more patients with cervical myelopathy than is found on conventional neurological examination. The combination of Hoffman’s reflex and walking Romberg sign has a potential as useful screening tests to detect clinically significant cervical myelopathy.
The purpose of the study is to assess changes in cortical activity in chronic low back pain patients with and without illness behaviour.
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.
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.