Giesecke T, Nachemson A, et al. “Evidence of Augmented Central Pain Processing in Idiopathic Chronic Low Back Pain. (2004) Arthritis and Rheumatism 50(2) 2/2004; pp613-623.
Methods | Results | Discussion
In 2004, famed author and researcher Alf Nachemson et al published the results of a preliminary investigation into the role augmented central pain processing (also known as central sensitization) played with regard to the perception of pain as experienced by a group of chronic back pain patients, which were diagnosed with idiopathic back pain--i.e., their imaging reveals no annular tears, disc herniations, stenoses, or any other detectable abnormality--nothing seemed to be wrong.
The reason I chose this study--very small cohort notwithstanding--is because it was only the second study in history to use functional MRI (fMRI) to visualize what was going on in the brains of these chronic pain patients before, during, and after they were exposed to a painful stimulus. Then (to make this study even cooler), fMRI was performed on normal subjects that were exposed to the same painful stimulus.
An attempt was made to gather a cohort of consecutive patients all of whom suffered either chronic low back pain of unknown origin (CLBP) or fibromyalgia syndrome (FMS). Although the consecutive pooling of patients didn't work out, groups were gathered that consisted of 11 patients with CLBP, 16 patients with FMS and 11 control subjects brought in from a newspaper ad.
Before the experiment, all patients submitted to self-report questionnaires, which included Center for Epidemiological Studies Depression Scale (CES-D), State-Trait Personality Inventory (STPI), the short form of the McGill pain questionnaire (SF-MPQ). They also made pain diagrams and were specifically asked about the presence of "tender points” in any one of the 18 different regions of the body that these tender points have been known to exist. (> 11 = FMS).
In order to quantify the magnitude of pain sensation in all patients, a thumb-nail compression device (who’s efficacy for precisely testing pain had been proven in the past [x]) was constructed. When started, this devise would "pinch" or clamp-down upon the thumbnail of the group members with any desired degree of pressure. In other words, the researchers wanted to see how the different groups of patients would perceive the same amount of pinch/pain.
For only the second time in history, functional MRI scans of the group's brains were made before, during and after the "pinching/pain" event in order to elucidate just what region(s) of the brains were "lighting up" (or showing the activity of pain perception).
"Both patient groups (CLBP and FMS) reported significantly more clinical pain on the SF-MPQ as compared with that reported by the controls (subjects without pain)." With regard to pain magnitude, there was no difference between that reported by the CLBP versus the FMS.
Tender Points: The FMS patients reported a greater number of "tender points" when compared to both the CLBP group and healthy controls.
Distress (depression / anxiety): With regard to psychological distress, the FMS group displayed significantly higher levels when compared to the healthy controls. Although there was a trend toward higher psychological distress in the CLBP group, there was not enough statistical evidence to confirm its existence.
fMRI Testing: When each of the three groups was exposed to pain (i.e., the 2 kg of pressure on the thumbnail), the brains of both the FMS and CLBP light up like crazy! More specifically, a mere 2 kg of nail-pressure caused multiple regions in the brains to light-up (indicating pain was being experienced), including the somatosensory cortex (multiple regions), the parietal lobe, and the cerebellum. In the healthy control group, however, there was only a faint signal increase in one region of the somatosensory cortex--i.e., there was no activity in the parietal lobe or cerebellum.
This small pilot study--which was only the second in history to use functional MRI (fMRI) as a means to confirm the pain response in the brain--suggested that the phenomenon of central pain amplification (a.k.a. central sensitization) is alive and well in patients of whom suffer chronic back pain and/or fibromyalgia syndrome, but not present in a group of normal, non-pain sufferers.
More precisely, it is theorized that a "modification" has occurred within the brains of chronic pain and fibromyalgia patients. And this "modification" has allowed such patients to become more "sensitive" to the perception of pain--both with regard to the intensity and duration of pain. This phenomenon was illustrated in the experiment by the fact that a relatively small amount of thumbnail pressure (2 kg) produced moderate pain in every single patient that suffered either chronic back pain or fibromyalgia, yet control subjects felt no sensation of pain at all.
This was not the first study that described the phenomenon of nervous system sensitization. We know from the work of Woolf et al (Harvard medical), that a repeated or particularly intense noxious stimuli (such as that of a compressive disc herniation) can result in a sensitization of the nociceptive system of some patients. In other words, in some patients the system that delivers the sensation of pain to the brain has become too easily triggered. That is, even in the absences of ongoing tissue injury/inflammation and even though the original problem/injury has long been healed, the nerves of the nociceptive system still fire and a erroneously send pain messages to the brain. [Latremoliere & Woolf – 2009]
And chronic pain is not the only abnormal human sensation invoked by the phenomenon of central sensitization; we also know from these same researchers that central sensitization contributes to neuropathic pain ; inflammatory pain [26,274,395]; migraine , fibromyalgia [6,68,301-303] and irritable bowel syndrome. as well.
The $64,000 question that remains is how do you treat central sensitization? Nachemson et al states that tricyclic antidepressants are more effective in the management of centralized pain than other medications such as nonsteroidal anti-inflammatories and/or opioids.
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