Changes in the pain-sensing circuits of the spinal cord may contribute to a greater sensitivity to pain in patients with fibromyalgia, a study has found.
Spinal cord reflexes were more sensitive to pain in fibromyalgia patients than in those who didn’t have fibromyalgia, even though this response was not correlated with pain duration or tender points.
The study, “Can aberrant spinal nociception be a marker of chronicity of pain in fibromyalgia syndrome?” was published in the Journal of Clinical Neuroscience.
Chronic pain associated with fibromyalgia is rooted in a process of central sensitization, known to originate from the hyperexcitability of certain nerve cells in the spinal cord, specifically the dorsal horn neurons. These neurons process sensory information that is then transmitted to several brain regions, including those responsible for pain perception.
In this study, a team of researchers at All India Institute of Medical Sciences (AIIMS) in India were interested in studying the role of a different spinal cord pathway in pain processing related to fibromyalgia — the nociceptive flexion reflex (NFR), or withdrawal reflex. This is an automatic response where a painful stimuli activates an effector response to protect the body from potential damage. An NFR can occur, for instance, when a person accidentally touches something hot and almost instantly withdraws his or her hand.
The NFR is easily measurable in a clinical setting, and has been extensively used as an objective measure of an individual’s pain experience, as well as a marker of central nervous system hyperexcitability.
Prior studies have reported that patients with fibromyalgia have alterations in the NFR that are consistent with an enhanced response to pain.
To explore more deeply the role of this spinal cord circuitry for fibromyalgia, the researchers investigated what the NFR threshold is and its association with pain duration and tender points in 103 patients with fibromyalgia. They compared these data with NFR measures from 74 healthy individuals used as controls. Patients were recruited at the rheumatology clinic of AIIMS.
To measure NFR, the researchers applied a low-intensity electrical stimulus over the skin at a sensory nerve of the calf (sural nerve) and recorded the subsequent reflex response (electrical activity) in a muscle in the back thigh.
Data showed that patients’ reflexes were triggered by stimulus of significantly lower intensity than healthy individuals. In other words, the threshold for NFR activation was lower, indicating this circuit was more sensitive to pain in the context of fibromyalgia.
Unlike threshold, other NFR parameters, such as latency (the time interval between the stimulus and the reflex) and amplitude, were similar between the two groups, and no significant correlation was found between NFR thresholds and pain duration or tender points.
“Results of the present study show that there is decrease in NFR threshold in patients with [fibromyalgia]. These results indicate insufficient function or a reduced top down effect of the spinal nociceptive system in [fibromyalgia],” the researchers wrote.
“Future investigation may elucidate how ethnic differences in NFR relate to clinical pain states or can explore the underlying mechanisms contributed to ethnic differences by examining the involvement of descending pain modulatory pathways,” they added.
In addition, they stress that the NFR may be used as a potential diagnostic tool for studies investigating therapeutic effects on spinal pain processing in fibromyalgia.