Background: The cause of FMS is unknown, but compelling evidence implicates a pain amplification process, resembling allodynia, that involves pro-nociceptive neurochemicals like substance P [SP], nerve growth factor, and excitatory amino acids. It was reasonable to expect that fMRI of the central nervous system [CNS] might provide a resource for evaluating the anatomy and physiology of allodynic pain processing in FMS.  

Methods: An experimental system was developed to allow non-invasive fMRI of the brain to determine the CNS effects of graded stimulation of a typical TeP. FMS patients and demographically-matched healthy controls [HNC] were recruited. All had known levels of lumbar spinal fluid SP. Clinical measures of subjective pain, insomnia, depression, and functional ability were obtained. The pressure pain threshold [PPT] was pre-determined for each subject by algometry. A computer driven cutaneous electrical stimulator device [invented locally] used a random testing protocol to separately determine the heat sensory and heat pain thresholds. A semi-automated, air pressure-driven algometer [invented locally, safe for use with MRI] reproducibly delivered sequential sets of graded pressure stimuli to the right medial knee TeP while the subject was being continuously monitored by fMRI. These fMRI experiments were performed on a 1.9 T GE/Elscint Prestige MRI scanner located in the Research Imaging Center at the UTHSCSA. A T2-weighted, multiple slices, echo-planar, gradient-echo pulse sequence was used with the parameters of TR/TE/flip angle = 2000 ms/45 ms/90-deg, slice thickness = 6 mm, and image spatial resolution = 2.9 mm x 2.9 mm. The sequence for each of the 10 identically repeated test sets was: resting [i.e., no contact] for 30 seconds, non-painful pressure below the PPT for six seconds, resting for 30 seconds, painful pressure above the PPT for six seconds. The averaged resting fMRI signals were separately subtracted from the averaged signals obtained with each of the active stimuli. The resultant, stimulus-specific activation fMRI images were overlaid on the relevant MRI anatomic images to facilitate identification of the activated CNS structures.

Results: Pressure applied to the medial knee TeP produced distinct fMRI images, indicating stimulus-induced changes in CNS blood flow and/or metabolic function within the brains of both HNC and FMS. Involved brain areas included thalamus, caudate nucleus, supplemental motor area in the paramedial cortex of the frontal lobe, sensory cortex, visual cortex, and cerebellum. Dramatic, stimulus-dependent, differences in the localization and in the magnitude of the CNS responses readily distinguished FMS from HNC [examples will be shown]. The CNS responses of FMS subjects were substantially more intense and distinctively more bilateral than those of the HNC. Correlations of the fMRI results with key clinical and laboratory variables will be discussed.

Presented at the National Fibromyalgia Research Association's Subgroups in Fibromyalgia Symposium, September 26-27, 1999, in Portland, Oregon.