Somatosensory dysfunctin in fibromyaligia : implications for pathophysiological mechanisms

Abstract: Fibromyalgia is a chronic pain syndrome characterized by generalized pain, tenderness, disturbed sleep and pronounced fatigue. The pathophysiology is unknown but peripheral mechanisms (i.e., muscle ischemia) as well as central mechanisms (dysfunction in endogenous pain modulation) have been implicated. The aim of this thesis was to increase the understanding of pathophysiological mechanisms in fibromyalgia by studying the location of tenderness, the perception of somatosensory stimuli, the relationship between ongoing pain and perception of somatosensory stimuli and, furthermore by studying the modulation of somatosensory perception during isometric muscular contraction, vibratory stimulation and heterotopic noxious conditioning stimulation. Methods: Thirty-one female fibromyalgia patients, all meeting the classification criteria proposed by the American College of Rheumatology, and 26 healthy females participated in the study. Von Frey filaments were used to test low-threshold mechanoreceptive function. Pressure pain sensitivity was assessed with a pressure algometer and thermal sensitivity with a Thermotest. A computerized isokinetic system was used for determination of maximalisometric strength and force registration during contraction. Vibratory stimulation (lOOHz) was delivered by an electromechanical vibrator and a submaximal effort tourniquet test was used for heterotopic noxious conditioning stimulation. Skin hypoesthesia was induced by a local anesthetic cream (EMLA). Results: Fibromyalgia patients exhibited a generalized, non-modality specific increase in pain sensitivity and a further increase in sensitivity to pressure pain and innocuous warmth in areas with high intensity of spontaneous ongoing pain. The increased pressure pain sensitivity in fibromyalgia patients was located deep to the skin but not restricted to muscle tissue. Anabnormal increase in pressure pain sensitivity over the contracting muscle during and following isometric contraction was demonstrated in fibromyalgia patients, as opposed to a decrease insensitivity in healthy controls. No abnormalities were found in the endogenous modulation of somatosensory perception by activity in large myelinated fibers set up by vibratory stimulation. Decreased sensitivity to innocuous thermal stimulation was seen during and following the tourniquet test in both groups alike, but no modulation of pressure pain sensitivity was found in fibromyalgia patients during the tourniquet test, as opposed to healthy controls, suggesting a dysfunction of 'diffuse noxious inhibitory controls'. Conclusions: The lack of normal modulation of pressure pain sensitivity in fibromyalgia patients during isometric contraction could be explained by peripheral as well as central mechanisms. However, the findings that fibromyalgia patients had a generalized, non-modality specific increase in pain sensitivity, only partially related to the intensity of ongoing pain in the assessed area, and that the increased pressure pain sensitivity was not restricted to muscle tissue support central mechanisms. The absence of normal inhibition of pressure pain sensitivity during heterotopic noxious conditioning stimulation in fibromyalgia patients can only be explained by a central nervous system dysfunction.