Fibromyalgia Pain: Do We Know the Source?
Fibromyalgia Pain: Do We Know the Source?
Purpose of review: Fibromyalgia Syndrome (FMS) is a chronic pain condition of unknown origin. Multiple abnormalities have been described, including peripheral tissue and central nervous system changes. The relation of these mechanisms, however, is likely bidirectional. FMS pain clearly depends on peripheral nociceptive input as well as abnormal central pain processing. This review will focus on the role of peripheral nociceptive input for pain in FMS.
Recent findings: There is strong evidence for abnormal central pain processing in FMS. Sensitized spinal cord neurons in the dorsal horn are responsible for augmented pain processing of nociceptive signals from the periphery. In addition, glial activation, possibly by cytokines and excitatory amino acids may play a role in the initiation and perpetuation of this sensitized state.
Summary: Nociceptive input clearly plays an important role in FMS. Acute or repetitive tissue injury has been associated with FMS pain. Cytokines related to such injuries may be responsible for long-term activation of spinal cord glia and dorsal horn neurons, thus resulting in central sensitization. A better understanding of these important neuro-immune interactions may provide relevant insights into future effective therapies.
Chronic pain and tenderness exist as a continuum in the general population and the severity of these symptoms appears to be normally distributed with more women than men affected. In 1990 the American College of Rheumatology convened a group of experts to better characterize the large number of chronic musculoskeletal pain patients diagnosed with Fibrositis that crowded the offices of rheumatologists. The experts agreed on several criteria for the new syndrome Fibromyalgia, which captures this chronic pain population with excellent sensitivity and specificity. In addition, the new FMS criteria of widespread chronic pain (> 3 months) and tender points (≥ 11 of 18) provide a useful characterization of patients with chronic musculoskeletal pain for research studies. The use of the same FMS criteria for clinical practice, however, turned out to be problematic because chronic musculoskeletal pain patients fulfilling the FMS criteria differ mostly in symptom severity from pain patients who do not satisfy the same criteria. Although this criticism has led many physicians to question the usefulness of the FMS criteria for clinical practice, they nevertheless seem to capture the most afflicted patients. Similar to FMS, several other clinically important syndromes also represent extremes of a continuum of symptoms including hypertension and diabetes. The particular usefulness of the latter syndromes, however, relies on their ability to predict significant morbidity and mortality in large numbers of patients. Although in the past the diagnosis of FMS appeared only predictive for increased dysfunction and emotional distress, recent epidemiological studies provided important evidence for excessive mortality in patients with widespread chronic pain syndromes like FMS. These findings seem to support the relevance of FMS as a distinct clinical syndrome and provide impetus for the identification of relevant FMS pain mechanisms that may result in better diagnosis and treatments.
Abstract and Introduction
Abstract
Purpose of review: Fibromyalgia Syndrome (FMS) is a chronic pain condition of unknown origin. Multiple abnormalities have been described, including peripheral tissue and central nervous system changes. The relation of these mechanisms, however, is likely bidirectional. FMS pain clearly depends on peripheral nociceptive input as well as abnormal central pain processing. This review will focus on the role of peripheral nociceptive input for pain in FMS.
Recent findings: There is strong evidence for abnormal central pain processing in FMS. Sensitized spinal cord neurons in the dorsal horn are responsible for augmented pain processing of nociceptive signals from the periphery. In addition, glial activation, possibly by cytokines and excitatory amino acids may play a role in the initiation and perpetuation of this sensitized state.
Summary: Nociceptive input clearly plays an important role in FMS. Acute or repetitive tissue injury has been associated with FMS pain. Cytokines related to such injuries may be responsible for long-term activation of spinal cord glia and dorsal horn neurons, thus resulting in central sensitization. A better understanding of these important neuro-immune interactions may provide relevant insights into future effective therapies.
Introduction
Chronic pain and tenderness exist as a continuum in the general population and the severity of these symptoms appears to be normally distributed with more women than men affected. In 1990 the American College of Rheumatology convened a group of experts to better characterize the large number of chronic musculoskeletal pain patients diagnosed with Fibrositis that crowded the offices of rheumatologists. The experts agreed on several criteria for the new syndrome Fibromyalgia, which captures this chronic pain population with excellent sensitivity and specificity. In addition, the new FMS criteria of widespread chronic pain (> 3 months) and tender points (≥ 11 of 18) provide a useful characterization of patients with chronic musculoskeletal pain for research studies. The use of the same FMS criteria for clinical practice, however, turned out to be problematic because chronic musculoskeletal pain patients fulfilling the FMS criteria differ mostly in symptom severity from pain patients who do not satisfy the same criteria. Although this criticism has led many physicians to question the usefulness of the FMS criteria for clinical practice, they nevertheless seem to capture the most afflicted patients. Similar to FMS, several other clinically important syndromes also represent extremes of a continuum of symptoms including hypertension and diabetes. The particular usefulness of the latter syndromes, however, relies on their ability to predict significant morbidity and mortality in large numbers of patients. Although in the past the diagnosis of FMS appeared only predictive for increased dysfunction and emotional distress, recent epidemiological studies provided important evidence for excessive mortality in patients with widespread chronic pain syndromes like FMS. These findings seem to support the relevance of FMS as a distinct clinical syndrome and provide impetus for the identification of relevant FMS pain mechanisms that may result in better diagnosis and treatments.
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