Evidence for shared pain mechanisms in osteoarthritis, low back pain, and fibromyalgia.

Denne nevner at mange smertelidelser har samme smertemekanisme som utgangspunkt: lavere nivå av intern smertedemping og central sensitering. De reagerer kraftigere på nococetive signaler som andre ikke reagerer så mye på.


Osteoarthritis (OA), low back pain (LBP), and fibromyalgia (FM) are common chronic pain disorders that occur frequently in the general population. They are a significant cause of dysfunction and disability. Why some of these chronic pain disorders remain localized to few body areas (OA and LBP), whereas others become widespread (FM) is unclear at this time. Genetic, environmental, and psychosocial factors likely play an important role. Although patients with OA, LBP, and FM frequently demonstrate abnormalities of muscles, ligaments, or joints, the severity of such changes is only poorly correlated with clinical pain. Importantly, many patients with these chronic pain disorders show signs of central sensitization and abnormal endogenous pain modulation. Nociceptive signaling is actively regulated by the central nervous system to allow adaptive responses after tissue injuries. Thus, abnormal processing of tonic peripheral tissue impulse input likely plays an important role in the pathogenesis of OA, LBP, or FM. Tonic and/or intense afferent nociceptive barrage can result in central sensitization that depends on facilitatory input from brainstem centers via descending pain pathways to the spinal cord. Abnormal endogenous control of these descending pathways can lead to excessive excitability of dorsal horn neurons of the spinal cord and pain. Ineffective endogenous pain control and central sensitization are important features of OA, LBP, and FM patients.

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