The mechanisms underlying
chronic pain states, including
osteoarthritis, differ from those underlying
acute pain. In
chronic pain states, central nervous system (CNS) factors often play a particularly prominent role. In many individuals with
chronic pain,
pain can occur with minimal or no evidence of ongoing nociceptive input. Medical subspecialties have applied a wide-range of labels to these
pain conditions including
fibromyalgia,
irritable bowel syndrome and
interstitial cystitis to name just a few. These same CNS processes can augment or magnify
pain when there is ongoing nociceptive input, as in conditions such as
osteoarthritis or autoimmune disorders. The hallmark of these 'centrally driven'
pain conditions is a diffuse hyperalgesic state identifiable though the use of experimental sensory testing, that has been corroborated by functional neuroimaging. Characteristic symptoms of these central
pain conditions include multifocal
pain,
fatigue, poor sleep, memory complaints and frequent co-morbid mood and
anxiety disorders. In contrast to acute and peripheral
pain states that are responsive to non-steroidal anti-inflammatory drugs (
NSAIDs) and
opioids, central
pain conditions respond best to CNS neuromodulating agents, such as
serotonin-
norepinephrine reuptake inhibitors (
SNRIs) and
anticonvulsants. While
osteoarthritis is generally considered a peripherally mediated
pain state, a subset of these patients also manifests centrally driven
pain characteristics. Thus,
osteoarthritis can also be thought of as a "mixed"
pain state and this requires a more tailored approach to treatment.