, Sensory-Motor Interaction (SMI) Center, School of Medicine, Aalborg University, Aalborg, Denmark
It is generally accepted that pain diagnosis and therapy should be mechanism based and hence pain assessment tools (pain biomarkers) should be sufficiently sensitive and advanced to provide such mechanistic information. Translating clinical observations to mechanisms and vice versa is not trivial, and tools to assess quantitatively the different phenomena are mandatory. This approach has provided new insight into how reorganization of the pain system is manifested in fibromyalgia and other chronic pain conditions. Common features across different pain patient populations have been identified utilizing this approach. Peripheral and central sensitization are important mechanisms for fibromyalgia (FM) and musculoskeletal pain conditions in general. Many similarities exist between different chronic musculoskeletal pain conditions. Musculoskeletal pain may transit from a localized pain problem through a regional representation to a widespread pain condition such as FM. As the pain condition transit from one to the other, more and more sensory abnormalities occur with many sensory abnormalities in FM. There is evidence that as well the intensity of ongoing pain as the duration of pain determine the degree of generalized hyperalgesia. This is important to realize as it underpins the importance of the ongoing nociception for the chronification process in conditions (e.g. osteoarthrosis) where the peripheral nociceptive drivers are known, whereas it is more complicated in, e.g. FM where the drivers are less obvious.
Such techniques for assessing the peripheral/central pain sensitization mechanisms in patients with FM and other patients with musculoskeletal pain have been developed and provide the opportunity to quantify pain mechanisms such as temporal summation, descending inhibition, spreading sensitization, and additional modality-specific hyperalgesic reactions. Such tools can help to phenotype patients with FM based on the role of the various pain sensitization mechanisms involved and have recently been used as tools to predict pain outcomes after pharmacological or surgical interventions in various groups of musculoskeletal pain conditions.
Relating clinical benefit of a given therapy with quantitative assessment of the pain sensitization mechanisms involved provides new opportunities for better diagnostics and hence for tailored and individualized management regimes.
Although assessed differently in specific tissues for various musculoskeletal pain conditions, the underlying mechanisms share common underlying features An example of similar mechanisms across chronic pain conditions could be cutaneous allodynia in neuropathic pain assessed by brush, which corresponds to pain evoked by weak muscle pressure in musculoskeletal pain and to pain provoked by a weak colonic distension in visceral pain. Another example can be facilitated temporal summation and impaired descending modulation across many different chronic pain conditions including fibromyalgia. This mechanistic understanding is of importance for developing better diagnostics and for implementing tailored pain management programs. The understanding that FM and other musculoskeletal conditions share common fundamental features has positioned FM as the one extreme end as opposed to, e.g. a myofascial pain problem at the other end. This has provided some new insight into the development of the sensitization processes from one extreme to the other. Some of the current available mechanistic human pain biomarkers translate back to animals, providing new possibilities for bridging findings between pre-clinical and clinical studies. Data on the clinical applicability are increasingly available.