Abstract
The transition from acute to chronic musculoskeletal pain is not well understood. To understand this transition, it is important to know how peripheral and central sensitization are manifested and how they can be assessed. A variety of human pain biomarkers have been developed to quantify localized and widespread musculoskeletal pain. In addition, human surrogate models may be used to induce sensitization in otherwise healthy volunteers. Pain can arise from different musculoskeletal structures (e.g. muscles, joints, ligaments, or tendons), and differentiating the origin of pain from those different structures is a challenge. Tissue-specific pain biomarkers can be used to tease these different aspects. Chronic musculoskeletal pain patients in general show signs of local/central sensitization and spread of pain to degrees which correlate to pain intensity and duration. From a management perspective, it is therefore highly important to reduce pain intensity and try to minimize the duration of pain.
Introduction
Musculoskeletal pain is a major clinical problem and further research into peripheral and central neurobiological mechanisms is required to improve understanding, diagnosis and management. Peripheral and central sensitization are important mechanisms for musculoskeletal pain conditions. This paper will focus on the clinical manifestations of localized and widespread musculoskeletal pain, and the methods to assess the underlying mechanisms involved. Several experimental techniques to assess deep-tissue hyperalgesia, temporal summation of pain, descending pain control, and referred pain are available. These methods reflect different mechanisms relevant for symptoms seen in patients (e.g. spreading of pain, tenderness, widespread hyperalgesia) and offer additional information to be used for revisions of treatment strategies. A progressive sensitization of central mechanisms (central sensitization) is a potential mechanism involved in the transition from acute to chronic pain, and needs to be assessed by appropriate biomarkers.
This paper will follow the translational pain research strategy in the presentation where basic animal science is translated into human experimental pain models for investigating fundamental pain mechanisms in healthy volunteers. As healthy volunteers do not behave as for example a sensitized chronic patient, pain models are needed where the healthy volunteers can transiently be transformed into a surrogate model of a patient, i.e. the models act as a proxy for clinical symptoms where mechanisms such as peripheral or central sensitization can be mimicked. Finally, the discovered mechanisms can be further investigated and possibly modulated in individuals with musculoskeletal pain problems.
Basic aspects of muscle pain
Muscle pain presents as localized, regional, or widespread pain. As the clinical pain condition transits from one to the other, more and more sensory abnormalities occur with widespread hyperalgesia in chronic conditions. There is evidence from the literature that the intensity of ongoing pain2 as well as the duration of pain determine the degree of generalized muscle hyperalgesia. This is important to note as it underpins the importance of the ongoing nociception for the chronification process.
The myofascial pain syndrome is an example of a regional muscle pain condition characterized by localized tenderness and pain caused by active myofascial trigger points. The affected muscles often display increased fatigability, stiffness, subjective weakness, pain in movement, and restricted range of motion that is unrelated to joint restrictions.
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