Recognition of central sensitization in patients with musculoskeletal pain: Application of pain neurophysiology in manual therapy practice

Nevner det aller meste om sentral sensitering og hvordan de gjenkjennes i klinisk praksis.

http://www.thblack.com/links/RSD/ManTher2010_15_135_CSinMusculoskelPain-PainNeurophys.pdf

«Even with acute pain the nervous system undergoes some changes. When tissue is damaged and pain persists for a few days with adaptation of unimodal nociceptors, the responsiveness of polymodal nociceptive endings is enhanced by substances released from various sources (i.e. serotonin released by platelets) (Purves et al., 1997). This process is called primary hyperalgesia or peripheral sensitization of nociceptors, and represents a protective action by the human body in order to prevent further use of damaged structures and consequent further damage of the traumatized and surrounding tissues.»

«Secondary hyperalgesia refers to increased responsiveness of dorsal horn neurons localized in the spinal segments of the primary source of nociception.»

«Central sensitization is defined as an augmentation of responsiveness of central neurons to input from unimodal and polymodal receptors (Meyer et al., 1995). Central sensitization encompasses altered sensory processing in the brain (Staud et al., 2007), malfunctioning of descending anti-nociceptive mechanisms (Meeus et al., 2008), increased activity of pain facilitatory path- ways, temporal summation of second pain or wind-up (Meeus and Nijs, 2007; Staud et al., 2007), and long-term potentiation of neuronal synapses in the anterior cingulate cortex (Zhuo, 2007).»

«The presence of central sensitization in patients with musculoskeletal pain implies an increased complexity of the clinical picture (i.e. an increase in unrelated symptoms and hence a more difficult clinical reasoning process) (Nijs et al., 2009), as well as decreased odds for a favorable rehabilitation outcome (Jull et al., 2007).»

«Central sensitivity syndromes is a term first used by Yunus in 2000 to describe a group of overlapping conditions bound by a common pathophysiological mechanism of central sensitization (Yunus, 2007a).»

«Another example is chronic non-specific low back pain. Some studies provided evidence in support of the presence of central sensitization in patients with non-specific chronic low back pain (Giesecke et al., 2004; Schmidt-Wilcke et al., 2006), while others refute such an association (Hoffman et al., 2005; Julien et al., 2005). It is concluded that central sensitization is present in some cases of chronic non-specific low back pain, possibly representing one of the subgroups of this frequent musculoskeletal disorder (Wand and O’Connell, 2008).»

«The myofascial variety within the heterogeneous group of temporomandibular disorders is also characterized by central sensitization (Yunus, 2007a). Likewise, regional chronic pain conditions that present with tender and/or trigger points in the absence of structural pathology (frequently referred to as myofascial pain syndrome) should alert the manual therapist to the possibility that central sensitization is determining the clinical picture (Yunus, 2007a). However, to our knowledge available evidence in support of central sensitization in patients with myofascial pain syndrome is limited to chronic whiplash associated disorders, temporoman- dibular disorders and chronic non-specific low back pain.»

«Furthermore, various subgroups of headache, chronic tension-type headache (Langemark et al., 1993; Pielsticker et al., 2005) and migraine (Burnstein et al., 2000; Weissman-Fogel et al., 2003) can be viewed as central sensitivity syndromes. Finally, rheumatoid arthritis and osteoarthritis are examples of local musculoskeletal disorders possibly causing continuous activation of polymodal nociceptors that initiate or sustain central sensitization (Yunus, 2007a).»

table1

«Central sensitization entails much more than generalized hypersensitivity to pain: it is characterized by an increased responsiveness to a variety of stimuli including mechanical pressure (Desmeules et al., 2004), chemical substances (Morris et al., 1997), cold temperature (Kasch et al., 2005), heat temperature (Meeus et al., 2008), electrical stimuli (Banic et al., 2004; Desmeules et al., 2004), stress, emotions, and mental load. The clinical picture is suggestive of a general intolerance to all kinds of physical and emotional stressors and hence a large decreased load tolerance of the human body in general.»

table2

«An ongoing source of peripheral nociception is required before the process of peripheral sensitization can establish central sensitization (Nijs and Van Houdenhove, 2009). Tissue injury healing and focal pain recovery should occur as soon as possible to prevent development of central sensitization (Vierck, 2006).»

«One of the main characteristics of central sensitization in patients with musculoskeletal pain is a generalized rather than a localized decrease in their pressure pain threshold. Here, ‘generalized’ implies more than a segmental spreading of the symptom area, in that it means that the increased sensitivity is localized at sites segmentally unrelated to the primary source of nociception (e.g. the lower limbs in case of a whiplash trauma).»

«Lower pressure pain thresholds at symptomatic areas most often represent primary hyperalgesia due to sensitized polymodal noci- ceptors within injured musculoskeletal structures. By measuring pressure pain thresholds outside the area of primary nociception, widespread hyperalgesia or secondary hyperalgesia can be detec- ted.»

«In cases of secondary hyperalgesia, a reduced pressure pain threshold in the various tissues innervated by the same segment (or two neighboring segments) can be detected.»

«Findings of numerous areas of hyperalgesia at sites outside and remote from the symp- tomatic site, together with a non-segmental general decrease in pressure pain threshold, may imply a generalized hyperexcitability of central nociceptive pathways (Sterling et al., 2004).»

«Pressure algometry provides a reliable and valid measure of the pressure pain threshold (Vanderweeen et al., 1996; Farasyn and Meeusen, 2003). In the absence of a pressure algometer, manual palpation can be used. Even when a manual therapist is not sus- pecting central sensitization, the finding of generalized hypersen- sitivity to manual palpation during routine clinical examination should alert the clinician.»

«Like every other tissue in the human body, peripheral nerves and nervous tissues (including connective tissue) themselves can become hypersensitive to mechanical stimuli such as tension and pressure.»

«Besides the passive tests listed above (Table 3), altered sensory processing can be demonstrated during exercise. Pain thresholds increase during physical activity in healthy individuals and can stay augmented for up to 30 min post-exercise. This is the result of endogenous opioid release (Koltyn and Arbogast, 1998) and related activation of several (supra)spinal anti-nociceptive mechanisms such as the adrenergic and serotonergic pathways (Millan, 2002).»

 

«Stress (particularly when chronic) may well trigger lower pain thresholds. This was demonstrated by Suarez-Roca et al. (2008) who reported reduced GABA neurotransmission and consequent hyperalgesia in rats after repeated forced swimming stress.»

«A constant or decreased pain threshold during and following exercise suggests malfunc- tioning of these anti-nociceptive mechanisms (Whiteside et al., 2004) and hence central sensitization. An abnormal pain threshold response to exercise should be regarded as one of the many possible signs of central sensitization.»

table4

 

 

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