The current definition of central sensitisation (CS) pain describes CS as manifesting in a generalised hyper-sensitivity of the somatosensory system (Nijs et al., 2010). We are familiar with the current clinical guidelines to help us identify CS as a predominant pain mechanism in our musculoskeletal pain patients (Nijs et al., 2014, 2015) with the assistance of the central sensitisation inventory (CSI) (Mayer et al., 2012, Neblett et al., 2013). However, patients sometimes present with CS and significant elements of sensory hypo-sensitivity. This may be local, such as the reduced tactile acuity over the painful area in chronic low back pain observed by Wand et al. (2011). Alternatively the hypo-sensitivity may be widespread (Egloff et al., 2012). Such examples from the clinic are described in the following brief case studies:
1. A 49 year old female, diagnosed with bilateral lower limb Complex Regional Pain Syndrome (CRPS) following lumbar surgery 5 years ago. She now presents with full body widespread pain with mild and episodic colour changes in her feet. Her CSI score is 63 on Gabapentin (severe CS). She exhibits motor extinction as described by McCabe (2011) whereby she becomes increasingly less able to move her legs when she cannot see them. Sensory hypo-sensitivity may play a role in motor extinction. Her bilateral leg pain increases when she cannot see her feet and diminishes as soon as she looks at them (similar to work described by Wand et al., 2012 in chronic low back pain in which pain diminished with visual feedback of the lumbar region). In sitting, she has tactile awareness in her anterior thighs when visualising the skin being touched but cannot feel the same applied touch when a board is placed between her knees to block the visual feedback. She also cannot feel the touch when the board is replaced by a mirror and bilateral touch is applied to both thighs. Even mirror visualisation does not apparently assist her ability to feel tactile input, but this may be due to her difficulty reaching the stage of ownership of the body reflection image, as discussed by McCabe (2011). On assessment of her Sensory Profile, using the Adolescent / Adult Sensory Profile (AASP) (Brown et al., 2001) (currently being validated for use in CS pain), she tests extremely positively for trait sensory hypo-sensitivity and within normal range for trait sensory hyper-sensitivity (i.e. not abnormally hyper-sensitive as a trait characteristic). Yet when her body is touched without warning, such as her hip, shin or foot, she experiences immediate pain amplification. This may relate to the threat perception model recently described again by Moseley and Butler (2015), and may be associated with the history of physical abuse in her adult lifetime (Seery et al., 2010; Egloff et al., 2012).
2. A 45 year old female presents with 4 years of chronic bilateral facial pain since visual correction laser surgery, averaging 7/10 on the visual analogue scale daily; tests have not identified any pathology nor pathogens; no widespread pain and no pattern of aggravating and easing factors. Her CSI score is 48 (moderate CS) on Gabapentin and she scores positively for trait sensory hypo-sensitivity on the AASP. She has diminished tactile acuity of two point discrimination on her cheeks and nose of 2.8 cm.
Individuals such as these cases appear to present with altered central pain processing in line with the clinical guidelines for CS, but exhibit a paradox of both hyper- and hypo-sensitivity. This paradox has been observed previously among researchers in psychiatry, primarily Mailis-Gagnon (see Mailis-Gagnon and Nicholson review, 2010) and subsequently Egloff et al. (2012). Mailis-Gagnon and Nicholson (2010) estimate a prevalence of sensory hypo-sensitivity to various sensory modalities in as many as 25-50% of chronic pain populations. They use the term non-dermatomal somatosensory deficits (NDSDs) which they define as, "unexplainable hypo-aesthesiae (e.g. to cutaneous or other sensory modalities) ipsilateral to the site of pain (or worse pain), which do not conform to the distribution of peripheral nerves or dermatomes" (Mailis-Gagnon and Nicholson, 2012; p. 1787). This definition overlaps with the definition of CS, in that the CS pain distribution is not anatomically plausible (Nijs et al., 2014, 2015).
Egloff et al. (2012) compared chronic pain patients with and without sensory hypo-sensitivity, or NDSDs. They recruited, from an in-patient pain centre, two groups of chronic pain patients, 90 without NDSDs and 90 with NDSDs in a hemi-body widespread distribution. None of the 180 participants tested positively for an identifiable nociceptive source of their chronic pain. Identification of CS pain also involves exclusion of specific neuropathic pain (Nijs et al., 2014). Although this was not documented, the definition of NDSDs itself excludes neuropathic pain because of the non-dermatomal pain distribution. Furthermore, neurological testing for reflexes and myotomes were reported as normal. It is therefore most likely that both groups had predominantly CS pain, which the authors described as “functional pain syndromes” (p. 1848), meaning pain without anatomical origin. The NDSD assessment for grouping included quantitative sensory testing, comparing both sides of the body to identify sensory hypo-sensitivity, although this was not described in detail. Both groups received musculoskeletal and psychosocial assessments and psychometric questionnaires.
The results show the non-NDSD (i.e. not hypo-sensitive) group contained significantly more patients with fibromyalgia (p<.001), non-specific chronic low back pain (p<.001) and atypical thoracic pain (p<.05), personality disorders (according to ICD-10 criteria, undescribed; p<.001) and no inciting traumatic event (56.7%). Conversely, nearly three quarters (74.4%) of the NDSD (hypo-sensitive) group reported an acute pain onset event and this was ipsilateral to the side of NDSD. Adult trauma and co-morbid post-traumatic stress disorder were significantly greater in the NDSD (hypo-sensitive) group (p<.001) and childhood trauma significantly greater in the non-NDSD group (p<.001). Both groups showed comparative levels of anxiety, depression and insomnia.
These observed differences between chronic pain groups likely to have predominantly CS, with and without sensory hypo-sensitivity, along with ongoing clinical enquiry, provoke an interesting question: Might there be two (or more) sub-groups within the CS population such as CS with 1) predominantly sensory hyper-sensitivity and 2) predominantly sensory hypo-sensitivity?
Furthermore, on the basis that altered sensory processing is closely associated with chronic pain, what might be the nature of such sensory sensitivity differences? Might they be a) trait characteristics of sensory hypo- or hyper-sensitivity to various sensory modalities, suggesting a normal or abnormal pre-morbid, generally stable characteristic? This would concur with studies describing ranges of trait sensitivity across populations, such as work described by Diatchenko et al., (2005) in the genetics of pain sensitivity; or might they be b) transient, “state” sensitivity alterations in various senses at the time of measurements resulting from post-morbid altered central pain processing and possibly influenced by the context of the testing. These differences might be similar in distinction to trait and state anxiety (Spielberger et al., 1970).
“Remind me where it is so I can feel it”
Either way, CS is commonly only associated with sensory hyper-sensitivity, based on the evidence to date. Not all non-neuropathic, non-nociceptive chronic pain patients (presumably with CS by definition) exhibit sensory hyper-sensitivity, identified using QST, such as seen in Egloff’s work above and in idiopathic neck pain (reviewed by Malfliet et al., 2015). Furthermore, Rehm et al. (2010) identified a subgroup (21.3%) of a large cohort of 3035 people with fibromyalgia (FM), which is characterised by CS, in which thermal and pressure pain sensitivity were absent. (However, painful prickling sensations were a dominant feature of this subgroup indicating other features of altered central pain modulation.) Only 58% of the whole cohort reported pressure pain sensitivity, which they reported as strong or very strong. Despite the participants fulfilling all the 2010 ARC criteria for FM (Wolfe et al., 2010), the variation in sensory profiles and symptom expression was diverse.
Rehm’s attempt to sub-group FM based on sensory profiles is admirable and substantiates the idea that CS populations may contain sub-groups based on different sensory profiles, including hypo-sensitivity profiles. On this basis, and as an additional comment, I endorse the use of terms such as altered central nociceptive processing, or even altered central somatosensory processing, instead of CS, which may represent a more encompassing view of sensory profiles across CS populations. Further research and discussions are warranted.
2016 Pain in Motion
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