2015
DOI: 10.1097/ajp.0000000000000194
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Clinical Value of Serum Neuroplasticity Mediators in Identifying the Central Sensitivity Syndrome in Patients With Chronic Pain With and Without Structural Pathology

Abstract: Neuroplasticity mediators could play a role as screening tools for pain clinicians, and as validation of the complex and diffuse symptoms of these patients.

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Cited by 54 publications
(83 citation statements)
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“…Only the main effect observed was interaction between timepoint and orofacial pain on the BDNF levels, with the levels of this mediator returning to baseline levels 7 days after the end of tDCS treatment. Also, a study involving patients with central sensitivity syndrome showed an increase in serum BDNF levels compared to control subjects, suggesting that this neuroplasticity mediator could be a screening tool for pain clinicians …”
Section: Discussionmentioning
confidence: 99%
“…Only the main effect observed was interaction between timepoint and orofacial pain on the BDNF levels, with the levels of this mediator returning to baseline levels 7 days after the end of tDCS treatment. Also, a study involving patients with central sensitivity syndrome showed an increase in serum BDNF levels compared to control subjects, suggesting that this neuroplasticity mediator could be a screening tool for pain clinicians …”
Section: Discussionmentioning
confidence: 99%
“…Symptoms of CS include allodynia, hyperalgesia, expansion of the receptive field beyond the area of peripheral nerve supply, and prolonged pain after a stimulus has been removed (Latremoliere & Woolf, ). A number of CS‐related biological mechanisms have been identified, including dysregulation of ascending and descending tracks in the central nervous system (Ren & Dubner, ; Yunus, ; Heinricher et al., ; van Wijk & Veldhuijzen, ; Kindler, Bennett, & Jones, ); over‐activation of glial cells, resulting in the release of pro‐inflammatory cytokines (Ji, Berta, & Nedergaard, ; Loggia et al., ; Nijs et al., ); dysfunction of the stress system, including the hypothalamic–pituitary–adrenal axis (Van Houdenhove & Luyten, ); decreased production of pain‐inhibiting neurotransmitters, and increased production of pain‐augmenting neurotransmitters, including excess production of brain‐derived neurotropic factor (BDNF) (Caumo et al., ; Deitos et al., ; Nijs, Meeus et al., ; Phillips & Clauw, ; Trang, Beggs, & Salter, ).…”
Section: Central Sensitizationmentioning
confidence: 99%
“…Subjective evidence for central‐related pain hypersensitivity has been demonstrated by differences in self‐reported pain severity ratings to heat, cold, electrical, and pressure stimuli between subjects with and without pain disorders (Yunus, ). Objective measures of CS, including brain imaging (Robinson, Craggs, Price, Perlstein, & Staud, ; Walitt, Ceko, Gracely, & Gracely, ), cortical excitability parameters assessed by transcranial magnetic stimulation (TMS), and levels of brain‐derived neurotrophic factor (BDNF) (Caumo et al., ; Deitos et al., ) have demonstrated biological differences between control subjects and those with CS‐related pain disorders.…”
Section: Central Sensitizationmentioning
confidence: 99%
“…Conditions where a noxious stimulus is no longer present and shares this phenomenon includes: fibromyalgia, irritable bowel syndrome, chronic fatigue syndrome, temporomandibular joint disorder, chronic whiplash, and others (Deitos et al., ; Robinson, Durham, & Newton, ). These conditions together have been described as a group called central sensitivity syndromes (CSS; Yunus, ).…”
Section: Introductionmentioning
confidence: 99%