Distinct quantitative sensory testing profiles in nonspecific chronic back pain subjects with and without psychological trauma

Abstract

Psychological trauma is associated with an increased risk for chronification of nonspecific chronic back pain (nsCLBP) independent of posttraumatic stress disorder (PTSD). However, the mechanisms underlying the role of psychological trauma in nsCLBP are less clear than in PTSD. Therefore, this study considered whether psychological trauma exposure (TE) is accompanied by specific alterations in pain perception. The study included 56 participants with nsCLBP and TE (nsCLBP-TE), 93 participants with nsCLBP without TE (nsCLBP-W-TE), and 31 pain-free controls. All participants underwent a thorough clinical evaluation. The standardized quantitative sensory testing protocol of the "German Research Network on Neuropathic Pain" was used to obtain comprehensive profiles on somatosensory functions in painful (back) and non-painful areas (hand). The protocol consisted of thermal and mechanical detection as well as pain thresholds, vibration thresholds, and pain sensitivity to sharp and blunt mechanical stimuli. Psychological trauma was validated by structured clinical interview. Trauma-associated symptom severity, anxiety, and depressive symptomatology were assessed by self-report questionnaires. Differences in somatosensory function were seen only for pressure pain thresholds. Compared with controls, nsCLBP-TE revealed hyperalgesia generalized in space with lower thresholds in painful and non-painful areas, whereas nsCLBP-W-TE demonstrated localized alterations with decreased thresholds only in the pain-affected area of the back (P ≤ 0.006). Our findings suggest an augmented central pain processing in nsCLBP-TE (alterations in painful and non-painful areas), whereas nsCLBP-W-TE show only local changes (alterations only in the painful area) suggesting regional sensitization processes. This finding might explain why TE without PTSD is associated with an increased prevalence of chronic pain.

Pain Catastrophizing and Anxiety are Associated With Heat Pain Perception in a Community Sample of Adults With Chronic Pain

“…38, 39 40 Previous studies suggest central pain processing, distinct from peripheral nociceptive input, may be responsible for mediating the effects anxiety has on pain perception. 41,42 For example, patients with chronic low back pain who had previously been exposed to a psychologically traumatic event reported higher anxiety, greater use of pain medications, and demonstrated hyperalgesia to deep pain modalities in both that nonsteroidal anti-inflammatory drugs and acetaminophen have no effect on HP perception, 51 but the effects gabapentinoids (ie, pregabalin, gabapentin), 52-54 tricyclic antidepressants (ie, desipramine), 55 and local anesthetics (topical lidocaine, oral mexiletine) are mixed. 56,57 In conclusion, the findings of this study extend the use of a standardized method for assessing HP in a sample of community-dwellings adults with chronic pain.…”

Evidence for Central Sensitization in Patients with Temporomandibular Disorders: A Systematic Review and Meta‐analysis of Observational Studies

“…Moreover, Park et al and Greenspan et al included males and females, which could lead to variations in the results because of hormonal differences that were not controlled among females performing the measurements during the same menstrual cycle . QST is considered an assessment toll to identify CS and has been used by many researchers investigating various musculoskeletal conditions . Moreover, they have demonstrated the ability to discriminate between central and peripheral sensitization…”

Psychological Trauma Exposure and Pain-Related Outcomes Among People with Chronic Low Back Pain: Moderated Mediation by Thought Suppression and Social Constraints

“…Although CLBP is influenced by biological, psychological, and social factors, the experience of psychologically traumatic life events appears to be a particularly potent risk factor for increased pain intensity, interference, and depression (3). The mechanisms linking trauma exposure to these pain-related outcomes, however, are not clear.…”