The relationship between catastrophizing and altered pain sensitivity in patients with chronic low-back pain

Abstract

Changes in central pain processing have been shown in patients with chronic low back pain (cLBP). We used quantitative sensory testing (QST) methods to identify differences in pain sensitization between patients with cLBP (N=167) and healthy controls (N=33). Results indicated that, compared to healthy pain-free controls, cLBP patients showed increased sensitivity and greater painful aftersensations for mechanical pressure and pin prick stimuli and lower tactile spatial acuity in the two-point discrimination task (ps<.05). Then, we examined the role of pain catastrophizing as a mediator of the group differences in pain sensitization. We found that catastrophizing partially accounted for group differences in pressure required to produce moderate pain. Finally, we examined the relationship between pain sensitization, catastrophizing, and clinical pain among patients with cLBP. We found that catastrophizing and deep-tissue pressure pain were associated with greater pain intensity in the past month, week, and at the visit as well aslow back pain bothersomeness. Further, deep-tissue pressure pain mediated the associations between catastrophizing and both pain in the past month and low back pain severity. Taken together, these results indicate that not only do patients with cLBP demonstrate increased pain sensitization and decreased sensitivity to innocuous stimuli, but these changes are also linked with increased catastrophizing. Furthermore, both catastrophizing and sensitization are associated with increased clinical pain among cLBP patients.

Pain-free resting-state functional brain connectivity predicts individual pain sensitivity

“…We used a pre-registered, multicentre design and deployed a substantial sample size to perform a rigorous prospective validation of our predictive model. Therefore, the RPN-signature may serve as an objective neuromarker of interindividual differences and alterations in pain sensitivity [3][4][5] .…”

“…While heightened pain sensitivity is a characteristic for many pain conditions [3][4][5] , patterns of brain activity and connectivity are fundamentally distinct in experimentally evoked, acute and chronic pain 49 . A future, iterative research approach involving clinical populations promises to further improve the predictive capabilities and generalisability of the RPN-signature and may allow for assessing pain sensitivity even if reliable behavioural pain reports cannot be obtained.…”

“…P ain is a subjective, unpleasant sensory and emotional experience 1 that is highly variable across individuals 2,3 . Individual differences in pain perception are of key interest in clinical practice as altered pain sensitivity is both a characteristic and risk factor for many pain conditions [3][4][5] . In the past decades, brain imaging has revealed the richness and complexity of brain activity underlying both the acute pain experience 6 and pain sensitivity 7,8 .…”

Temporal aspects of endogenous pain modulation during a noxious stimulus prolonged for 1 day

“…Contrary to this, studies have found that CPM is not normalized when clinical pain is reduced (Petersen, Arendt-Nielsen, Simonsen, Wilder-Smith, & Laursen, 2015;Petersen, Simonsen, Olesen, Morch, & Arendt-Nielsen, 2019), indicating that other factors might interfere with the impairment of CPM. For example, studies have suggested that pain catastrophizing or sleep impairment can impair CPM and many of these factors are rarely assessed in mechanistic pain studies (Eichhorn, Treede, & Schuh-Hofer, 2018;Meints et al, 2019), which complicate the interpretation of these findings.…”

Individual Pain Sensitivity is Associated With Resting-state Cortical Activities in Healthy Individuals but Not in Patients With Migraine: A Magnetoencephalography Study

“…Pain sensitivity may determine the risk, severity, prognosis, and treatment e cacy of clinical pain [1,2].…”