Changes in central pain processing have been shown in patients with chronic low-back pain (cLBP). We used quantitative sensory testing methods to identify differences in pain sensitization between patients with cLBP (N = 167) and healthy controls (N = 33). Results indicated that, compared with 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 2-point discrimination task (ps < 0.05). 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 as low-back pain bothersomeness. Furthermore, 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.
Chronic low-back pain patients demonstrate greater pain sensitization and poorer spatial acuity, changes linked with greater catastrophizing. Catastrophizing and sensitization are also associated with greater clinical pain.
aDepartment of Anesthesiology and Pain Medicine, Brigham and Women's Hospital, Harvard Medical School, Chestnut Hill, MA, United States
bAthinoula A. Martinos Center for Biomedical Imaging, Massachusetts General Hospital, Harvard Medical School, Charlestown, MA, United States
cDepartment of Psychiatry, Massachusetts General Hospital, Harvard Medical School, Charlestown, MA, United States
dDepartment of Anesthesiology, Center for Pain Research, University of Pittsburgh, Pittsburgh, PA, United States
eBeth Israel Deaconess Medical Center, Harvard Medical School, Boston, MA, United States
Corresponding author. Address: Department of Anesthesiology and Pain Medicine, Brigham and Women's Hospital, Harvard Medical School, 850 Boylston St, Ste 308, Chestnut Hill, MA 02467, United States. Tel.: 857-307-5405; fax: 617-525-7900. E-mail address: firstname.lastname@example.org (S.M. Meints).
Sponsorships or competing interests that may be relevant to content are disclosed at the end of this article.
Received June 12, 2018
Received in revised form October 24, 2018
Accepted December 04, 2018