The journal of pain : official journal of the American Pain Society
-
Randomized Controlled Trial
Pain relief is associated with improvement in motor function in complex regional pain syndrome type 1: secondary analysis of a placebo-controlled study on the effects of ketamine.
There are indications of motor circuit changes in patients with complex regional pain syndrome (CRPS). Nevertheless, although several studies have analyzed motor behavior in CRPS, a relation with pain could not be detected. This might be explained by the use of cross-sectional designs in these studies, in which pain is considered as a trait- rather than a state-dependent variable. We therefore studied the time-dependent relation between pain and motor function in affected arms of 29 CRPS patients during their participation in a placebo-controlled ketamine study. Movement parameters (velocity, frequency, amplitude, and number of arrests) were assessed during a finger tapping task. Linear mixed model analysis of the effects of pain (numerical rating scale score), treatment (ketamine/placebo), and week (1, 3, 6, and 12 weeks after treatment) on the movement parameters revealed that pain intensity was significantly (inversely) related to motor function, irrespective of whether patients had received ketamine or placebo. Movement parameters changed 3-12% per point numerical rating scale change. Because patients were unaware of possible effects of ketamine on motor function, these findings suggest that motor function changes were mediated by, or occurred simultaneously with, changes in pain intensity. By improving motor function, pain relief may offer a window of opportunity for rehabilitation programs in CRPS. ⋯ This article provides evidence for a direct relation between pain and motor function in CRPS, which indicates that pain relief may be an important factor in the treatment of motor disturbances in this condition. These findings may help to advance our understanding of the pathways underlying motor disturbances in CRPS.
-
Despite the high prevalence of neck pain among women, menstrual effects on regional pain outcomes have not been investigated in this clinical population. This study evaluated menstrual effects on mechanical pain sensitivity (pressure pain threshold [PPT]), neck pain intensity (numeric pain rating scale [NPRS]), and neck-related disability (Neck Disability Index [NDI]) in 22 normally menstruating (NM) and 17 hormonal contraceptive users with chronic neck pain. Sex hormones, PPT, and NDI were measured during the early follicular (F1), late follicular (F2), and luteal (L) menstrual phases. Daily NPRS scores were recorded in an online symptom diary and averaged within each phase. Estradiol and progesterone increased only for NM women in F2 and L, respectively. Phase effects on PPT (η(2) = .003), NDI (η(2) = .003), and NPRS (η(2) = .016) for NM women were small and did not differ from those for the hormonal contraceptive users (P ≥ .386). Averaged across the menstrual cycle, PPT scores explained 29% of the variance in NPRS scores for NM women but were not associated with NDI scores in either group. Results indicate that the magnitude of menstrual effects on mechanical pain sensitivity and the severity of neck pain and disability do not exceed thresholds of clinically detectable change in women with chronic neck pain. ⋯ Fluctuations in evoked and clinical pain outcomes across the menstrual cycle do not appear to be of sufficient magnitude to impact clinical decision making for women with chronic neck pain.
-
Randomized Controlled Trial
Determinants of pain treatment response and nonresponse: identification of TMD patient subgroups.
The purpose of the present study was to determine if we could identify a specific subtype of temporomandibular disorder (TMD) pain patients that does not respond to treatment. Patients were 101 men and women with chronic TMD pain recruited from the community and randomly assigned to 1 of 2 treatment conditions: a standard conservative care (STD) condition or a standard care plus cognitive-behavioral therapy condition (STD + CBT) in which patients received all elements of STD but also received cognitive-behavioral coping skills training. Growth mixture modeling, incorporating a series of treatment-related predictors, was used to distinguish several distinct classes of responders or nonresponders to treatment based on reported pain over a 1-year follow-up period. Results indicated that treatment nonresponders accounted for 16% of the sample and did not differ from treatment responders on demographics or temporomandibular joint pathology, but that they reported more psychiatric symptoms, poorer coping, and higher levels of catastrophizing. Treatment-related predictors of membership in treatment responder groups versus the nonresponder group included the addition of CBT to STD, treatment attendance, and decreasing catastrophization. It was concluded that CBT may be made more efficacious for TMD patients by placing further emphasis on decreasing catastrophization and on individualizing care. ⋯ This article provides evidence that the TMD chronic pain population is heterogeneous and that a subsample of patients will be unresponsive to standard or psychosocial approaches. The addition of CBT to treatment may be helpful for this group, but new individualized approaches will be needed to treat all patients effectively.
-
Studies of peripheral nerve inflammation (neuritis) suggest that some symptoms of neuropathic pain can be generated from inflamed but otherwise uninjured axons. We have previously inferred a role for inflammation-induced axonal transport disruption in the underlying mechanisms. In the present study, we have investigated the development of sensory hypersensitivities following vinblastine-induced axonal transport disruption. Similar to neuritis, locally applied .1 mM vinblastine caused the rapid development of mechanical hypersensitivity within the first week postsurgery. The same animals did not develop heat hypersensitivity. Because aberrant firing from primary sensory neurons is considered necessary to drive spinal mechanisms that lead to hypersensitivities, the levels of ongoing activity and axonal mechanical sensitivity were examined. Recordings from A- and C-fiber neurons did not reveal differences in the levels of ongoing activity between vinblastine-treated (<5.8%) and saline-treated control animals (<4.6%). However, 28% of C-fiber axons were mechanically sensitive at the vinblastine treatment site. Using kinesin immunohistochemistry, we confirmed a reduction of anterograde axonal transport in vinblastine-treated and neuritis animals. In summary, this study has revealed an alternative pain model, which may be relevant to conditions that are not accompanied by frank nerve injury. ⋯ In this study, we expand our previous reports and demonstrate that focal reduced axonal transport causes distal mechanical hypersensitivity considered consistent with neuropathic pain but in the absence of nerve injury. These findings may inform pain conditions that have a neural inflammatory component.