Pain
-
The purpose of this study was to predict post-settlement pain intensity, psychological distress, disability, and financial struggle among African American (n=580) and non-Hispanic Caucasian (n=892) Workers' Compensation claimants with single incident low back injury. The study was a population-based telephone survey conducted in three population centers in Missouri. ⋯ The results suggest that African American race and lower SES-relative to Caucasian race and higher SES-are risk factors for poor outcomes after occupational low back injury. Mechanisms to explain these associations are discussed, including patient-level, provider-level, legal, and Workers' Compensation system-level factors.
-
Central neuropathic pain is well known in multiple sclerosis (MS), but the underlying mechanisms are unclear. In the present study we studied sensory function in MS patients with pain, MS patients without pain and healthy subjects in order to clarify the role of sensory abnormalities in pain. Fifty MS patients with pain were randomly recruited from a previous epidemiological MS study in Aarhus County, Denmark. ⋯ Central pain patients did not differ from musculoskeletal pain patients in quantitative sensory testing, but allodynia was more common in MS patients with central pain. Pain patients scored lower in all dimensions of SF-36 compared with pain-free patients and healthy subjects. The results suggest that pain in MS is central in more than half of the patients and is associated with mechanical or thermal hyperalgesia.
-
Animal studies have established a role for the brainstem reticular formation, in particular the rostral ventromedial medulla (RVM), in the development and maintenance of central sensitisation and its clinical manifestation, secondary hyperalgesia. Similar evidence in humans is lacking, as neuroimaging studies have mainly focused on cortical changes. To fully characterise the supraspinal contributions to central sensitisation in humans, we used whole-brain functional magnetic resonance imaging at 3T, to record brain responses to punctate mechanical stimulation in an area of secondary hyperalgesia. ⋯ Brainstem activation was localised to two distinct areas of the midbrain reticular formation, in regions consistent with the location of nucleus cuneiformis (NCF) and rostral superior colliculi/periaqueductal gray (SC/PAG). The PAG and the NCF are the major sources of input to the RVM, and therefore in an ideal position to modulate its output. These results suggest that structures in the mesencephalic reticular formation, possibly the NCF and PAG, are involved in central sensitisation in humans.
-
Surgery commonly causes pain and neural plasticity that are unique compared to other persistent pain problems. To more precisely study central sensitization and plasticity, we examined the role of ionotropic EAA receptors in dorsal horn neuron sensitization early after incision. Sensitization, in the form of increased background activity, increased mechanosensitivity or pinch receptive field expansion, was induced by plantar incision 1 h later in 30 neurons. (+)-5-Methyl-10,11-dihydro-5H-dibenzo(a,d)cyclohepten-5,10-imine (MK-801) or 1 mM 1,2,3,4-tetrahydro-6-nitro-2,3-dioxo[f]quinoxaline-7-sulfonamide (NBQX) was administered through a microdialysis fiber to block NMDA and nonNMDA EAA receptors, respectively. ⋯ The pinch receptive field (RF) expansion into uninjured areas of the paw and hindquarters occurred after incision. Only 1 of 13 neurons exhibited RF expansion after spinal NBQX administration; 9 of 12 neurons had RF expansion remaining after MK-801. Thus, nonNMDA receptors are critical and NMDA-independent factors influence the increased responsiveness of dorsal horn neurons that occur early after incision.
-
The 'facial feedback hypothesis' suggests that inhibiting or exaggerating pain displays produces parallel effects on subjective experience. Research on the regulation of emotional expressions suggests that the act of self-regulation may be detectable in the properties of facial behavior. Both issues were examined in this study. ⋯ The control and inhibit groups showed linear increases in pain expression with increasing pain intensity, which did not differ significantly. Fine-grained analysis of participants' facial behavior provided evidence that pain augmentation was accompanied by topographic changes in pain expression. Parallels with existing studies, methodological issues and practical implications of the findings are discussed.