Pain
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Lysophosphatidic acid (LPA) is a bioactive lipid that impacts neurological outcomes after neurotrauma by inhibiting neuroregeneration, promoting inflammation, and contributing to behavioral deficits. Blocking LPA signaling with a novel anti-LPA monoclonal antibody (mAb) is neuroprotective after traumatic brain injury (TBI) if given to injured animals whose blood-brain barrier (BBB) has been compromised. It is hypothesized that the anti-LPA mAb could improve chronic pain initiated by TBI. ⋯ Compared with control rats that received LT3114 but no TBI, TBI rats demonstrated significantly higher concentrations of intranasally administered LT3114 antibody in some tissues. In behavioral studies, a significant attenuation of mechanical allodynia after TBI was observed in the anti-LPA treatment group (P = 0.0079), when compared with vehicle controls within 14 days after TBI. These results suggest that intranasal application of the anti-LPA antibody directly accesses CNS sites involved in TBI-related pain and that this access attenuates pain sequelae to the neurotrauma.
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Review Meta Analysis
Defining chronic pain in epidemiological studies - a systematic review and meta-analysis.
The objective was to document the operational definitions applied in epidemiological studies of chronic pain and to examine whether pain definitions and other methodological factors are systematically related to prevalence estimates. MEDLINE, EMBASE, and PsychINFO were searched for original research reports with study samples of at least 1000 individuals, excluding studies of less than 5 out of 15 selected body regions and studies solely concerned with specific pain conditions. Meta-analyses and meta-regressions were applied with random effects models; covariates were geography, sampling year, survey method, sampling frame, participation rate, percentage women of all participants, pain duration, and pain location. ⋯ There were also interaction effect of survey method by sex (female-male prevalence ratio [95% confidence interval]: questionnaire = 1.20 [1.16 to 1.25], and interview = 1.38 [1.29 to 1.47]). The other covariates investigated were not significantly related to the prevalence estimates. Researchers and clinicians should be aware of the probability that interview survey method of collecting data may give lower chronic pain reporting than questionnaire survey method and that this effect may be stronger in men than women.