Pain
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The drugs available for treatment of neuropathic pain have somewhat disappointing efficacy with many patients left with limited or no effect. Individualized treatment based on phenotype according to presumed underlying pain mechanism(s) has been proposed to improve outcomes. We report a retrospective analysis of phenotype-specific effects of several neuropathic pain drugs, which were studied in a series of crossover, placebo-controlled, clinical trials. ⋯ No phenotype-specific effects were found for venlafaxine, escitalopram, oxcarbazepine, valproic acid, levetiracetam, or St. John's wort. Thus, this post hoc analysis of 8 drugs with mainly nonselective actions on neuropathic pain mechanisms found limited usefulness of sensory phenotyping in pain as the basis for individualized treatment.
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The classification of most chronic pain disorders gives emphasis to anatomical location of the pain to distinguish one disorder from the other (eg, back pain vs temporomandibular disorder [TMD]) or to define subtypes (eg, TMD myalgia vs arthralgia). However, anatomical criteria overlook etiology, potentially hampering treatment decisions. This study identified clusters of individuals using a comprehensive array of biopsychosocial measures. ⋯ Similar results were obtained when the same methodology was applied to a smaller case-control study consisting of 199 chronic TMD cases and 201 TMD-free controls. During a median 3-year follow-up period of TMD-free individuals, participants in the global symptoms cluster had greater risk of developing first-onset TMD (hazard ratio = 2.8) compared with participants in the other 2 clusters. Cross-cohort predictive modeling was used to demonstrate the reliability of the clusters.
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We developed the Michigan Body Map (MBM) as a self-report measure to assess body areas where chronic pain is experienced and to specifically quantify the degree of widespread body pain when assessing for centralized pain features (eg, fibromyalgia-like presentation). A total of 402 patients completed the measure in 5 distinct studies to support the validation of the original and a revised version of the MBM. Administration is rapid 39 to 44 seconds, and errors for the original MBM were detected in only 7.2% of the possible body areas. ⋯ Furthermore, the revised MBM showed convergent and discriminant validity with other self-report measures of pain, mood, and function. In conclusion, the MBM demonstrated utility, reliability, and construct validity. This new measure can be used to accurately assess the distribution of pain or widespread bodily pain as an element of the fibromyalgia survey score.
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Plasticity in inhibitory receptors, neurotransmission, and networks is an important mechanism for nociceptive signal amplification in the spinal dorsal horn. We studied potential changes in GABAergic pharmacology and its underlying mechanisms in hyperalgesic priming, a model of the transition from acute to chronic pain. We find that while GABAA agonists and positive allosteric modulators reduce mechanical hypersensitivity to an acute insult, they fail to do so during the maintenance phase of hyperalgesic priming. ⋯ Neurolide 2 treatment also reverses the change in polarity in GABAergic pharmacology observed in the maintenance of hyperalgesic priming. We propose that increased nlgn2 expression is associated with hyperalgesic priming where it promotes dysregulation of inhibitory networks. Our observations reveal new mechanisms involved in the spinal maintenance of a pain plasticity and further suggest that disinhibitory mechanisms are central features of neuroplasticity in the spinal dorsal horn.