The journal of pain : official journal of the American Pain Society
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Retraction Of Publication
Size does matter, but it isn't everything: the challenge of modest treatment effects in chronic pain clinical trials.
Available online This article has been withdrawn at the request of the author(s) and/or editor. The Publisher apologizes for any inconvenience this may cause. The full Elsevier Policy on Article Withdrawal can be found at https://www.elsevier.com/about/our-business/policies/article-withdrawal.
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Bilateral deficits in sensorimotor function have been observed in unilateral musculoskeletal pain conditions. Evidence suggests a reduction in interhemispheric inhibition (IHI) from the "affected" (contralateral to the side of pain) to the "unaffected" primary motor cortex (M1) could contribute. However, the effect of short-lasting acute muscle pain on IHI, and whether any changes are related to early sensorimotor changes in the unaffected limb, is unknown. ⋯ These findings suggest a decrease in IHI from the affected to the unaffected M1 that occurs rapidly after the onset of acute pain and could contribute to the development of bilateral symptoms. PERSPECTIVE: The affected M1 (contralateral to the side of pain) releases inhibition over the unaffected M1 within minutes after the onset of acute muscle pain. This finding could have relevance for the development of bilateral sensorimotor symptoms in unilateral pain conditions.
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Sexual assault (SA) is associated with an increased risk of chronic pain, but the mechanisms for this relationship are poorly understood. To explore whether disrupted descending inhibition is involved, this study used a conditioned pain modulation task to study the inhibition of pain and the nociceptive flexion reflex (NFR; a correlate of spinal nociception) in 32 pain-free SA survivors. This group was compared with 32 pain-free, trauma-exposed persons without SA and a group of 40 pain-free persons who reported no trauma exposure. ⋯ These findings suggest that trauma exposure may impair inhibitory cerebrospinal circuits, but that SA may specifically promote facilitation of spinal nociception. Perspective: This study suggests that trauma exposure disrupts the cerebrospinal inhibition of spinal nociception, but that exposure to SA further promotes chronic pain risk by facilitating spinal nociception. This finding help may help to elucidate the pain risk mechanisms in trauma survivors.
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Congenital insensitivity to pain is an umbrella term used to describe a group of rare genetic diseases also classified as hereditary sensory autonomic neuropathies. These conditions are intriguing, with the potential to shed light on the poorly understood relationship concerning nociception and the experience of pain. However, the term congenital insensitivity to pain is epistemologically incorrect and is the product of historical circumstances. ⋯ The suggested term better reflects the nature of the conditions and incorporates current understandings of nociception. PERSPECTIVE: The umbrella term congenital insensitivity to pain conflates pain and nociception, which is epistemologically unacceptable. We suggest a new term, namely, congenital nociceptor deficiency, that overcomes this problem and is concordant with current neurobiological knowledge.
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Randomized Controlled Trial
Tactile precision remains intact when acute neck pain is induced.
A growing body of evidence suggests that chronic pain is associated with perceptual changes, such as impaired tactile acuity and laterality judgements. A recent study on low back pain showed that tactile acuity was decreased immediately after acute pain induction. Biologically, acute pain should lead to enhanced rather than disruptive changes in tactile acuity to meaningfully respond to potentially damaging nociceptive stimuli. ⋯ PERSPECTIVE: In this study, a sensory adaptation to acute neck pain was investigated. It was found that experimental neck pain did not elicit changes in the sensory axis, leaving tactile acuity intact in otherwise healthy participants. These data support site-specific sensory adaptation to pain.