Pain
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Review Historical Article
A comprehensive categorical and bibliometric analysis of published research articles on pediatric pain from 1975-2010.
The field of pediatric pain research began in the mid-1970s and has undergone significant growth and development in recent years as evidenced by the variety of books, conferences, and journals on the topic and also the number of disciplines engaged in work in this area. Using categorical and bibliometric meta-trend analysis, this study offers a synthesis of research on pediatric pain published between 1975 and 2010 in peer-reviewed journals. Abstracts from 4256 articles, retrieved from Web of Science, were coded across 4 categories: article type, article topic, type and age of participants, and pain stimulus. ⋯ Most studies were original research articles; the most frequent topics were pain characterization (39.86%), pain intervention (37.49%), and pain assessment (25.00%). Clinical samples were most frequent, with participants most often characterized as children (6-12 years) or adolescents (13-18 years) experiencing chronic or acute pain. The findings provide a comprehensive overview of contributions in the field of pediatric pain research over 35 years and offers recommendations for future research in the area.
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Among many mechanisms implicated in the development of neuropathic pain after nerve damage is a profound dysfunction of GABAergic inhibitory controls, manifested by ongoing pain, mechanical hypersensitivity, and thermal hyperalgesia. In some respects, neuropathic pain can be considered a "disease" of the nervous system, with features in common with trauma-induced seizures. Indeed, first-line management involves anticonvulsant therapy. ⋯ In related studies, we demonstrated that medial ganglionic eminence cell transplants are also effective in a chronic neuropathic itch model in which there is a significant loss of dorsal horn inhibitory interneurons. Most importantly, in contrast to systemic or intrathecal pharmacological therapies, adverse side effects are minimized when the inhibitory control, namely, γ-aminobutyric acid release, occurs in a spinal cord circuit. These studies suggest that therapy targeted at repairing the GABAergic dysfunction is a viable and novel alternative to the management of neuropathic pain and itch, particularly those that are or become refractory to traditional pharmacotherapy.
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Brain responses to nociception are well identified. The same is not true for allodynic pain, a strong painful sensation in response to touch or innocuous cold stimuli that may be experienced by patients with neuropathic pain. Brain (or spinal cord) reorganization that may explain this paradoxical perception still remains largely unknown. ⋯ Both thalamic function and structure have been reported to be abnormal or impaired in neuropathic pain conditions including in the basal state, possibly explaining the spontaneous component of neuropathic pain. A further indication as to how the brain can create neuropathic pain response in SII and insular cortices stems from examples of diseases, including single-case reports in whom a focal brain lesion leads to central pain disappearance. Additional studies are required to certify the contribution of these areas to the disease processes, to disentangle abnormalities respectively related to pain and to deafferentation, and, in the future, to guide targeting of stimulation studies.
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Pain is a quite frequent complaint accompanying numerous pathologies. Among these pathological cases, numerous neuropathies are retrieved with identified etiologies (chemotherapies, diabetes, surgeries…) and also more diffuse syndromes such as fibromyalgia. More broadly, pain is one of the first consequences of most inherited diseases. ⋯ Among these ion channels, we and others revealed the important role of low voltage-gated calcium channels in cellular excitability in different steps of the pain pathways. These channels, by being activated nearby resting membrane potential, have biophysical characteristics suited to facilitate action potential generation and rhythmicity. In this review, we will present the current knowledge on the role of these channels in the perception and modulation of pain.