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      Juvenile Fibromyalgia and Headache Comorbidity in Children and Adolescents: A Literature Review

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          Abstract

          Juvenile fibromyalgia (JFM) is a chronic pain syndrome with onset in developmental age, characterized by widespread musculoskeletal pain associated with other neurological or nonneurological symptoms. Headache is one of the most frequent comorbid conditions with JFM, but this association is still poorly studied in the juvenile population. The literature review was conducted searching through PubMed, Scopus, and Web of Science with a combination of the following free-text terms: “fibromyalgia,” “juvenile fibromyalgia,” “headache,” “primary headache,” “migraine,” “children,” “adolescents,” and “comorbidity.” The research resulted only in two specific studies regarding comorbidity JFM + Juvenile Headache (JH). From each study, we extracted data about sample features, clinical characteristics of both JFM and PH, and assessment tools. The clinical approach to JFM and JH should include a complete examination of the main causes of comorbid diseases, thus improving the therapeutic approach to the patient in developmental age.

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          Most cited references26

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          Applying modern pain neuroscience in clinical practice: criteria for the classification of central sensitization pain.

          The awareness is growing that central sensitization is of prime importance for the assessment and management of chronic pain, but its classification is challenging clinically since no gold standard method of assessment exists.
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            Central sensitization theory of migraine: clinical implications.

            The clinical science of migraine headache continues to evolve. Theories of the pathophysiology of migraine have progressed from the early vascular basis of migraine to more complex current theories that emphasize the centrality of neuronal dysfunction. The most recently articulated theory of migraine is the central sensitization hypothesis, which proposes that altered processing of sensory input in the brainstem, principally the trigeminal nucleus caudalis, could account for many of the temporal and symptomatic features of migraine, as well as its poor response to triptan therapy when such treatment is initiated hours after the onset of pain. Both preclinical and clinical data support the central sensitization theory. A critical clinical implication of this theory is that drugs that are capable of either aborting or arresting the process of central sensitization, most prominently dihydroergotamine, may have a unique role in the treatment of migraine. An additional, and highly practical, implication is based upon the finding that cutaneous allodynia-pain arising from innocuous stimulation of the skin, as in hair brushing or the application of cosmetics-is an easily identifiable marker of central sensitization. Thus, the presence or absence of cutaneous allodynia can be integrated into the routine clinical assessment of migraine and utilized as a determinant of treatment. Future basic and clinical research on central sensitization is likely to be of ongoing importance to the field.
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              Mechanisms of disease: pain in fibromyalgia syndrome.

              Despite extensive research, the pathogenesis of pain in fibromyalgia syndrome is incompletely understood. Fibromyalgia pain is consistently felt in deep tissues including ligaments, joints and muscles. Increasing evidence points towards these tissues as relevant contributors of nociceptive input that might either initiate or maintain central sensitization, or both. Persistent or intense nociception can lead to transcriptional and translational changes in the spinal cord and brain resulting in central sensitization and pain. This mechanism represents a hallmark of fibromyalgia and many other chronic pain syndromes, including irritable bowel syndrome, temporomandibular disorder, migraine, and low back pain. Importantly, after central sensitization has been established, only minimal nociceptive input is required for the maintenance of the chronic pain state. Other factors, including pain-related negative affect, have been shown to significantly contribute to clinical fibromyalgia pain. An improved understanding of the mechanisms that characterize central sensitization and clinical pain will provide new approaches for the prevention and treatment of fibromyalgia and other chronic pain syndromes.
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                Author and article information

                Contributors
                Journal
                Pain Res Manag
                Pain Res Manag
                PRM
                Pain Research & Management
                Hindawi
                1203-6765
                1918-1523
                2019
                3 June 2019
                : 2019
                : 3190829
                Affiliations
                1Child Neuropsychiatry Unit, Department of Basic Medical Sciences, Neurosciences and Sense Organs, University “A. Moro”, Piazza Giulio Cesare 11, 70100 Bari, Italy
                2Children Epilepsy and EEG Center, Via Aldo Moro 32, 70019 Bari, Italy
                3Neurology Unit, Department of Basic Medical Sciences, Neurosciences and Sense Organs, University “A. Moro”, Piazza Giulio Cesare 11, 70100 Bari, Italy
                Author notes

                Academic Editor: Anna Maria Aloisi

                Author information
                http://orcid.org/0000-0001-6567-5373
                http://orcid.org/0000-0002-9203-3373
                Article
                10.1155/2019/3190829
                6589204
                74a319ba-2336-418b-9cb6-a2b151429a44
                Copyright © 2019 Emilia Matera et al.

                This is an open access article distributed under the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited.

                History
                : 5 April 2019
                : 16 May 2019
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