Headache
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New-onset migraine headache attacks (MHAs) can occur after atrial septal device implantation in patients without previous migraine. Plasma calcitonin gene-related peptide (CGRP), which plays a crucial role in migraine pathophysiology, has shown to be released from specific cardiac tissues. ⋯ Bigger ASD size and lower plasma CGRP levels before closure can be a potential predictor of new-onset MHAs. Furthermore, a significant increase of CGRP levels during migraine attack implies that the occurrences of new-onset MHAs after ASD closure correlate with the release of CGRP. This suggests CGRP sensitization from a lower baseline may be involved in the occurrence of new-onset MHAs after ASD closure.
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To compare prevalence of self-reported comorbid temporomandibular joint muscle disorder-type, neck, back, and joint pains in people with severe headache or migraine; and analyze these self-reported pains in the 2000-2005 US National Health Interview Survey by gender and age for non-Hispanic whites, Hispanics, and non-Hispanic blacks (African Americans). ⋯ Severe headache or migraine is often associated with other common pains, seldom existing alone. Two or more comorbid pains are common, similarly affecting gender and racial/ethnic groups.
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Burning mouth syndrome (BMS) is an idiopathic and chronic pain condition for which patients may experience high levels of pain, anxiety, and depression. So far, it has not yet been well investigated whether specific psychiatric features (anxious traits, personality disorder, or somatization) may play a role in the BMS pathogenesis or whether some BMS symptoms, or BMS itself, may cause secondary psychiatric symptoms. ⋯ We may hypothesize that anxiety could determine a secondary demoralization in BMS patients (depression) and depressive symptoms could contribute to pain, accordingly. Therefore, pain could be a somatic feature of depression. Our findings provide an example of a possible pathogenetic model for BMS.
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This study tests the hypothesis that injury to the somatosensory cortex is associated with periorbital allodynia and increases in nociceptive neuropeptides in the brainstem in a mouse model of controlled cortical impact (CCI) injury. ⋯ Injury to the somatosensory cortex results in persistent periorbital allodynia and increases in brainstem nociceptive neuropeptides. Findings suggest that persistent allodynia and increased neuropeptides are maintained by mechanisms other than activation of macrophage/microglia or astrocyte in the injured somatosensory cortex.