Current pain and headache reports
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Joint hypermobility syndrome (JHS) was initially defined as the occurrence of musculoskeletal symptoms in the presence of joint laxity and hypermobility in otherwise healthy individuals. It is now perceived as a commonly overlooked, underdiagnosed, multifaceted, and multisystemic heritable disorder of connective tissue (HDCT), which shares many of the phenotypic features of other HDCTs such as Marfan syndrome and Ehlers-Danlos syndrome. ⋯ There is hardly a clinical specialty to be found that is not touched in one way or another by JHS. Over the past decade, it has become evident that of all the complications that may arise in JHS, chronic pain is arguably the most menacing and difficult to treat.
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Curr Pain Headache Rep · Dec 2009
Randomized Controlled TrialMemantine for the prophylaxis of chronic tension-type headache.
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Curr Pain Headache Rep · Dec 2009
Randomized Controlled TrialPregabalin as treatment for fibromyalgia: the rest of the story?
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Curr Pain Headache Rep · Oct 2009
ReviewBrain manifestation and modulation of pain from myofascial trigger points.
The brain plays a prominent role in the generation and modulation of pain. It contains powerful endogenous pain modulatory systems that can be engaged in a beneficial way by therapeutical intervention. In contrast, pain chronification is associated with maladaptive structural and functional changes that may shift the balance of the modulatory systems. ⋯ Recent neuroimaging data suggest that hyperalgesia from MTrPs is processed in similar regions as hyperalgesia from other pain conditions. However, abnormal hippocampal hypoactivity suggests that dysfunctional stress responses may play an important role in the generation and maintenance of hyperalgesia from MTrPs. Other data suggest that short-term pain relief obtained with intramuscular electrostimulation within an MTrP is partially due to descending pain inhibitory mechanisms.
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Some studies suggest that platelet activation and aggregation are associated with migraine, likely secondary to changes occurring during the acute attack. Evidence also suggests that platelet clots can lodge in small cerebral vessels, and that the resultant ischemia and inflammation can induce cortical spreading depression with aura-like symptoms and pulsatile headache. ⋯ When associated with other factors, such as oral contraceptive use, there may be an increased tendency for thrombus formation, secondary migraine with aura, transient ischemic attacks, and stroke. Identifying those migraineurs at highest risk of developing endothelial dysfunction and platelet disorders may allow for preventive strategies to avoid the cerebral consequences.