The journal of pain : official journal of the American Pain Society
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Migraine with aura is a subtype of migraine characterized by transient neurological disturbances that usually precede headache. Cortical spreading depression (CSD) is the likely pathophysiological correlate of the aura phase of migraine, found in common and rare forms of migraine, such as familial hemiplegic migraine. CSD is a depolarization wave that propagates across the cerebral gray matter transiently suppressing neuronal activity. ⋯ In brainstem, CSD with and without treatment, although to a lesser extent, also induced gene expression changes involving genes related to apoptosis. Half of the genes altered in brainstem after CSD were also differentially expressed in the same direction in cortex. No differences in gene expression were identified after CSD as a consequence of the treatments, neither in cortex nor in brainstem.
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Although depression is associated with more clinical pain complaints, psychophysical data sometimes point to hypoalgesic alterations. Studying the more reflex-like facial expression of pain in patients with depression may offer a new perspective. Facial and psychophysical responses to nonpainful and painful heat stimuli were studied in 23 patients with major depressive disorder (MDD) and 23 matched control participants. ⋯ Pain psychophysics was unaltered in MDD patients compared with healthy control participants. In conclusion, the facial expression of pain in MDD patients indicates rather hyper- than hypoalgesia, with enhanced affective pain processing. Moreover, the linkage between subjective and facial responses was much stronger in MDD patients, which may be due to a reduced influence of social display rules, which normally complicate this relationship.
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Bone fracture with subsequent immobilization of the injured limb can cause complex regional pain syndrome (CRPS) in humans. Mechanisms of CRPS are still not completely understood but bone fracture with casting in mice leads to a similar post-traumatic inflammation as seen in humans and might therefore be an analog to human CRPS. In this article we report behavioral and spinal electrophysiological changes in mice that developed swelling of the paw, warming of the skin, and pain in the injured limb after bone fracture. ⋯ In all mice tested, all signs subsided 12 weeks after trauma. Our data suggest a significant reorganization of spinal circuitry after limb trauma, in a degree more comprehensive than most models of neuropathies. This process seems to be reversible in the rodent.