Pain
-
Controlled Clinical Trial
Anxiety and depression associated with migraine: influence on migraine subjects' disability and quality of life, and acute migraine management.
Anxiety and depression are reported to be frequently associated with migraine but how they impact on migraine-related disability, migraine subjects' quality of life, and medical and therapeutic management of migraine attacks has not been investigated. FRAMIG 3 is a nation-wide population-based postal survey carried out in France according to the 2004 international classification of headache disorders. ⋯ Although, migraine-associated anxiety and depression do not appear to influence the drugs taken by migraine subjects for the acute treatment of migraine attacks, perceived treatment efficacy and satisfaction with treatment are lower in subjects with anxiety alone or combined with depression than in subjects with neither anxiety nor depression. Anxiety and depression should be systemically looked for and cared for in subjects consulting for migraine.
-
Extracellular signal-regulated kinase (ERK), a mitogen-activated protein kinases (MAPK), transduces a broad range of extracellular stimuli into diverse intracellular responses. Recent studies have showed that ERK activation in the supraspinal level involved in the development of drug dependence, especially in psychological dependence. In this study, we reported that the spinal ERK signaling pathway was activated by chronic morphine injection. ⋯ The spinal ERK inhibition or knockdown also reduced morphine withdrawal-induced phosphorylation of cAMP response element binding protein (CREB), which is one of the important downstream substrates of ERK pathway, and Fos expression. The involvement of the spinal ERK in morphine withdrawal was supported by our finding that intrathecal N-methyl-D-aspartate receptor antagonist MK-801 or protein kinase C inhibitor chelerythrine chloride suppressed withdrawal-induced ERK activation in the spinal cord and attenuated morphine withdrawal symptoms. These findings suggest activation of the spinal ERK signaling pathway contributes naloxone-precipitated withdrawal in morphine-dependent rats.