“(Headache 2010;50:1126-1129) Background.— A pilot survey of 94 neurologists attending a continuing medical education meeting was performed to assess whether neurologists like to treat headaches and other common disorders and evaluate their personal prevalence of the disorders. Methods.— Physicians were asked to respond to the following statement using a 5-point Likert scale (from 1, strongly disagree to 5, strongly agree): “I like to treat patients with this disease or symptom. Results.— The response rate was 46% with a mean age of 52.5 years.
The respondents liked to treat migraine (mean = 4.32) similarly to carpal tunnel syndrome and Parkinson’s disease. Cluster headaches (mean = 3.90) are less liked than migraine similar to epilepsy and multiple sclerosis and respondents learn more are neutral to treating chronic daily headaches (mean = 3.02) similarly to insomnia and low back pain. The lifetime prevalence of migraine among respondents is 48% with those with and without migraine comparably liking to treat migraineurs. Conclusions.— Neurologists like to treat migraine more than cluster headaches and are neutral in treating chronic daily headaches. “
“To examine calcitonin gene-related peptide (CGRP) gene expression Atezolizumab mouse under inflammatory conditions using trigeminal ganglia organ cultures as an experimental system. These
cultures have increased proinflammatory signaling that may mimic neurogenic inflammation in the migraine state. check details The trigeminal nerve sends peripheral pain signals to the central nervous system during migraine. Understanding the dynamic processes that occur within the trigeminal nerve and ganglion may provide
insights into events that contribute to migraine pain. A neuropeptide of particular interest is CGRP, which can be elevated and play a causal role in migraine. However, most studies have overlooked a second splice product of the Calca gene that encodes calcitonin (CT), a peptide hormone involved in calcium homeostasis. Importantly, a precursor form of CT called procalcitonin (proCT) can act as a partial agonist at the CGRP receptor and elevated proCT has recently been reported during migraine. We used a trigeminal ganglion whole organ explant model, which has previously been demonstrated to induce pro-inflammatory agents in vitro. Quantitative polymerase chain reaction and immunohistochemistry were used to evaluate changes in messenger ribonucleic acid (mRNA) and protein levels of CGRP and proCT. Whole mouse trigeminal ganglia cultured for 24 hours showed a 10-fold increase in CT mRNA, with no change in CGRP mRNA. A similar effect was observed in ganglia from adult rats. ProCT immunoreactivity was localized in glial cells. Cutting the tissue blunted the increase in CT, suggesting that induction required the close environment of the intact ganglia. Consistent with this prediction, there were increased reactive oxygen species in the ganglia, and the elevated CT mRNA was reduced by antioxidant treatment.