Evidence from animal experiments shows that the brain stem is involved in the pathophysiology of migraine. To investigate human migraine, we used positron emission tomography to examine the changes in regional cerebral blood flow as an index of neuronal activity in the human brain during spontaneous migraine attacks. During the attacks, increased blood flow was found in the cerebral hemispheres in cingulate, auditory and visual association cortices and in the brain stem. However, only the brain stem activation persisted after the injection of sumatriptan had induced complete relief from headache and phono- and photophobia. These findings support the idea that the pathogenesis of migraine is related to an imbalance in activity between brain stem nuclei regulating antinociception and vascular control.
The results of PREEMPT 2 demonstrate that onabotulinumtoxinA is effective for prophylaxis of headache in adults with chronic migraine. Repeated onabotulinumtoxinA treatments were safe and well tolerated.
There was no between-group difference for the primary endpoint, headache episodes. However, significant reductions from baseline were observed for onabotulinumtoxinA for headache and migraine days, cumulative hours of headache on headache days and frequency of moderate/severe headache days, which in turn reduced the burden of illness in adults with disabling chronic migraine.
The authors followed 532 consecutive patients with episodic migraine (<15 days/month) for 1 year. Sixty-four patients (14%) developed chronic headache (>/=15 days/month). The odds ratios for developing CH were 20.1 (95% CI 5.7 to 71.5) comparing patients with a "critical" (10 to 14 days/month) vs "low" (0 to 4 days/month) and 6.2 (95% CI 1.7 to 26.6) in patients with an "intermediate" (6 to 9 days/month) vs "low" headache frequency and 19.4 (95% CI 8.7 to 43.2) comparing patients with and without medication overuse.
on behalf of the German Stroke Study CollaborationBackground and Purpose-To date, no validated, comprehensive, and practicable model exists to predict functional recovery within the first hours of cerebral ischemic symptoms. The purpose of this study was to externally validate 2 prognostic models predicting functional outcome and survival at 100 days within the first 6 hours after onset of acute cerebral ischemia. Methods-On admission to a participating hospital, patients were registered prospectively and included according to defined criteria. Follow-up was performed 100 days after the event. With the use of prospectively collected data, 2 prognostic models were developed and internally calibrated in 1079 patients and externally validated in 1307 patients. By means of age and National Institutes of Health Stroke Scale (NIHSS) score as independent variables, model I predicts incomplete functional recovery (Barthel Index Ͻ95) versus complete functional recovery, and model II predicts mortality versus survival. Results-In the validation data set, model I correctly predicted 62.9% of the patients who were incompletely restituted or had died and 83.2% of the completely restituted patients, and model II correctly predicted 57.9% of the patients who had died and 91.5% of the surviving patients. Both models performed better than the treating physicians' predictions made within 6 hours after admission. Conclusions-The resulting prognostic models are useful to correctly stratify treatment groups in clinical trials and should guide inclusion criteria in clinical trials, which in turn increases the power to detect clinically relevant differences.
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