The signs and symptoms have been well described but the pathogenesis remains a mystery. Most of the evidence suggests increased resistance to cerebrospinal fluid outflow as being pivotal to the disorder. Any comprehensive PI3K inhibitor theory on causation will have to explain the preponderance of obese women of childbearing age with primary PTCS and lack of ventriculomegaly in the disorder. It is possible that female sex hormones, along with endocrinologically active adipose tissue, directly result in the syndrome, in those genetically predisposed.
Aldosterone has been proposed also as important in the development of PTCS. Vitamin A, in the form of retinoic acid, may also play a pivotal role, and is influenced by both estrogen and adipose tissue. This article reviews proposed mechanisms of PTCS. “
“Objective.— To examine frovatriptan’s efficacy as preemptive treatment for fasting-induced migraine. Background.— Fasting is a common migraine trigger that cannot always be avoided. The development of a short-term preemptive approach would be of benefit.
Because of its longer half-life, frovatriptan has been effectively used for short-term daily use to prevent menstrually related migraines and might prove useful in the prevention of fasting-induced migraine. Tyrosine Kinase Inhibitor Library Methods.— This was a double-blind, placebo-controlled, randomized, parallel-group trial. Subjects.— With a history of fasting-induced episodic migraine were randomly assigned to receive either frovatriptan (5.0 mg) or placebo (ratio 1:1). Subjects.— Took a single dose of study medication at the start of their 20-hour fast. Information about headache intensity, associated symptoms, and use of rescue medication was captured at defined time points from the start of
the fast through 20 hours post-fast. Results.— Of the 75 subjects screened, 74 subjects were randomized and 71 subjects completed the study. Demographic characteristics of the placebo and frovatriptan treatment Metformin cost groups were not statistically different. Thirty-three subjects received active drug. Twelve (36.4%) developed a headache between 6 and 20 hours after the start of the fast (1/33 mild, 11/33 moderate or severe). In the placebo group, 18/34 (52.9%) developed a headache (4/34 mild, 14/34 moderate or severe). The difference between the 2 treatment groups did not achieve statistical significance; Pearson chi-square, P = .172. Kaplan-Meier survival analysis showed no difference between the 2 treatment groups with respect to the time of onset of headache of any intensity (log rank, P = .264) and for the time of onset of a moderate or severe intensity (log rank, P = .634). Conclusion.— More subjects on placebo developed a headache than those on frovatriptan. Perhaps because of the small number of subjects involved, the differences in headache incidences observed did not achieve statistical significance.