02-03-2018, 01:36 AM
(02-02-2018, 11:48 PM)Xfizzler Wrote: Hi Rafterman & Zman!!!
Thanks for your insight and response to my thread. Rafter.... here is something I found to support your wisdom on the mattter. And Zman thanks for letting my know that I was right to ask for the KP!n prescription.below is an article I found.
According to classic theory, a migraine attack is initiated by cerebrovascular spasm followed by extracranial vasodilatation. Results of recent studies support this theory and suggest that cerebral blood flow during the initial phase of migraine symptoms is, in fact, decreased and this decrease probably leads to ischemia and hypoxia. Cellular hypoxia, in turn, can cause an increase in the flow of calcium from the extracellular fluid to the intracellular space, resulting in calcium overload and cellular dysfunction. Because calcium-channel blockers selectively inhibit the intracellular influx of calcium ions, investigators have begun evaluating the efficacy of these agents for migraine prophylaxis. Nimodipine, a calcium-channel blocker that exhibits selective effects on cerebral vessels, seems to offer protection against the cerebral ischemia and hypoxia presumed to be operative during migraine attacks. In a double-blind, placebo-controlled study, nimodipine decreased the frequency and duration of migraine attacks by at least half in 69% of patients treated with this agent. Comparable reductions in migraine frequency and duration were attained in 58, 51, 41 and 52% of patients treated with methysergide maleate, pizotifen, clonidine hydrochloride and propranolol, respectively. The piperazine derivative flunarizine also has calcium-channel blocking properties. This agent prevents vasospasm in cerebral arteries and protects against cerebral hypoxia. Results of double-blind studies of migraine prophylaxis with flunarizine demonstrate the beneficial effects of this agent, particularly in younger patients. Flunarizine proved to be superior to pizotifen in decreasing the severity of migraine attacks and comparable to pizotifen in decreasing their frequency.
My pleasure, X,
Yep, Nimodipine is the cranial-selective CCB that I have seen work for several people. These are people who did not first try a benzo. They went right to the Nimodipine and experienced positive results. Do you think you might just keep this knowledge as a back up plan, while staying on the clowns for now? As we all know, finding a doc who will write for off-label use of a benzo is not easy. I have one that scripts clowns for me for a condition called costochondritis. It would seem a shame to not take advantage of the fact that your doc is broad-minded enough to go off label and treat migraine with it. Just curious as to what you think you might do. RM