The published research on Botox for Migraines generally suggests that it only works for Chronic and not Episodic Migraines.
However this is not my experience, and it does not fit with the history of how the effect was first a serendipitous discovery in people who were having Botox for their wrinkles!
I would suggest that the failure of Botox in treatine Episodic Migraines is a failure of the PREEMPT Protocol devised by Allergan. Because they were scared that injecting the corrugator muscles would cause a high incidence of lid ptosis so the existing protocol actively avoids injecting them, even though it suggests it does.
It is interesting that Silberstein/Allergan are now teaching people how to inject into the corrugators directly, though this is not yet published. Indeed one neurologist in the UK, who was shown the 'new' technique, was told that perhaps she shouldn't use it because it wasn't yet published
I use a much higher dose in the corrugators (see the articles in my project) and find it very effective in both chronic and episodic migraines
What have other people found?
Most likely an effect may be small, if any. My own experience in chronic migraine suggests that the reported reduction of headache days occurs first, with (subjectively?) stronger migraine attacks, followed by control / decline of attack intensity / frequency in most patients. But I wouldn't conclude that Botox is effective in episodic migraine as I cannot distinguish from spontaneous course triggered by transforming chronic to episodic migraine as well as possible effects of other non-specific measures (changes in lifestyle etc.) might become efficient. I wouldn't bet that the corrugator is really a treatment focus, as I don't see any difference between my injected and non-injected (ptosis) patients.
Hi Dirk
I would certainly agree that the effects of botox on migraines are not mediated through paralysis of the corrugators (or any other muscles). Instead they are on the free pain nerve endings which appear to have the highest incidence in the fibrous muscle attachments/aponeuroses> Perhaps this is related to the common embryological origins from neural crest cells. Active short chain BoTN/A is found centrally by axonal transport, though it is unclear how much clinical effect this central BoTN/A has.
There is considerable discussion on whether the active short chain BoNT/A can jump from neuron to neuron because it is found in multiple locations. There is no theory that can account for this jump and personally I don't believe this is the explanation. There is however evidence that individual trigeminal neurons project to multiple locations (eg the dura, skin and brain stem) and I think this is far more likely an explanation
I'm not sure I understand your last comment about ptosis patients. Ar you talking about brow or lid ptosis. Brow ptosis comes from too large a dose laterally to the frontalis (as opposed to too little which causes exaggerated lift/mephisto brows. Lid ptosis comes from botox that has got behind the the superior orbital septum to weaken the fibres of levator palpebrae. Allergan's fea was that injecting lower down into the corrugators (rather than the frontalis where the botox really goes in the PREEMPT protocol) would cause lid ptosis because of migration. This is purely about injection technique as the Botulinum molecule is far too big to pass through fascia and if injected into the corrugators will remain within the corrugator fascial compartment. I regularly inject 1.5ml - 60U into the corrugators and have only had one case of lid ptosis where the anatomy had been disrupted by an old deep brow laceration
Hi Pete
Leaving aside the discussions on Botox, and responding to your comments on Vit D, I agree that the importance of Vit D in many situations is only recently being explored, and that perhaps everybody should be taking supplements.
I appreciate that the purported dangers of Hypervitaminosis D are greatly exaggerated and that you can certainly take 1000-2000 IU a day without problem. However I feel a little concerned that 10,000 IU a day is a pretty high dose. Does Vit D have an effect at lower doses such as 2000 IU a day?
A separate discussion revolves around the mode of action. If the effect begins to wear off after a few days, in spite of a long course of treatment then it would suggest that the effect is not mediated directly from general body Vit D status as it is inconceivable that the stores that have been built up over weeks will be depleted in a few days
I remain concerned about the wholesale suggestion that it is safe to take 10,000 IU Vit D3 for extended periods. Anybody contemplating this dose should perhaps read
https://en.wikipedia.org/wiki/Hypervitaminosis_D
This discussion is not whether high doses of Vit D helps for Cluster Headache can help, but that anybody contemplating it should be fully informed on the potential long-term effects that take more than a few months to develop. It may be that the risks are low at 10,000 IU but I don't see any suggestion in what I have read that they are zero. Quite the opposite in fact. I'm not at all convinced that one can rely upon such simplistic measurements as Blood Calcium levels to ensure safety
It is well accepted that CoQ10 can help migraines,and if this added to 4,000 IU Vit D3 a day can help then perhaps this is a route forward with a much better safety margin.
For some with severe CH not controlled by any other means then perhaps the potential risks are worth taking, but I believe that claiming it is risk free is irresponsible
https://en.wikipedia.org/wiki/Hypervitaminosis_D
Pete Batcheller has written on Clusterheadache.com that "Regarding the optimum maintenance dose of vitamin D3... The best information available indicates the average sustained 25(OH)D response to a dose of 5,000 IU/day is 60 ng/mL while a maintenance dose of 10,000 IU/day results in a sustained average 25(OH)D response of 80 to 85 ng/mL."
I am unclear where these assertions come from, along with the variation in individual responses to the doses.
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