Not good for CH, it's a vasodialator and we need vasoconstictors. CH pain is caused by dialation of blood vessels in the brain. And yes many have tried it.

If you don't have it, look into O2 and read all you can on this site, especially the "oxygen info" on the left of this screen.

Good Luck, Don

Most here are likely to confirm that marijuana is a trigger more so than an abortive.

Quote:

Cannabinoid Research J Pharmacol Exp Ther. 2006 Oct 3 [Epub ahead of print] Cannabinoid (CB1) receptor activation inhibits trigeminovascular neurons. Akerman S, Holland P, Goadsby PJ. Institute of Neurology, London. Migraine is a common and disabling neurological disorder that involves activation, or the perception of activation, of the trigeminovascular system. Cannabinoid receptors are present in brain and have been suggested to have an anti-nociceptive role. Here we determine the effect of cannabinoid receptor activation on neurons with trigeminovascular nociceptive input in the rat. Neurons in the trigeminocervical complex - trigeminal nucleus caudalis (TNC) and dorsal horn of the C1 region- were studied using extracellular electrophysiological techniques. Responses to both dural electrical stimulation and cutaneous facial receptive field activation of the ophthalmic division of the trigeminal nerve, and the effect of cannabinoid agonists and antagonists were studied. Non-selective CB receptor activation, with WIN55,212 (1 mgkg(-1), i.v) inhibited neuronal responses to A- (by 52%)and C-fiber (by 44 %) afferents, an effect that was blocked by the CB1 receptor antagonist, SR141716 (3 mgkg(-1), i.v), but not the CB2 receptor antagonist, AM630 (3 mgkg(-1), i.v). Anandamide (10 mgkg(-1), i.v) was also able to inhibit both A- and C-fiber elicited trigeminocervical complex (TCC) firing, but only after TRPV1 receptor inhibition. Activation of cannabinoid receptors had no effect on cutaneous receptive fields when recording from TCC neurons. The data show that manipulation of CB1 receptors can affect the responses of trigeminal neurons with A- and C-fiber inputs from the dura mater. This may be a direct effect on neurons in the trigeminocervical complex itself, or an effect in discrete areas of the brain that innervate these neurons. The data suggest that CB receptors may have therapeutic potential in migraine, cluster headache or other primary headaches, although the potential hazards of psychoactive side-effects that accompany cannabinoid treatments may be complex to overcome. PMID: 17018694 ---------- Br J Pharmacol. 2004 Aug;142(8):1354-60. Epub 2004 Jul 26. Anandamide acts as a vasodilator of dural blood vessels in vivo by activating TRPV1 receptors. Akerman S, Kaube H, Goadsby PJ. Headache Group, Institute of Neurology, Queen Square, London, WC1N 3BG, U.K. Migraine pathophysiology is believed to involve the release of neuropeptides via the activation of trigeminal afferents that innervate the cranial vasculature. Anandamide, the endogenous ligand to the cannabinoid receptor, is able to inhibit neurogenic dural vasodilatation, calcitonin gene-related peptide (CGRP)-induced and nitric oxide-induced dural vessel dilation in the intravital microscopy model. In an in vitro setting anandamide is also able to activate the vanilloid type 1 (TRPV1) receptor and cause vasodilation, via the release of CGRP. In this study we used intravital microscopy to study whether anandamide behaves as a TRPV1 receptor agonist in the trigeminovascular system. We examined if anandamide-induced dural vasodilation involves CGRP release that can be reversed by the CGRP receptor antagonist, CGRP(8-37), and whether like capsaicin the anandamide effect could be reversed by the TRPV1 receptor antagonist, capsazepine. Anandamide 1 (19+/-9%, n=12), 3 (29+/-5%, n=37), 5 (74+/-7%, n=13) and 10 mg kg(-1) (89+/-18%, n=6) was able to cause a dose-dependent increase in dural vessel diameter. Capsazepine (3 mg kg(-1), t(5)=6.2, P<0.05) and CGRP(8-37) (300 micrograms kg(-1), t(6)=11.1, P<0.05) attenuated the anandamide-induced dural vessel dilation when compared to control (Student's paired t-test). AM251 (3 mg kg(-1)), a cannabinoid type 1 (CB(1)) receptor antagonist, was unable to reverse this anandamide-induced dilation. The study demonstrates that anandamide acts as a TRPV1 receptor agonist in the trigeminovascular system, activating TRPV1 receptors that promote CGRP release and cause vasodilation independent of any action at the CB(1) receptor. Anandamide has been shown previously to inhibit trigeminovascular neurons and prevent vasodilation, through an action at CB(1) receptors. PMID: 15277315 ---------- J Pharmacol Exp Ther. 2004 Apr;309(1):56-63. Epub 2004 Jan 12. Anandamide is able to inhibit trigeminal neurons using an in vivo model of trigeminovascular-mediated nociception. Akerman S, Kaube H, Goadsby PJ. Headache Group, Institute of Neurology and National Hospital for Neurology and Neurosurgery, Queen Square, London WC1N 3BG, UK. Arachidonylethanolamide (anandamide, AEA) is believed to be the endogenous ligand of the cannabinoid CB(1) and CB(2) receptors. CB(1) receptors have been found localized on fibers in the spinal trigeminal tract and spinal trigeminal nucleus caudalis. Known behavioral effects of anandamide are antinociception, catalepsy, hypothermia, and depression of motor activity, similar to Delta(9)-tetrahydocannanbinol, the psychoactive constituent of cannabis. It may be a possible therapeutic target for migraine. In this study, we looked at the possible role of the CB(1) receptor in the trigeminovascular system, using intravital microscopy to study the effects of anandamide against various vasodilator agents. Anandamide was able to inhibit dural blood vessel dilation brought about by electrical stimulation by 50%, calcitonin gene-related peptide (CGRP) by 30%, capsaicin by 45%, and nitric oxide by 40%. CGRP(8-37) was also able to attenuate nitric oxide (NO)-induced dilation by 50%. The anandamide inhibition was reversed by the CB(1) receptor antagonist AM251. Anandamide also reduced the blood pressure changes caused by CGRP injection, this effect was not reversed by AM251. It would seem that anandamide acts both presynaptically, to prevent CGRP release from trigeminal sensory fibers, and postsynaptically to inhibit the CGRP-induced NO release in the smooth muscle of dural arteries. CB(1) receptors seem to be involved in the NO/CGRP relationship that exists in causing headache and dural blood vessel dilation. It also seems that some of the blood pressure changes caused by anandamide are mediated by a noncannabinoid receptor, as AM251 was unable to reverse these effects. It can be suggested that anandamide is tonically released to play some form of modulatory role in the trigeminovascular system. PMID: 14718591 Note: Anandamide is a fatty-acid derived compound that possesses pharmacological properties similar to delta 9-THC, the psychoactive component in cannabis. ----------

Thanks OUCH.  When California legalizes recreational use of pot in November, we''ll see if it wipes out clusters on the west coast.

Pot, cigarettes, cigars, burning leaves, chimney smoke etc... for me = BAD trigger

Quote:

I recently spent a week in Gulf Shores in a drunken daze....

Wow. Sounds like fun.

Not.

It was always a trigger for me, so no benefit.

How did you manage to get into a drunken haze on verapamil and topamax.  Neither of those work well with alcohol for me, much less both.

You are very lucky that you did not suffer ill affects  Are you aware of the warnings associated with taking Topamax and drinking?  "Avoid drinking alcohol. It can increase some of the side effects of Topamax, and can also increase the risk of a seizure".

Quote:

How did you manage to get into a drunken haze on verapamil and topamax.

I believe he was talking about alcohol..not Verapamil or Topmax.

Hey smoke.....

As a former pot-head and now a 24 year sufferer of chronic cluster headaches, I have to admit that FOR ME, pot is a trigger.  I was in denial for a long time, but it was a trigger.  Sorry about that.

Alcohol is definately a big trigger for most.  I don't know how you avoided the "beast" in your drunken haze.  I wouldn't expect that to last...

Ray

Linda_Howell wrote on Apr 16^th, 2010 at 7:23pm:

Quote: How did you manage to get into a drunken haze on verapamil and topamax. I believe he was talking about alcohol..not Verapamil or Topmax.

I meant, being on verapamil and topamax, and getting into a drunken haze would be difficult for me.  I'd get sick far too soon to get really drunk, the drinks wouldn't taste good, and I'd know how hung over I'd feel that it'd never happen.  Either of those drugs + a lot of alcohol is bad news for me (topamax and a little bit of alcohol), much less both.

Within five minutes of a sip of wine during a cluster cycle, I'm in a Kip 5 to 7.  It's much less predictable with weed.  I haven't had a drink in three weeks -- don't smoke anything any more (never did smoke tobacco).  Still can't get the damned things under control, despite steroids, Topamax, and occasional use of Imitrex.  Haven't slept more than two continuous hours in more than 18 days, both from fear of waking up with headache and from effects of meds.  This is the longest cluster I've ever had.  Do they get worse with age?

If you want to try to treat clusters by altering the anandamide/cannabindoid pathways, I would suggest beta-caryophyllene. While cannabis affects mostly the CB1 receptors, caryophyllene hits the CB2 receptors. The CB2 receptors turn down inflammation and dampens some of the key immune hormones that are turned up too high in people with cluster headaches. Foods that include caryophyllene include cloves, basil, rosemary, cinnamon, and hops. There have been a few isolated reports here of hops being helpful for clusters. My money is on a mild pesto (without garlic, which can trigger for some people).  I think if this approach does help, it would be via gradual action and it would be preventive, not abortive. Echinacea also stimulates the CB2 receptors, and might be a good packaged alternative... drops of extract under the tongue 3x-5x a day is pretty easy. With echinacea drops held in the mouth, the prickly or tingling sensation is a good indicator of the active ingredient.

START PRINTPAGEMultimedia File Viewing and Clickable Links are available for Registered Members only!!  You need to or END PRINTPAGE

i enjoyed smoking pot more than most! i dont recomentd it for your CH! agree more of a triger. gave up smoking to see if the demon would go away and no still getem but still not smoking any more. been about 2yrs and yes sometime i still think id like to 8-)