Today, in part two, we’ll go over a remarkable study that clearly demonstrates the potent effects of pot smoking on cluster headaches. We’ll also start our review on the possible mechanisms that underlie the cerebrovascular events that result in cluster or migraine headache, and how they are intimately involved with CB receptors.
Thankfully, cluster HA is fairly rare yet that fact fails to placate those who suffer from it. That’s because cluster headache is horrifically painful: a former patient of mine, a medieval history professor, once quipped that he would prefer the strappado rather than endure another debilitating series of cluster attacks. Really? If that’s the case it has to hurt.
Briefly, when an attack occurs it produces severe, stabbing pain on one side of the face and cranium, a runny nose, drooping eyelid and dilated pupil. The attacks occur in clusters for several weeks to months, and then just as quickly, it disappears, only to return again months later.
A NOVEL AND HIGHLY EFFECTIVE TREATMENT
Recently a groundbreaking article was published in Headache by Robbins et al, which clearly showed an astonishing, near complete, reduction in cluster HA symptoms within five minutes in a patient who smoked marijuana for relief of his condition.
We present a patient with cluster headaches who was refractory to multiple acute and preventive medications but successfully aborted his attacks with recreational marijuana use; subsequent use of dronabinol provided equally effective pain relief.
The author commented that the benefit may be related to the high concentration of cannabinoid receptors in an area of the brain called the hypothalamus. This region “lights up” as a site of dysfunction in neuroimaging studies of patient who suffer from cluster HA. I’m in awe because nothing in a doctor’s medicine cabinet comes close to this kind of success, not even the cabinet of Dr Caligari.
THIS YEARS MODEL
Even if we cannot prove something, it’s essential in scientific studies to be able to provide a model for how a disease might manifest. Then further testing will either prove or disprove the hypothesis.
At least in theory there are a number of good reasons why cannabinoids may have a positive pharmacologic effect on headache. In The Use of Marijuana or Synthetic Cannabinoids for the Treatment of Headache, Uri Napchan MD et al, had this to say:
Cannabinoids are active in areas of the brain known to be involved in migraine pathophysiology, including areas suspected of being involved in the generation of migraine. The endogenous compound anandamide appears to modulate pain signaling in the central nervous system. It also potentiates 5-HT1A and inhibits 5-HT2A receptors, [5HT receptors are serotonin receptors] so effects on serotonergic pain transmission also may be involved in any therapeutic effects on headache.
Right now the best drug for treating migraine is called Imitrex which stimulates serotonin receptors within the brain. That in turn acts on blood vessels causing them to constrict which relieves migraine symptoms.
MEHCANISM OF ACTION
Sumatriptan binds with high affinity to human cloned 5-HT1B/1D receptors. Sumatriptan presumably exerts its therapeutic effects in the treatment of migraine headache through agonist effects at the 5-HT1B/1D receptors on intracranial blood vessels and sensory nerves of the trigeminal system, which result in cranial vessel constriction and inhibition of pro-inflammatory neuropeptide release.
However, Imitrex is fraught with serious side effects. Compared to pot’s benign profile, sumatriptan looks more like a 12th century poison. Mary Jane’s effects seem quite similar on the serotonin system, yet it doesn’t produce the adverse drug effects that are legion with Imitrex or many of today’s pharmaceuticals.
In part three we’ll continue our discussion on scientific models that explain pot’s potent actions on headache. Can you say endocannabinoid deficiency?