Why does Oxygen work for CH ? Possibly not why you think.

30 Apr, 2015 - 9:41 am

I've never seen a good explanation of why oxygen treatment can abort a cluster headache - but I've certainly experienced it many times. I've read many of the papers on the subject from Horton in '52 through Kudrow's work in California through 80's and 90's. The text on this site puts forward the hypothesis:

"Why does it work? Your brain very closely monitors the amount of oxygen it receives, so it always gets the right amount. When it starts to get too much, it simply constricts the blood vessels that supply it with oxygenated blood. Because Cluster headaches are from Dilated blood vessels applying pressure the the Trigeminal Nerve, this command from the brain to constrict them reverses the cause of the attack, and abruptly ends it."

I never really bought that. Why does the flow rate have to be so high to achieve an increased blood oxygen saturation level leading to constriction? Why does this treatment have much less effect on other types of vascular headache ?

There's a growing body of evidence that Cluster Headaches may be caused by an enlarged and under-active Hypothalamus e.g.: http://www.ncbi.nlm.nih.gov/pmc/articles/PMC3002651/

and

http://journals.lww.com/neurotodayonline/Fulltext/2006/07180/Hypoth
alamic_Stimulation_Offers_Relief_for_Cluster.1.aspx

A few years ago when researching the possible dangers of breathing pure oxygen I came across this research from UCLA: http://www.sciencedaily.com/releases/2007/05/070521213022.htm

That suggests to me that the real reason O2 is effective in treating a CH attack is more likely to be related to massive stimulation of Hypothalamus activity than it is to a simple constriction of blood vessels due to an elevated blood O2 saturation. Note that there is also a strong suggestion in the research that concentrated O2 inhalation is not as benign as many people assume - however that's not going to put me off (getting my delivery today from MEGA as my clusters are back after 2 years).

I'm interested to hear the thoughts of other members here on my hypothesis.This post was edited on 30/04/2015 at 9:42 am

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01 May, 2015 - 9:54 am

I was informed by a paramedic who came to my home to give me oxygen that long term use of pure oxygen would cause my lungs to become lazy and therefore depend on receiving the oxygen.
I have also wondered, (as it seems that my chs have seemed worse since having my own oxygen supply at home) If the use of oxygen is helping in the short term, but creating a vicious cycle in the long term.
I will check out your links now.

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15 May, 2017 - 3:43 pm

Hi the cluster headache is caused when the blood vessels dilate .Scientists think a malfunction or abnormality of the hypothalamus causes the carotid arteries that feed the brain to enlarge and press on the trigeminal nerves, causing incredible pain. The trigeminal is a bundle of nerves, one bundle on each side of the head, that split into three to serve the upper jaw, face, forehead and temple. This idea got complicated, though, when researchers found that the pain of cluster headache seems to start before the artery expands and touches the trigeminal but
Oxygen at 15 to 25 litres a minute will 1st dilate the blood vessels also then as they are getting a lot of oxygen , the brain then relaxes the blood vessels and the cluster goes away . This is the way it seems to work .
Long term oxygen will not make your lungs lazy as its only short term on each cluster.

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08 Feb, 2018 - 4:33 pm

Oxygen inhalation suppresses CGRP, that's how it works.
You're correct Fiemus, the vascular theory of headache is no longer considered correct.
Peter Goadsby wrote a paper on it: https://tinyurl.com/y956kdek

"Treatment with both oxygen and subcutaneous sumatriptan reduced the CGRP level to normal,"

Human in vivo evidence for trigeminovascular activation in cluster headache. Neuropeptide changes and effects of acute attacks therapies.

Goadsby PJ1, Edvinsson L.

Cluster headache is a rare very severe disorder that is clinically well characterized with a relatively poorly understood pathophysiology. In this study patients with episodic cluster headache fulfilling the criteria of the International Headache Society were examined during an acute spontaneous attack of headache to determine the local cranial release of neuropeptides.

Blood was sampled from the external jugular vein ipsilateral to the pain before and after treatment of the attack. Samples were assayed for calcitonin gene-related peptide (CGRP), vasoactive intestinal polypeptide (VIP), substance P and neuropeptide Y. Attacks were treated with either oxygen inhalation, sumatriptan or an opiate.

Thirteen patients were studied of whom 10 were male and three female. All had well-established typical attacks of cluster headache when blood was sampled. During the attacks external jugular vein blood levels of CGRP and VIP were raised while there was no change in neuropeptide Y or substance P.

Calcitonin gene-related peptide levels rose to 110 +/- 7 pmol/l (normal: < 40) while VIP levels rose to 20 +/- 3 pmol/l (normal: < 7).

Treatment with both oxygen and subcutaneous sumatriptan reduced the CGRP level to normal, while opiate administration did not alter the peptide levels.

These data demonstrate for the first time in vivo human evidence for activation of the trigeminovascular system and the cranial parasympathetic nervous system in an acute attack of cluster headache. Furthermore, it is shown that both oxygen and sumatriptan abort the attacks and terminate activity in the trigeminovascular system.


https://www.ncbi.nlm.nih.gov/pubmed/7518321This post was edited on 08/02/2018 at 4:35 pm

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