So I've had a nasty outer-ear infection for almost a week now, and I've noticed that its always worse at night. Now the pain is caused by the inflammation of my ear canal. My ear canal is cinched tight, completely closed, which I'd assume is why the further inflammation makes it hurt like hell.

Now I'm wondering why is it worse at night? Why do I have worsening inflammation at night? Most of you can follow the train of thought here. CH's are caused by inflammation, which puts pressure on the trigeminal nerve, and certainly worse at night.

I Googled "why is inflammation worse at night?" and there are lots of conditions which people complain about their pain being worse at night.
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There's also lots, and lots of theories, but that in itself suggests the cause either isn't known or often mistaken for another.

I know the theory and data suggests the hypothalamus as the 'culprit' for the timing of CH's. Yet I wonder if there is more known data regarding why, for example ear inflammation is worse at night. By that I mean perhaps there's another explanation as to the 'culprit'.

Is the hypothalamus responsible for my ear inflammation being worse at night? Or someones Arthritis, Sciatica, Hip Bursitis, Sinus headaches, Back Pain? I'm sure they all don't have the same 'culprit' but I'd imagine there's commonalities.

Just some food for thought.

co2 buildup

Simple enough, Thanks for the info. Much appreciated.

I wonder if wearing a Nasal cannula with O2 at a low volume level, during sleep effects, or prevents to some extent CH's during sleep?

I've noticed lately, coincidentally around the time I had a cycle start, that I wake up with a clogged nostril(s). I blame the furnace for the dry air, and the stuffed nose, and perhaps it increases a CO2 build up?

Just brainstorming, and thinking 'out loud' but maybe there's a connection with some kind of respiratory disorder? A sort of Central sleep apnea, or even snoring.

Morning headaches
One of the more mysterious symptoms of COPD is waking up after a night's sleep with a dull, throbbing headache. "What's happening is that you're not breathing deeply enough at night, and the carbon dioxide builds up while you're sleeping," says physician Norman Edelman, chief medical officer for the American Lung Association. The buildup of carbon dioxide causes blood vessels in the brain to dilate, resulting in headaches.

Many people don't connect the headaches to COPD, though; instead they treat them as a separate symptom. But unless you treat the underlying cause -- making sure you get enough oxygen into your lungs while you sleep -- the headaches won't go away. Talk to your doctor about setting up a treatment regimen for COPD designed to reduce inflammation and increase the absorbent capacity of the lungs. via START PRINTPAGEMultimedia File Viewing and Clickable Links are available for Registered Members only!!  You need to or END PRINTPAGE

I'm not suggesting we all have COPD, or a form of it, just brainstorming here. Please no flames.  :P

Hypercapnia
is an unusually high concentration of carbon dioxide in the blood which may be accompanied by hypoxemia, in which the oxygen level in the blood is low. This condition occurs as a result of poor gas exchange at the lungs which makes it difficult for people to eliminate carbon dioxide from their bodies.
Patients with hypercapnia can develop respiratory acidosis, in which the pH content of the blood drops because of the change in its chemical composition. via START PRINTPAGEMultimedia File Viewing and Clickable Links are available for Registered Members only!!  You need to or END PRINTPAGE

I watched a show once on health, and ironically I believe it was the first time I heard the term "executive headache". It followed a few "Executives" during a normal day. During some paper-work one of the subjects stopped breathing for a short, (imperceptible to him) length of time, and the person conduction the study was pointing out how he was tense and conveyed the related health issues resulting from it.
I wish I knew what the show was called, but it was a long time ago. Only now do I have a database of educational shows.  :)

Now again, I'm not suggesting this is the case for anyone with CH, but I do know that I get tense and I'm sure my O2 and CO2 levels are effected. I regularly relax my shoulders and take a deep breath to keep it in check. I also try to meditate, yet with a 15 month old running around of late, that is getting hard to schedule. lol

While I'm sleeping, perhaps my tension builds, with nothing to keep it in check, or even notice its happening? I went through a fairly stressful period before my latest cycle started, and I've been having fantastically vivid dreams for the past few months.

Exercise is a great preventative for some, its also a great reliever of stress.

Maybe CH's are even due to us all having a blood vessel uncommonly close to our trigeminal nerve? And during times of stress, that cause a slight increase in CO2 levels for everyone, as we sleep or rest, triggers a CH in CH'ers?

Perhaps its the pain itself that activates the hypothalamus, which is why its the only different activity?

If you've followed me this far, you'll know I'm letting the thoughts fly. Call it guessology if you will, but I've had renewed hope that this medical issue can be solved, and fully understood. From where I'm sitting the future looks bright and perhaps completely pain-free thanks to Batch's Regime. O2 therapy and the work people have done to design, create, and share it, has saved me an incalculable amount of pain. Even Mushrooms seemed to give me a great deal of relief.

Please feel free to share your wild ideas with me. I'm as 'open-minded' as they get, and I Respect everyone's thoughts and beliefs. Even when I feel they couldn't be more wrong. I've learned more from being wrong then being right.

lol, 50,000+ characters = time to stop.

A neighbor of mine has a bumper sticker which says:
"You don't have to believe every thought you have!" <bg>

Cluster is not caused by inflammation.
==
Headache:lessons learned from functional imaging
British Medical Bulletin 2003; 65: 223-234

Arne May
Department of Neurology, University of Regensburg, Regensburg, Germany

Using PET in a larger patient series, significant activations ascribable to the acute cluster headache were observed in the ipsilateral hypothalamic grey matter when compared to the headache-free state44. This highly significant activation was not seen in cluster headache patients out of the bout when compared to the patients experiencing an acute cluster headache attack45. In contrast to migraine25, no brainstem activation was found during the acute attack compared to the resting state. This is remarkable, as migraine and cluster headache are often discussed as related disorders and identical specific compounds, such as ergotamine and sumatriptan, are currently used in the acute treatment of both types of headache46. These data suggest that while primary headaches such as migraine and cluster headache may share a common pain pathway, the trigeminovascular innervation, the underlying pathogenesis differs significantly as might be inferred from the different patterns of presentation and responses to preventative agents46.
Just as it is striking that no brainstem activation occurs in contrast to acute migraine, no hypothalamic activation was seen in experimental pain induced by capsaicin injection into the forehead47. This is important because injection of the forehead would activate first (ophthalmic) division afferents which are the trigeminal division predominantly responsible for pain activation in cluster headache. Thus two other types of first division of trigeminal nerve pain, while sharing neuro-anatomical pathways with cluster headache, do not give rise to


VASCULAR HEADACHE: ARE BLOOD VESSELS INVOLVED?

Taking these observations on acute cluster headache together with what has been observed in experimental head-pain and migraine, the data establish that migraine and CLUSTER HEADACHE, FAR FROM BEING PRIMARILY VASCULAR DISORDERS, ARE CONDITIONS WHOSE GENESIS IS TO BE FOUND IN THE CENTRAL NERVOUS SYSTEM IN PACEMAKER OR CIRCADIAN REGIONS SPECIFIC TO THE SYNDROME. If further studies confirm these findings, a better understanding will be gained of where and how acute and preventative therapy can be targeted.
====
That you have found material which links CH to inflammation can be misleading because it's out of date. When looking at medical literature it's necessary to start with the latest material and work back in time so that you can see any evolution in the knowledge.

The hypothalamus gland triggers the timing of the attack, whether it be to trigger the beginning of a cycle (Spring/Fall, etc) or time of day or night of each attack.

To answer your question specifically in more detail....inflammation is worse at night because of naturally occurring Carbon Dioxide (co2) buildup.

Respiratory, COPD, etc may cause additional co2 buildup for those afflicted by those issues.  Most CH'ers report no history of COPD, respiratory issues, etc; so there is not a credible link to CH's.

In general, co2 buildup naturally occurs when the body is resting. 

It is not that we CH'ers have a lack of o2, so a need for additional o2 while sleeping such as a nasal canula is not going to be of help.  Many insurance co's have been known to test for lack of o2 among CH'ers to determine if the patient will qualify for an o2 prescription  Again, we do not have a lack of o2, so this test is irrelevant to treatment of CH's.

Too much Co2 creates (vasodilation) an inflammation in the trigeminal nerve which triggers pain.  i.e. eye, temples, neck, cheek, nose, teeth, ear, etc.  Co2 is the enemy! 

However, O2 is our friend! ;)  Oxygen (o2) will reduce the swelling/inflammation (vasoconstriction) and relieve the pain.

Hyperventilating 100% o2 with a NRB (Non-Rebreather Mask) at high flow rates (25 lpm to 40 lpm) will abort an attack within 15 minutes or less, IF the CH'er gets on the o2 at onset of attack.  It is important to breathe in the o2 in as fast and deep of a an inhalation possible, equally important as it is to exhale the co2 pushing it out as fast as possible.  Inhale deeply, exhale deeply, fast!  Like a panting dog, or after you've run out of breath chasing the puppy around the block.

If the CH'er gets on the o2 after the pain has reached unbearable pain levels, the attack may subside but most likely the CH'er will suffer for whatever length of time the duration of the attack is.  It is vital to get on o2 at onset of the attack!

If low flow rates are used, the CH'er will not have the opportunity to hyperventilate.  This often results in increased pain intensity and abort times will be lengthened.  The CH'er will often give up o2 and go for an Imitrex shot and conclude o2 does not work for them.

The concept behind o2 therapy is to increase the o2 levels greater than the co2 levels.  Once the pain reduces and the attack is aborted, it is very important to continue breathing the o2 for an addtl 5 or 10 minutes to avoid a re-attack.  This part of o2 therapy can be at lower flow rates such as 15 lpm.

Unfortunately, there is no credible neurological literature regarding o2 therapy at high flow rates (25 lpm - 40 lpm) that support hyperventilation.  The inside scoop is this literature is in the process of getting the "gold standard of approval" and should be out next year.  Until then, the only literature available is outdated showing 7 lpm to 10 lpm for 20 minutes, which is non-effective treatment.

Hope what i've shared helps you understand a bit more why inflammation is worse at night ;)

-Gregg in Las Vegas

Bob Johnson;
This is from Wikipedia
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Pathophysiology
Cluster headaches have been classified as vascular headaches. The intense pain is caused by the dilation of blood vessels which creates pressure on the trigeminal nerve. While this process is the immediate cause of the pain, the etiology (underlying cause or causes) is not fully understood.

I've listen to Dr's tell me and others things that sounded great, yet turned out to be completely wrong so many times I'm learned to be a skeptic.

Seeing unique activation in the Hypothalamus isn't proof-positive that its responsible. I don't doubt the FMRI data, and I'm not suggesting I know more then all those people who've interpreted the findings. I'm just not convinced.

I know for a fact there is a physiological difference in my brain when I'm in a CH, compared to when I'm not. Now an FMRI can show me what area is active, in comparison, yet I think its premature to 'assume' its responsible. Why is it not just as possible its being activated by the pain/CH?

Again, I'm just guessing without a medical education. I'm not suggesting the hypothalamus is not, in whole, or in part, responsible for CH pain. But I feel its fair to assume it may not be.
CONDITIONS WHOSE GENESIS IS TO BE FOUND IN THE CENTRAL NERVOUS SYSTEM IN PACEMAKER OR CIRCADIAN REGIONS SPECIFIC TO THE SYNDROME. If further studies confirm these findings, a better understanding will be gained of where and how acute and preventative therapy can be targeted.

This seems no more then an educated guess IMO, and a fairly general one at that. This from someone who's been spewing uneducated ones. lol

I did find this interesting,
Testosterone Replacement Therapy for Treatment Refractory Cluster Headache
Article first published online: 29 MAR 2006

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LasVegas
Thanks for the info. I'm actually quite well read on O2 therapy for CH, and even on respiratory O2 therapy.

I know low levels of O2 wont assist in an abort, and in fact may worsen a CH. Yet I'd assume that being on a low level O2 all night would increase one's O2 level, and by doing so, reduce CO2 levels.

Your system can only contain so much gas. Add more O2 and something has to be displaced. Co2, nitrogen and even O2.

I'm not suggesting its practical or anything, but just hypothesizing. Yet to be honest if I was getting hit still, I'd probably give it a try.  :)

There may be a buildup of CO2, I don't know, but for many the night attacks coincide with periods of REM sleep.

If my feeble memory serves me correctly, the hypothalamus monitors blood pressure and dialates or constricts the blood vessels as needed to maintain the requisite BP.  It would figure that if the hypo is screwed up, it could dialate the vessels an abnormal amount rather than being caused by inflamation.

From Cleveland Clinic:

Quote:

Inflammation is a process by which the body’s white blood cells and chemicals protect us from infection and foreign substances such as bacteria and viruses. Fig 1: When inflammation occurs normally, chemicals from the body’s white blood cells are released to protect us from foreign substances. Sometimes, however, the white blood cells and their inflammatory chemicals cause damage to the body’s tissues. In some diseases, however, the body’s defense system (immune system) inappropriately triggers an inflammatory response when there are no foreign substances to fight off. In these diseases, called autoimmune diseases, the body’s normally protective immune system causes damage to its own tissues. The body responds as if normal tissues are infected or somehow abnormal.

I doubt there is any inflamation going on.

Bob, Gregg, PlayDoh,

Great discussion.  Please allow me to chime in with my 2 cents...

I'm comfortable siding with all your positions as neither appears mutually exclusive when you take them in context...  For example:

Kudrow, with the benefit a few others before him, gave us oxygen therapy at a flow rate of 7 to 9 liters minutes with a non-rebreathing mask as a CH abortive.

Rozen gave us oxygen therapy at 15 liters/minute to treat CH'ers refractory to oxygen therapy at 7 to 9 liters/minute. 

When this mechanism of aborting cluster headache was taken into perspective, vascular and neurogenic theorists squared off all over the world for many years over which theory of cluster headache pathophysiology should prevail. 

Then Arne May gave us the latest and most learned explanation of CH pathogenesis in his Seminar Cluster headache: pathogenesis, diagnosis, and management, attached, where he plays a clever straddle with a very compelling use of "neurovascular factors..." in the following opening statement:

"Headaches often start about 1–2 h after falling asleep or in the
early morning, and show seasonal variation, suggesting that the hypothalamus has a role in the illness.  Consequently, the vascular theory has been superseded by recognition that neurovascular factors are more important."

Imagine the impact of seasonal variations in 25(OH)D levels suggesting vitamin D3 production and total intake plays a role in the pathophysiology of cluster headache...

I've had the pleasure of meeting with Dr. May over a two day period in July of 2010 at his UKE research facilities in Hamburg.  I had a fascinating two-hour, one-on-one meeting with him in his office looking at the results of his functional neuroimaging and its impact on explaining the pathophysiology of cluster headache and its pathogenesis.  A continuation of these same discussions and impact that oxygen therapy with hyperventilation would have on that pathogenesis over a delightful three-hour dinner with him at a great little Italian restaurant a short walk from the UKE campus was equally fascinating.

Regarding the respective roles of oxygen and carbon dioxide on cluster headache... In 2005 after turning chronic, and not knowing any better other than being confident it was perfectly safe after 3,000 hours of breathing 100% oxygen while flying jets, I cranked the oxygen flow rate up from 15 liters/minute to 60 liters/minute in 15 liter/minute increments during successive attempts to abort a night's worth of head-bangers.  To my surprise, the abort times came down with each increase in flow rate. 

After less than 24 hours, I settled on a procedure to abort my CH with oxygen therapy that called for an initial few seconds of relaxed deep breathing with 100% oxygen at forced vital capacity tidal volumes to clear nitrogen and let the coughing caused by atelectasis clear followed by a very rapid respiration rate breathing oxygen as deeply as possible at a flow rate of 60 liters/minute for 30 seconds to a minute or until I experienced the symptoms of paresthesia with a slight tingling or prickling sensation of the lips, face, back of the neck, and fingertips which ever came first.  At that point I reduced the oxygen flow rate to 45 liters/minute and continued breathing at forced vital capacity tidal volumes until the abort.

It took me nearly a year reading respiratory physiology texts, articles and studies as well as several conversations with one of my old Navy Flight Surgeons and an Aviation Physilogists to get my head completely around the respiratory physiology involved in this method of oxygen therapy. 

What I learned and later reproduced using oxygen therapy at a flow rate of 7 to 9 liters/minute was that while this flow rate provided all the oxygen I needed to abort a CH, when there was any physical activity and the total lung ventilation was limited to that flow rate, it was insufficient to remove excess CO2, the levels built up above normal and eventually prevented the oxygen therapy from aborting my CH. 

I verified this using a capnometer and saliva pH test strips during an attempted abort of a CH at this flow rate and found my CO2 levels were above normal and pH was below normal (more acidic) when this method of oxygen therapy was unable to abort my CH.

I repeated these tests using the same 7 to 9 liters/minute oxygen flow rate, but alternated taking two full breaths of air between each breath of oxygen.  I got a fairly rapid abort with my CO2 levels lower than normal and pH higher than normal.  I repeated these tests a third time at an oxygen flow rate of 45 liters/minute, and got the same rapid abort with nearly identical CO2 and pH readings.

After that I started taking what I'd learned to three of the leaders in the field of neurology specializing in cluster headache and other TACs: Todd Rozen, Arne May, and Peter Sandor.  We discussed the respective roles of oxygen and carbon dioxide in process of aborting the cluster headache and the cluster headache triggering mechanism.

My cut on why we tend to have more CH while sleeping is more an adaptation.  I'm comfortable that the CH starts in the hypothalamus. It's the chain of events or processes that take place in the rest of the triggering mechanism where I think there is room for enabling and perturbation factors to influence the outcome either way... a full fledged cluster headache... or its prevention.

In short, I'm confident with the notion that somewhere between the hypothalamus deciding it's time for a cluster headache and one actually occurring, that there are a number of dependent and independent processes taking place.  Some of these processes result in a cluster headache...  and some can prevent it.  I realize that's likely an oversimplification... but that's the way I see it...  I'm just an old fighter pilot... not a neurologist or biochemist...  It's kind of like the aviation saying:  Power plus attitude equals performance, or input equals output less some inefficiencies...  simple concepts, easy to grasp.

When we sleep there are several factors that can come into play that help enable the cluster headache triggering mechanism making it more effective with an increase in the frequency of cluster headache: slightly lower oxygen levels, slightly higher CO2 levels, a slight increase in vascular pressure and blood flow due to the inclined position with the head at the same level as the heart.  Any one of these factors may be insignificant by themselves.  However, when they all occur at the same time, a synergistic effect is clearly possible.

Some of this is still half-baked even in my mind...  but when we consider the impact of vitamin D3 supplementation and the role of 25(OH)D levels on the pathogenesis of cluster headache...  I think the gene is out of the bottle...  and all bets are off.

Again, a great discussion...

Take care,

V/R, Batch

---

WoW again Batch. Thanks for the thoughts. Thanks for all the input, everyone.

I've been pondering a similar idea that there's likely a symphony of factors that ultimately determine the outcome of a CH. From shadow to kip 9+.

I've also considered the possibility that there are multiple 'types' of CH, with different or partially different pathogenesis-es (culprits). Perhaps the ineffectiveness of O2, for some, is proof of that. Yet I cant help but be skeptical that it might be a matter of improper use then O2 being ineffective. Yet with as many reports as I've seen it seems quite likely that O2 is ineffective for at least some.

Perhaps for some its a Inflammation/dilation/vascular pathogenesis, yet for others its something like cranial pressure on the Trigeminal nerve. Or perhaps some/all/most are effected by both, using only 2 pathogenesis for example.

If your Trigeminal was receiving pressure from a physical force, other then vascular, O2 probably wouldn't do anything for you.

I noticed that my CH career  ;) started not too long after a couple car accidents. I know enough not to make any 'certain' assumptions, yet my CH pain seems to be effected by heat and pressure on the back of my neck. My neck was injured in both accidents. 

I've wondered if after those accidents the blood flow in my head has been altered, making me 'susceptible' to CH's. When I have the symphony of factors occur, like for the sake of hypothesis, laying down, increased co2 levels, muscle tension, Vit D deficient, neck position, I end up with a CH.

Take away say one or two of those factors and I end up with say a Kip 6. Only one or two present, perhaps Kip 2. All possible conditions, Head-banger.

Change the level of blood flow deviation significantly, and I have Chronic CH, or vice-versa.

One thing that bothers me about the Hypothalamus theory is the spontaneous onset of CH, as a condition. To go from normal to CH's routinely doesn't seem to mesh with an abnormality deep in the brain. At least not entirely.

I feel some 'event' is more likely a cause, since if it was just a 'birth defect' with my hypothalamus, I don't see how I could go 24 or so years without any 'hint' or even HA's of any significance, to one day I have CH. I'm not suggesting its impossible, but seems illogical and unlikely to me.

I've also considered if my exposure to 'unhealthy' levels of co2 a number of times (faulty furnace and improperly vented welding shop), around the time my CH's started, could be related to my 'CH career'. It seems likely that 1 in a 1000 others could have received a similar exposure with CH's as a possible "injury".

More guessology. lol

Thanks again for joining me Batch, Bob P, LasVegas and Bob Johnson.

I LOVE think-tank debates.  ;D

PlayDoh,

Hmmm... you just knocked another electron out of orbit or flipped a bit somewhere in my memory banks with your comment about a faulty furnace and welding fumes... 

Carbon monoxide (CO) can be particularly nasty.  It does an OWS on hemoglobin and that screws the pooch slowing the normal transport and exchange of oxygen and CO2 between the lungs and body. 

When CO occupies hemoglobin molecule's sockets... the same ones used to transport oxygen and CO2, there's no room for oxygen or CO2 molecules so serum oxygen levels drop like a rock, CO2 levels spike...  and BINGO!  You have CO poisoning.

We used to carry CO test kits in the older piston driven transport aircraft as cabin heating was accomplished by passing cockpit air through a radiator like heat exchanger on the firewall heated by engine exhaust or burning avgas. 

A cracked weld in a heat exchanger was not uncommon.  What made it worse is CO is odorless and colorless and the symptoms of CO poisoning are similar to hypoxia (lack of oxygen)...  Fortunately the treatment for both was to get on 100% oxygen... if you detected the symptoms before passing out.

Welding fumes can pose a similar problem as they contain some really exotic metallic and molecular vapors that are highly reactive so can also play heck with hemoglobin chemistry.

The 2005 Seminar by Arne May is close to, if not the Gold Standard when it comes to explaining cluster headache. That said, the attached paper on Cluster headache: Epidemiology, clinical features, and diagnosis, also authored by Arne May, provides some interesting stats on brain injuries and cranial lesions associated with cluster headache you might find interesting...

Take care,

V/R, Batch

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Hi Batch,
pdf file did not open.
-Gregg

CLUSTER+HEADACHE+09

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attached below

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hmmm

Works now (attachment)

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