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AussieBrian
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Re: CH history, genetic link and nicotine
« Reply #75 on: May 7th, 2008, 1:24am »
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on May 6th, 2008, 10:44pm, BMoneeTheMoneeMan wrote:
...until you can come up with hard concrete proof of what exactly causes CH, there's no sense in researching theories regarding the cause of CH.

You're gunna have to run that one by me again, BMonee. I know I'm old and slow but how can the proof be found without researching the theories?
 
All the theories.
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Re: CH history, genetic link and nicotine
« Reply #76 on: May 7th, 2008, 1:54am »
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First of all, let me commend you for the work you've done on this subject.
 
That said, let me just comment on a couple points.  
 
 
on May 6th, 2008, 10:46am, Annette wrote:

 
Although medical record prior to the 1960s did not report much on the prevalence of rare condition, but it is interesting that there had been NO record of a description of any headache with symptoms classical of CH prior to 1641. There had been no record of any headache that occured several times a day at exactly the same times, I would have thought that anyone observing that would find it interesting enough to document.  

 
This may or may not be true. It certainly isn't something that you can make a statement of fact.  
The only fact is that you didn't find anything on the internet from before 1641.  
The world was much different before 1641.
My guess is that at least some of those skulls they find from 1000 BC that have trepanning holes drilled into their temples, just might have had clusters.
 
We still find ancient writings (ex; dead sea scrolls) that describe things we hadn't known to have existed prior to the microwave.
 
Between 1300 and 1700, I think the Black Plague and the other plagues were keeping most of the record keepers and physicians pretty busy, or dead. Maybe a little too busy to worry about someone with a "headache"?
 
Before this time period (1300s), record keeping was sparse at best. It's also very possible that before that time, they had a very good treatment for clusters and it wasn't that big a deal. If you go back and read the Rig Veda (circa 1000 - 1500 BC) you'd find that they were treating dibilitating headaches, with magic mushrooms.
 
Then again, people banging their heads on the cave walls most likely would have been clubbed to death as being useless for the hunt.  
 
Just because it isn't there (yet), doesn't prove anything.
 
on May 6th, 2008, 10:46am, Annette wrote:

 
I would love it if anyone who believes in different theories can actually come up with researched evidences, rather just personal hunches and impression. That way it will make the discussions more interesting and valid.  
 

 
Many of your passages are littered with your own personal hunches and impressions, although you state them as facts. Many statements, just like the one about nothing before 1641, are just what you are telling others not to make. That's not playing very fair IMHO.
 
I was also a little offended by your suggestion that it would be good to sue tobacco companies.  
First of all, as was pointed out, it wouldn't do any good because it would have been an unintended consequence, not like hiding data on it's cancer causing effects.
Second of all, even if sued, they would never throw billions of dollars at trying to find the "real" cause of clusters. They'd have no reason to. That research, even with billions of dollars, would still most likely take decades. Even if it took 10 years, it would never be completed before a lawsuit was settled. They would have absolutely no incentive to search for the cause of clusters.
I would also never sue anyone or any entity, for personal gain, just because they "have the money"
and that is what you intimated. Even if they didn't cause it, they'd spend the money to defend themselves by researching the "real" cause.
 
Lastly, as I said in the beginning, you did a lot of work on this and have come up with some interesting theories, and for that I do commend you.
 
Bobw
 
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Re: CH history, genetic link and nicotine
« Reply #77 on: May 7th, 2008, 3:23am »
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on May 7th, 2008, 1:24am, AussieBrian wrote:

 
 
All the theories.

 
 I am with you 100% mate! The key word is theories. Use it while you are postulating and it changes the tone of the entire post and throws it back to where it should be.......we are all searching.
 
 Don't make that clear and you are running the risk of making visitors to the site think that we have more answers than we do.
 
 
 Been away awhile but I still think the micro-brew research may still be our best bet.........................Cheers...........Tim
 
   
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Re: CH history, genetic link and nicotine
« Reply #78 on: May 7th, 2008, 7:33am »
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on May 7th, 2008, 3:23am, tanner wrote:
Been away awhile but I still think the micro-brew research may still be our best bet..

You've caught me out completely on that one, Tim, because this is the first I've heard about 'micro-brew research'' and while you believe it to be our best bet, I'm not happy leaving it as our only bet.
 
As you say, it's 'research', and all research is good research until proven otherwise.
 
It may surprise you to learn that some people are even researching magic mushrooms (of all things) with a view towards finding a cure.  
 
Research has given us oxygen and Imetrex while suggesting capsaicin and voodoo may be a little less than effective.  Kudzu, melatonin and Red Bull  as opposed to dentistry, sinal surgery and tin-foil hats.
 
Annette's research seems to be towards possible causative factors, as opposed to palliative care,  and no harm can from it while we all remain open minded.
 
 
 
 
 
 
 
 
 
 
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Re: CH history, genetic link and nicotine
« Reply #79 on: May 7th, 2008, 9:46am »
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We can sit here and theorize until the cows come home.
 
Gathering info from the Internet may be helpful for us personally, but in order for real research to happen, we would have to come up with some convincing evidence and present it to a university or hospital to pursue.
 
In the case of psychedelic treatments and kudzu, the anecdotal evidence came from sufferers.  
 
Annette, I do have to ask how you arrived at this conclusion:
on May 6th, 2008, 9:30pm, Annette wrote:

 
I guess this is why Flo dont come here anymore and why Lee said he preferred to keep all his findings to himself.

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Re: CH history, genetic link and nicotine
« Reply #80 on: May 7th, 2008, 9:54am »
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on May 7th, 2008, 1:24am, AussieBrian wrote:

You're gunna have to run that one by me again, BMonee. I know I'm old and slow but how can the proof be found without researching the theories?
 

 
In order to get an egg, you need to have a chicken.
 
 
It's too bad sarcasm doesn't work so well on the internets, cause i am laying it on pretty thick.
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Re: CH history, genetic link and nicotine
« Reply #81 on: May 7th, 2008, 11:14am »
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on May 7th, 2008, 7:33am, AussieBrian wrote:
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You've caught me out completely on that one, Tim, because this is the first I've heard about 'micro-brew research'' and while you believe it to be our best bet, I'm not happy leaving it as our only bet.

 
It may surprise you to learn that some people are even researching magic mushrooms (of all things) with a view towards finding a cure.  
 

 
Wasn't the 'micro-brew' a veiled reference to the mushrooms?  I can't imagine that producing beer on a small scale would be beneficial to clusters in any way. Or am I missing something?
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Re: CH history, genetic link and nicotine
« Reply #82 on: May 7th, 2008, 11:33am »
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on May 7th, 2008, 11:14am, monty wrote:

 
It may surprise you to learn that some people are even researching magic mushrooms (of all things) with a view towards finding a cure. Wasn't the 'micro-brew' a veiled reference to the mushrooms?  I can't imagine that producing beer on a small scale would be beneficial to clusters in any way. Or am I missing something?

 
Just venturing a guess here, but the micro-brew reference could be addressing the fact that for some CHers, beer/alcohol is a trigger for a hit, where for others it is not?
 
 
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Re: CH history, genetic link and nicotine
« Reply #83 on: May 7th, 2008, 12:11pm »
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on May 6th, 2008, 8:24pm, Annette wrote:
That is because CH is multifacets ie many things can lead to CH. Its not caused by ONE thing.

This is a crucial statement and is one that I've been banging on about for years.  It only works though if you agree with the theory of predisposition i.e. some people are predisposed to develop cluster headache and some more so than others.  I've posted the following before on a couple of occasions in slightly different guises, and it's been a real thread-killer in the past, but ho hum, here it is again.
 
As with many things in life, I believe cluster headache is a factor of both nature and nurture.  Firstly, I think that sufferers are born with a natural propensity to develop the symptoms and pain of these so-called headaches.  This is a hereditary factor based on genes of one of the parents; and the reason why it can and does skip generations is that the abnormal genes that cause CH can lie dormant unless triggered by external factors.
 
All the clinical evidence suggests that we have to start with the hypothalamus.  Most practitioners who specialise in CH agree that the abnormality within the hypothalamus is the root cause of the pain, which when in cycle releases hormones and chemicals that innervate (stimulate) the trigeminal ganglion, which in turn causes the domino effect of pain and cranial autonomic symptoms through the trigeminal nerve down one side of the face and head.  This theory is backed up by the uncanny regularity of attacks (circannual and circadian), much lower levels of plasma testosterone (amongst men) during attacks and bouts, and alterations in the natural production of hormones/chemicals that affect endogenous biologic clocks.  The most recent research involving PET studies amongst CH sufferers put the icing on the cake for me, which in summary showed an increase in functional activity of the hypothalamus amongst CH sufferers, which up until very recently has not seen in migraine.
 
Furthermore, it has always been assumed that primary headaches are caused by abnormal brain function rather than an abnormality in the brain.  However, by using magnetic resonance imaging (MRI), which visualises the structure and function of the brain by providing detailed images in any plane, it showed that there is a significant increase in the volume of grey matter in the brain.  This increased area was consistent with the location of activation seen in the PET studies; that is, the hypothalamus.  This is the prime reason why CH is thought to be caused by an abnormality within the hypothalamus.  These abnormalities were seen when sufferers were both in and out of bout and were interpreted as an excessive growth of grey cells within the hypothalamus, or more probably, within the suprachiasmatic nucleus (SCN), the previously mentioned master-clock.  I also think the pineal gland is closely linked with this theory, but I won't throw a spanner in the works on this one as yet.
 
So, sufferers may possibly inherit a brain abnormality from their parent's genes.  The extent of this abnormality determines the pattern(s) of CH amongst sufferers; so in fact, there may well be a variety of different types of CH based on the extent of this abnormality and how sufferers live their lives.  This may be why specific triggers of attacks are not ubiquitous and not all medications work for everyone.
 
I've no idea as to how many different types of CH there are, we're all different, but it's likely to be on a sliding scale based on the current yardstick of episodic to chronic; perhaps something like this:
  • Extreme abnormality: chronic from onset at any age
  • High abnormality: episodic with limited remission
  • Medium abnormality: half on half off
  • Low abnormality: episodic yearly  
  • Slight abnormality: single/infrequent episodes

The crucial thing is that the abnormality that sufferers are born with is not fixed.  Everyone who is unlucky enough to have the abnormality has the propensity for it to develop over time - classically from episodic to chronic and sometimes vice versa.  This is where the controversy may start creeping in.  Although the abnormality is pre-determined at birth, I also believe that there are other external factors (nurture) that can influence the pattern and type of CH.  Sufferers who are born with a particularly low abnormality may not develop CH until they are exposed to specific external forces.  So in a nutshell, someone who has a slight abnormality may move up the "intensity" scale because of external forces, and conversely, sufferers who have extreme abnormalities can and do move down the scale also due to external forces.
 
Here's the tricky bit: what are these external forces?  I would suggest that they are anything that can alter the natural balance of hormones and chemicals in the body; so it would make sense that it's all to do with consumption and lifestyle, possibly (not exclusive and in no particular order) as follows:
  • Diet: especially alcohol, nicotine and caffeine
  • Trauma: bangs to the head, disease etc.
  • Stress: particularly stark changes in the level of stress
  • Environment: temperature, humidity, seasons, altitude, latitude
  • Medication: preventatives, abortives, suppressives, regulators of neurogenesis
  • Health: general well being, sleep behaviour and illness
  • Lifestage: hormonal imbalance

So in summary, I believe that there is just one type of CH (which is closely linked to the other TACs), but within this, there are many different strains.  To understand the potential mechanisms involved we have to go right back to the root cause, which is currently thought to be due to an abnormality within the hypothalamus.  The extent of an individual's abnormality (possibly genetically linked) will dictate the initial onset and subsequent pattern of CH, but these are not fixed and in turn are influenced by specific external factors.  As external factors change over time, so does the pattern of an individual's CH, modifying these different strains.  So CH isn't black or white (episodic or chronic) but should be classified more in terms of a continuum: still largely dictated by periods of remission, but also frequency of occurrence and attack intensity, and the extent of influence of differing external factors.
 
There's more of course, if anyone is interested, but that should do for now.
 
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Re: CH history, genetic link and nicotine
« Reply #84 on: May 7th, 2008, 6:01pm »
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on May 6th, 2008, 8:21pm, Brew wrote:
The hypothalamus is considered to be the pain/pleasure center of our brains. Leading theories as to the cause of CH point to the hypothalamus. If our defective hypothalamuses are responsible for CH, could it not then be responsible for our collective penchant for addictions? And would it then be plausible that statistically we might be outside the norm when it comes to what we consider to be painful and/or pleasurable? I wonder if, for example, CH'ers represent a higher than normal percentage of sado/masochists, or anything else where pain and pleasure get opposite billing, as compared to a cross section of society?
 
Sorry - it's just how my mind works sometimes.

 
Brew, I wonder why my undefective hypothalamus became suddenly defective at the age of 47?
 
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Re: CH history, genetic link and nicotine
« Reply #85 on: May 7th, 2008, 6:14pm »
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on May 7th, 2008, 6:01pm, Giovanni wrote:

 
Brew, I wonder why my undefective hypothalamus became suddenly defective at the age of 47?
 
John  

My humble opinion - it has always been defective. The defect is only a gateway of sorts. But I'm not a doctor, so my opinion and $1.50 will get you a cup of coffee, but you better have the $1.50.
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Re: CH history, genetic link and nicotine
« Reply #86 on: May 7th, 2008, 6:31pm »
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on May 7th, 2008, 12:11pm, LeeS wrote:

 
This is a crucial statement and is one that I've been banging on about for years.  
 
As with many things in life, I believe cluster headache is a factor of both nature and nurture.  
 
-Lee

 
 
This is exactly what I have come to realise . We all agree that everyone's cluster is different. The only common denominator is the amount of pain and the characteristics of it. However, when we compare the history of one CHer to another, there is often nothing similar. Even in ones history, CH appears to morph and change and become influenced by different things at different times. That is an indication of the multifacet nature of it. When one starts to look into the biochemistry of CH and see how many factors are involved, how many neurotransmitters are involved... its no longer a surprise.
 
The difficulty arises when we pursuit one factor deeper and discuss about this particular factor, there will always be people who protest " but that does not affect me". However, if one tries to discuss enough factors to include everyone, the discussion will become so diluted that it loses its value.  
 
In regard to nature, researchers have finally come up with a gene that is strongly associated with CH. Even then there were people who did not have this gene and still had CH. Prof Goadsby came up with the anatomical abnormality in the hypothalamus, again this was not detected in all the CHers who had the scan.  
 
When looking at nurture, its so vast a subject where should one start? It would be wise to start with something that is most common in CHers. Personally I have looked at two in details : stress and cigarette smoking. Both have evidences to support their role in the development of CH. The next one I am interested in is the pineal gland with its involvement in the sleep/wake cycle and REM sleep.
 
The hypothesis and the theories are put forward not as gospel for people to take for granted. They are put forth as interesting findings that people might like to look into further for themselves and to discuss. Its there to be shred apart the way all hypothesis and theories should be. What I was looking for is for people to contribute with what they know or with personal experiences one way or another. For eg, if putting it forward encouraged people to come share that how stopping/starting smoking helped or did not help with CH then we would gain further information that is currently not available. Even if the theory gets completely disproved by the majority reporting that stopping smoking permanently does not do a thing for their CH then we have learnt something new too. Either way its useful and helpful.  
 
What doesnt help is when personal attack which has nothing to do with the topic of discussion get thrown in or when opinions are voiced just for the sake of argument. Still someone PMed me commented that since the personal attack did not start until page 3 that indeed for me its a new record. I guess I cant complain.
 
Thank you very much to everyone who have read the thread and have contributed.
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Re: CH history, genetic link and nicotine
« Reply #87 on: May 7th, 2008, 8:40pm »
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During my research, I came across this thread started by Flo in 2004, which barely had any interest/response to it at all.
 
http://www.clusterheadaches.com/cgi-bin/yabb/YaBB.cgi?board=medsarchive2 004;action=display;num=1097672966
 
 
This is what happens when information is presented purely in its scientific form, no one understands it enough to become interested or excited about it. Most people will read it and think " I dont understand so it doesnt apply to me".
 
However, when one presents the same information interpreted at a more personal level with ones own thoughts and speculations then the discussion tends to turn into personal issues and comments instead.  
 
How do we get past this ? Or we cant ?  
 
 
Modified to add: In hindsight I would say I have achieved more than Flo did by adding my personal theory and interpretations to the material. I dare say more people became interested on the topic this time around than 4 years ago. However that meant I got swiped at more than Flo did. Was it worth it ? YES !  
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Re: CH history, genetic link and nicotine
« Reply #88 on: May 7th, 2008, 11:52pm »
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on May 7th, 2008, 6:31pm, Annette wrote:

 
 Even if the theory gets completely disproved by the majority reporting that stopping smoking permanently does not do a thing for their CH then we have learnt something new too. Either way its useful and helpful.  
 
 

 
It has been looked at (by meducal professions) and stopping smoking does not appear to make any beneficial difference in one's clusters.
 
Long term smoking does cause damage in various ways. Can smoking, and the resulting damage  potentiate the onset of clusters, possibly. Maybe even probably in those people predisposed to cluster headaches.  
Stopping smoking does not reverse this damage nor does it "cure" clusters. The damage has been done. Can it possibly make then a little less severe? The only possibility for this in my opinion is that once the lungs clear as much as they can, it may make things better due to a more efficient oxygen supply.
The damage to the vascular system that most likely contributes to the pain cycles, won't be significantly repaired, in long term smokers.
 
Clusters are not alone in being triggered by a myriad of different combinations. Most, if not all, vascular related headaces are also caused by differing combinations of events and circumstances. This is one reason that  different treatments work for different people and why different triggers are sometimes present from one person to the next.
 
The human body in it's state of perfection, is a finely tuned instrument. If you, or your environment F**k with it, there are consequences. Many of which we still don't fully understand.
 
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Re: CH history, genetic link and nicotine
« Reply #89 on: May 7th, 2008, 11:56pm »
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on May 7th, 2008, 8:40pm, Annette wrote:
This is what happens when information is presented purely in its scientific form, no one understands it enough to become interested or excited about it. Most people will read it and think " I dont understand so it doesnt apply to me".
 

 
Really? I think you underestimate the people on this board.
But then, maybe you are just too smart for us.
 
<geeesh>
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Re: CH history, genetic link and nicotine
« Reply #90 on: May 8th, 2008, 1:07am »
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Annette,
 
Outstanding! I still say Your efforts here are worth publication if for no other reason than to stimulate a similar exchange among neurologists and medical scientists working on the cluster headache disorder.  I'd say that you and Lee took us way beyond Red Bull and Kudzu with help from AussieBrian and others tuned into your hypothesis and willing to contribute and stand by your right offer it as a discussion.  You also carried on multiple dialogs on as many different levels of understanding our disorder in a most professional and scientific manner.  We do need more science...  Thank you and Well done.
 
I've been following the writings and letters to the editor at JNNP offered by Dr. Vinod Gupta M.D. and neurologist.  Being a fighter pilot it was easy to recognize another Type 1 personality.  I think you and Lee may find the following provides yet another structure that can be used to shape our search for the cause(s), treatment, and someday a cure or lasting preventive for our disorder.
 
Please take care, and again, Well Done!
 
V/R, Batch
 
"Science is a process; accretion of data in the absence of a central concept thwarts or impedes the process.
 
Key issues that can evolve into a comprehensive theory for cluster headache include:[4][5][6][7][8][9][10]
 
1. The self-limited nature of cluster headache (15-180 minutes) indicates primary involvement of a system that has the intrinsic ability to limit or dampen the headache attack initiating physiological event. Such a system is highly unlikely to be purely vascular or neuronal.
 
2. Strict lateralization of headache indicates an idiosyncratic cranial structural or anatomical variation that localizes the headache.
 
3. Absence of vomiting despite a variant of headache that is frequently far more intense and distressing than migrainous headache indicates that vomiting – while frequently remitting migraine – might exacerbate the underlying pathophysiological mechanism in cluster headache.
 
4. Non-pulsatile nature of headache indicates occurrence of the maximum possible attack-related stretching of the cranial structure primarily involved in cluster headache.
 
5. Therapeutic effect of oxygen and ergotamine and aggravation / precipitation by alcohol or nitroglycerine (glyceryl trinitrate) strongly indicate primary involvement of peripheral non-neuronal mechanisms.
 
6. Prophylaxis with verapamil practically confirms a peripheral non- neuronal origin of cluster headache.
 
7. Long periods of remissions indicate operation of adaptive mechanisms, possibly involving tissue creep.
 
It is illusionary to believe that advanced neuro-imaging or other laboratory advancements have unlocked the “biology” of cluster headache. All laboratory procedures have their limitations; nothing can supplant careful thinking about the research question(s). Technology is a tool of science, it is not science itself. Also, undirected epidemiological investigations and nosological or statistical-mathematical sophistication do not further our understanding of cluster headache.
 
Vinod K Gupta, Physician. dr_vkgupta@yahoo.com
 
References
 
1. van Vliet JA, Favier I, Helmerhorst FM, Haan J, Ferrari MD. Cluster headache in women – relation with menstruation, use of oral contraceptives, pregnancy and menopause. J Neurol Neurosurg Psychiatry published online 11 Jan 2006; doi:10.1136/jnnp.2005.081158
 
2. Gupta VK. Migraine: Migraine: “how” versus “what” of a disease process. BMJ (published online 8 February 2006). Available at: http://bmj.bmjjournals.com/cgi/eletters/332/7532/25
 
3. Skrabanek P. The poverty of epidemiology. Persp Biol Med 1992;35:182-185.
 
4. Gupta VK. Trigeminal autonomic cephalalgias: ‘noso-physiology’ or pathophysiology? J Neurology Neurosurgery & Psychiatry (22 February 2005). Available at: http://jnnp.bmjjournals.com/cgi/eletters/76/3/301
 
5. Gupta VK. Intractable cluster headache and therapeutic stimulation of the hypothalamus: pathophysiological and management insights from a rare experiment. Brain 2005;128: E26. [Extract] [Full Text]
 
6. Gupta V. Does the eye modulate the clinical expression of cluster headache? BMC Neurology (17 May 2005) Available at: http://www.biomedcentral.com/1471-2377/5/6/comments#201461
 
7. Gupta VK. Is verapamil-triptan combination for cluster headache therapy pharmacologically valid? Headache [In press].
 
8. Gupta VK. Change in frequency pattern in cluster headache induced by subcutaneous sumatriptan. Headache [In press].
 
9. Gupta VK. Neuroimaging in hemicrania continua: dissociation between technology and basic sciences? Headache [In press].
 
10. Gupta VK. MRI imaging in primary headaches. Radiology 2006:238:754-755."
 
The complete text of the above letter to the editor can be found at the following link:   http://jnnp.bmj.com/cgi/eletters/jnnp.2005.081158v1
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Re: CH history, genetic link and nicotine
« Reply #91 on: May 8th, 2008, 2:37am »
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on May 7th, 2008, 11:56pm, Pinkfloyd wrote:

 
Really? I think you underestimate the people on this board.
But then, maybe you are just too smart for us.
 
<geeesh>
Bobw

 
 
I never said I am smarter than the people of this board although I did spent 7 years going through medical school and another 12 years working in various hospitals and clinics and am exposed daily to scientific and medical terms which many here are not familiar with.
 
I said that in the context of the responses Flo got 4 years ago trying to discuss the same topic.  When he simply posted the medical findings on this board, here were the responses he got :
 
on Oct 13th, 2004, 1:10pm, nani wrote:
Good Lord you guys are smart!  When you figure it all ou can you post in regular people words so I can get it?  laugh

 
 
on Oct 13th, 2004, 3:39pm, Woobie wrote:

 
 
 
 
Ditto!   laugh
 
I'm not the brightest crayon in the box ..........

 
 
on Oct 21st, 2004, 10:43am, Valerie wrote:

 
......  None of this makes sense to me - I appreciate the research you all are doing  Smiley  Smiley  Smiley
 
Valerie

 
 
on Oct 13th, 2004, 10:31am, ozzy wrote:

......
 
Then again, I probably didn't understand a thing....
 
 
Ozzy

 
 
When I read that I realised that if I just posted the studies without any comment or interpretation I most probably would get similar responses, people would say " interesting" and then not think twice about it. That was not the response I was hoping for.  
 
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Re: CH history, genetic link and nicotine
« Reply #92 on: May 8th, 2008, 2:46am »
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on May 7th, 2008, 11:52pm, Pinkfloyd wrote:

 
It has been looked at (by meducal professions) and stopping smoking does not appear to make any beneficial difference in one's clusters.
 
 
Bobw

 
 
Have you actually got concrete evidence of that ? Which medical professionals have looked at it and where did they publish their findings that stopping smoking does not make any beneficial difference to CH ?  
 
Can you please post these results ? I would love to see it as I have not found anything like that.  
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Re: CH history, genetic link and nicotine
« Reply #93 on: May 8th, 2008, 4:51am »
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on May 8th, 2008, 2:46am, Annette wrote:
Have you actually got concrete evidence of that ? Which medical professionals have looked at it and where did they publish their findings that stopping smoking does not make any beneficial difference to CH ?

Goadsby et al have been saying it for donkey's years Annette, just pick up one of their articles which review TACs.  There is this too, which was compiled by Arne May.  I've posted the whole extract, because it's interesting in its own right, and is pertinent to the whole thread:
 
Quote:
The medical history often reveals a high incidence of head trauma with brain concussion,23–25 but it is hard to prove a cause-and-effect relation. Interestingly, up to 85% of patients with chronic headache are also chronic cigarette smokers.23 Quitting smoking has no effect on the disease. The question arises whether chronic nicotine consumption is needed as a trigger to initiate the syndrome, possibly on the basis of some genetic background.  Before 1990, cluster headache was not generally thought to be an inherited disorder.26,27 However, reports of cluster headache in monozygotic twins28 and familial occurrence of cluster headache in 7% of families, resulting in a 14-fold increase in risk of cluster headache in first-degree relatives and a two-fold increased risk for second-degree relatives,29 show that genetic factors should be considered. In a study of 186 index patients and 624 first-degree relatives, investigators showed a positive family history of cluster headache in 11% of the index patients. They concluded that no precise mode of inheritance could be ascertained.30 A complex segregation analysis of cluster headache has suggested that an autosomal dominant gene has a role in some families,31 although some evidence exists for autosomal recessive or multifactorial inheritance in others.12 However, future studies should take into account that since cluster headache can start between the ages of 7 years32 and 83 years,33 the distinction between affected and unaffected individuals is clearly provisional. To date, the increased familial risk strongly supports the hypothesis that cluster headache has a genetic component, at least in some families.21 However, no clear molecular genetic clues have yet been identified. In view of the paroxysmal character and circadian and circannual rhythmicity of the disease, future studies need to focus on ion channel genes and clock genes.
 
Source: http://www.thelancet.com/journals/lancet/article/PIIS0140673605672170/fu lltext

 
BTW Annette, careful when you quote Ozzy out of context.  He is one of the most knowledgeable and smartest people here; I think that comment was somewhat tongue in cheek Cool
 
 
I've been following Dr Gupta's missives too Batch.  I don't agree with much he says, but he certainly provides an interesting perspective Wink
 
-Lee
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Re: CH history, genetic link and nicotine
« Reply #94 on: May 8th, 2008, 3:17pm »
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on May 8th, 2008, 4:51am, LeeS wrote:

 
Goadsby et al have been saying it for donkey's years Annette, just pick up one of their articles which review TACs.  There is this too, which was compiled by Arne May.  I've posted the whole extract, because it's interesting in its own right, and is pertinent to the whole thread:
 
 
BTW Annette, careful when you quote Ozzy out of context.  He is one of the most knowledgeable and smartest people here; I think that comment was somewhat tongue in cheek Cool
 
 
-Lee

 
 
I could not find any work done by Goadsby on the effect of smoking on CH. Have you got anything on hand that you can share please Lee ? Or BobW ?
 
From what BobW posted I thought he meant many medical professionals have actually done studies or trials on the effects of stopping smoking on CH specifically.  
 
I might have quoted Ozzy out of context but what else he posted in the thread did not make a lot of sense, at least to me. Ozzy, if you are here and read this please come correct me and share what you know on this topic. I would really appreciate it. Thank you.
 
 
Your quote from the Lancet article is somewhat not accurate.
 
" The medical history often reveals a high incidence of head trauma with brain concussion,23–25 but it is hard to prove a cause-and-effect relation. Interestingly, up to 85% of patients with chronic headache are also chronic cigarette smokers.23 Quitting smoking has no effect on the disease. The question arises whether chronic nicotine consumption is needed as a trigger to initiate the syndrome, possibly on the basis of some genetic background. "
 
1- The article must be old as it had no mention of the finding of the hypocretin receptor gene. The discovery of it and the fact that nicotine acts on it have shed new light on the topic.
 
2- It mentioned that medical history showed high incidence of head injury with concussion. I am not sure whether that statistic is still valid ?
 
3- It actually mentioned the possibility of chronic nicotine consumption required to trigger the gene for CH.  
 
4- 85% chronic CHers are also chronic smokers.
 
 
Therefore although it said stopping smoking may not change the course of CH but it sure raised the possibility that smoking could cause CH to start in the first place and that CH somehow links to chronicity.
 
In effect, it said basically the same thing I did, which is that chronic nicotine consumption in some people "causes" or " triggers" the condition to happen, by acting on the CH gene, but for those whose damage has been done and became "fixed", stopping smoking later in life may not help anymore as it is too late.  
 
However, if this " triggering" effect on the gene can be proven, young people who test positive to this gene may be able to avoid triggering CH in themselves by not starting to smoke ?  
 
Finding this out may not be worthwhile for people of this generation but it can help their children , grandchildren, great grandchildren .... Wouldnt that be a good thing ?  
 
 
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Re: CH history, genetic link and nicotine
« Reply #95 on: May 8th, 2008, 4:32pm »
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on May 8th, 2008, 3:17pm, Annette wrote:

Ozzy, if you are here and read this please come correct me and share what you know on this topic. I would really appreciate it. Thank you.

 
Ozzy hasn't been around in a long time. I hope my ignorance didn't chase him away, too.  Embarassed
 
Annette, Batch suggests your info here is publishable. Why not submit it somewhere?
Once it's published, it should be easy to get a university, or even your own hospital to back a study, no?
You could even be the lead researcher!
 
/ for spelling, LOL
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Re: CH history, genetic link and nicotine
« Reply #96 on: May 8th, 2008, 6:08pm »
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on May 6th, 2008, 9:31pm, Redd wrote:
Just to keep the topic on CH and it's realated qualities lets leave schizophrenics out of the equasion.  
 
Schizophrenia is not caused by hypothalamic disfunction so therefore does not enter into this querry.  
 
Just because some of the same neurotransmitters are involved doesn't give liberty to make any compairisons between one condition with the other.
 
Since I can't access the reports, please link to a study where I can see conclusively that hypothalamic cell abnormality and dysfunction is related to Schizophrenia.  
 
Then I can comment further.
 

 
Annette, why don't you post the link on this thread? I would also like to read the study about hypothalamic cell abnormality, and how it relates to schizophrenia, and to see if there are any correlations to CH, or how it parallels with CH. Or, if you wish, feel free to pm it to me. I think there are others who would like to see it too, so they can draw their conclusions, as Pegg will, and as I would like to.
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Re: CH history, genetic link and nicotine
« Reply #97 on: May 8th, 2008, 6:57pm »
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50% of clusterheads smoke.
72% of clusterheads drink.
 
Alcohol is a definite trigger.
 
Maybe it's an alcohol gene instead of smoke gene?
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Re: CH history, genetic link and nicotine
« Reply #98 on: May 8th, 2008, 7:23pm »
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Quote:
Am J Psychiatry 98:385-392, November 1941
doi: 10.1176/appi.ajp.98.3.385
© 1941 American Psychiatric Association
   
 
 ELECTROENCEPHALOGRAPHIC STUDIES OF CORTICOHYPOTHALAMIC RELATIONS IN SCHIZOPHRENIA  
ROY R. GRINKER M. D.1, and HERMAN M. SEROTA M. D., PH. D.1  
1 The Department of Neuropsychiatry of the Michael Reese Hospital.
 
 
 
Using hypothalamic and cortical leads electroencephalographic studies in schizophrenics give the following preliminary results.
 
1. Reaction to external cold is deficient in that no reactive hyperthermia results and little electrical activity in hypothalamus or cortex can be observed. The normal or neurotic shows a definite reaction in both leads.
 
2. Adrenalin injected intravenously causes violent subjective and objective reactions but intramuscularly causes little subjective and usually no objective effect on hypothalamus or cortex in schizophrenics. The intramuscular injection, however, causes a prompt and striking effect in normals and neurotics electrically as well as subjectively demonstrable.
 
3. Electrical stimulation of the hypothalamus of schizophrenics caused minimal or no reaction in that structure demonstrable by the EEG or secondarily in the cortex. Normal and neurotics showed a profound excitation of hypothalamus and cortex, frequently with prolonged "condensor" effect, and usually subjective responses as well.
 
4. Verbal stimuli when applied to schizophrenics elicited no excitation in either lead whereas excitability from both has been recorded in neurotic subjects.
 
5. Sodium amytal injected intravenously showed a typical hypothalamic and cortical response, more striking in the hypothalamus, which further study may correlate with the "amytal interview" effect, and be related to the selective action of barbiturates.
 
6. Speculations have been presented regarding the fundamental deficiency of dynamic action of the hypothalamus in schizophrenia and its possible secondary effects in the production of the essential psychosis in the psychomotor system.
 

 
This is the first link Annette, and I guess I'd want to see the conclusions to these postulations and speculations, and something much more recent than 1941.  There is nothing conclusive in this.
 
Quote:
: Eur Neuropsychopharmacol. 2008 Apr;18(4):312-5. Epub 2008 Jan 28. Links
Hypothalamus volume in twin pairs discordant for schizophrenia.Koolschijn PC, van Haren NE, Hulshoff Pol HE, Kahn RS.
Rudolf Magnus Institute for Neuroscience, Department of Psychiatry, University Medical Center Utrecht, Utrecht, The Netherlands. p.c.m.p.koolschijn@umcutrecht.nl <p.c.m.p.koolschijn@umcutrecht.nl>
 
Monozygotic and same-sex dizygotic twin pairs discordant for schizophrenia were compared with matched control twin pairs in order to disentangle genetic and environmental contributions to variation in hypothalamus volume. A decrease in hypothalamus volume was found in patients or discordant twin pairs compared to healthy controls which could be attributed to the decrease in total brain volume. Higher within-twin pair similarities in monozygotic compared to dizygotic twin pairs, suggests that hypothalamus volume might be partly genetically controlled.
 
PMID: 18222652 [PubMed - indexed for MEDLINE]
 

 
It is my understanding that Goadsby and his tean found that there was an increace in cell volume in the inferior postierior region of the hypothalamus.  I could be wrong but this is what I remember.
 
http://books.google.com.au/books?id=6pyv4cWRkSIC&pg=PA133&lpg=PA 133&dq=hypothalamus+schizophrenia&source=web&ots=defY6d4jy8&sig=jgD41JcrUrgg0czJ6N9DQBM_JOg&hl=en
 
I can't copy the page so I'll post the link.  Page 133.
 
Third ventrical of the hypothalamus located in the antirior region and a tissue loss in this region.  
 
This reads to be the opposite of Goadsbys findings.
 
Quote:
Volume 61, Issue 8, Pages 935-945 (15 April 2007)
 
 
 
Hypothalamic Abnormalities in Schizophrenia: Sex Effects and Genetic Vulnerability
 
Jill M. Goldsteinabcde, Larry J. Seidmancde, Nikos Makrisf, Todd Aherncde, Liam M. O’Brieng, Verne S. Caviness Jr.e, David N. Kennedye, Stephen V. Faraoneh, Ming T. Tsuangcdij
 
 
Received 15 August 2005; received in revised form 11 April 2006; accepted 8 June 2006. published online 17 October 2006.
 
Background
This is a unique hypothalamic magnetic resonance imaging (MRI) study in schizophrenia, an important region in the limbic system. We hypothesized abnormal volumetric increases, with greater severity in multiplex families (more than one ill member) compared with simplex families (one ill). We tested the hypothesis that normal hypothalamic sexual dimorphism is disrupted in schizophrenia.
 
Methods
Eighty-eight DSM-III-R schizophrenia cases (40 simplex and 48 multiplex), 43 first-degree nonpsychotic relatives, and 48 normal comparisons systematically were compared. A 1.5-Tesla General Electric scanner was used to acquire structural MRI scans, and contiguous 3.1-mm slices were used to segment anterior and posterior hypothalamus. General linear model for correlated data and generalized estimating equations were used to compare cases, relatives, and controls on right and left hypothalamus, controlled for age, sex, and total cerebral volume. Spearman’s correlations of hypothalamic volumes with anxiety were calculated to begin to examine arousal correlates with structural abnormalities.
 
Results
Findings demonstrated significantly increased hypothalamic volume in cases and nonpsychotic relatives, particularly in regions of paraventricular and mammillary body nuclei, respectively. This increase was linear from simplex to multiplex cases, was positively correlated with anxiety, and had a greater propensity in women.
 
Conclusions
Findings suggest important implications for understanding genetic vulnerability of schizophrenia and the high rate of endocrine abnormalities.

 
This one contradicts the previous ones but does give some information that is more in line with what the most recent findings in CH are.  I'm not quite sure how it makes the leap to comparing schizophrenia with CH, but I hope you can clue me in.
 
Quote:

 
Dopamine-Hypocretin/Orexin Interactions  
The Prefrontal Cortex and Schizophrenia  
Book Hypocretins  
Publisher Springer US  
DOI 10.1007/b107412  
Copyright 2005  
ISBN 978-0-387-25000-7 (Print) 978-0-387-25446-3 (Online)  
Part Part 8  
DOI 10.1007/0-387-25446-3_23  
Pages 339-351  
Subject Collection Biomedical and Life Sciences  
SpringerLink Date Wednesday, April 25, 2007  
 
 
Hypocretins
Integrators of Physiological Functions  
10.1007/0-387-25446-3_23  
Luis de Lecea and J. Gregor Sutcliffe  
 
23. Dopamine-Hypocretin/Orexin Interactions  
The Prefrontal Cortex and Schizophrenia
Ariel Y. Deutch2, Jim Fadel3 and Michael Bubser2
 
(2)  Vanderbilt University Medical Center, Nashville, TN, 37212  
(3)  University of South Carolina School of Medicine, Columbia, SC, 29208  
 
6. Conclusions
The discovery of the hypocretins/orexins has allowed us to understand the etiology and proximate cause of narcolepsy, and continued advances in other neuropsychiatric disorders, including a role for the orexin in schizophrenia, seems likely. The advantages of having a small number of defined cells integrate a broad function, such as arousal, would seem intuitively attractive. However, continued data point to orexin cells forming several distinct functional systems, each with a correspondingly distinct anatomy, and each with its own set of pharmacological interactions. The elucidation of these systems and the roles they play will likely drive new means of treating several neuropsychiatric disorders.

 
Now I see the prefrontal cortex being the focus of this abridged article.  Discussing the involvement of hypocretins/orexins and neuropsychiatric conditions would be very interesting indeed.
 
Personally, I find there simply is not enough information presented for me to come to the conclusion that Hypothalamic abnormality is causal to the development of schizophrenia, especially when one very recent study shows,  
Quote:
Findings demonstrated significantly increased hypothalamic volume in cases and nonpsychotic relatives, particularly in regions of paraventricular and mammillary body nuclei, respectively.
 Let alone how this makes the leap to be compared with CH and nicotine consumption.
 
I'm pretty adept at interpreting reports such as these, and maybe being out of college for 9 years has somethinng to do with my not being able to make the same connections bwteen this information as you are.  
 
Please tell me how you tied this information together to reach your hypothosis.
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Re: CH history, genetic link and nicotine
« Reply #99 on: May 8th, 2008, 8:46pm »
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Pegg, you misunderstood something I said. I did not use the finding in the anatomical abnormality of schizophrenia to reach my hypothesis.
 
My hypothesis is this  
 
1- Hypocretin receptor gene has been found to be strongly associated with CH.
 
2- Hypocretin acts on the hypothalamus affecting the circadian clock via the sleep-wake cycle and on various neurotransmitters such as dopamine, noradrenaline,etc.
 
3- Nicotine has been found to bind to these same receptors.
 
4- CHers tend to be heavy smokers therefore would chronic or excessive exposure to nicotine play a causative or triggering role in the development of CH.
 
 
Prior to arriving at this hypothesis I had the same notion  as many here that it was CH that makes people more addicted to cigarettes. When I set out to research this angle I came across several stumbling blocks. I decided to study about the mechanism of addiction first. I learnt that addiction to anything ( chemicals or otherwise ) is caused by the release of dopamine. Dopamine is the chemical that makes a person feels rewarded. Whatever makes your brain releases more dopamine you will like it and potentially can become addicted to it. This is the same from chocolate to being in love to cigarette to cocaine. This can happen to ANYONE regardless of whether or not you have any existing condition, just to a different degree.
 
Pathological addiction occurs in people where the dopamine pathway is malfunctioning. This has been extensively studied in schizophrenics. They have anatomical abnormalities in the hypothalamus as well as other areas of the brain which makes them MORE addictive than the normal person. The abnormalities that they have are obviously different from the ones seen in CH, otherwise they would be more likely to develop CH and not schizophrenia and vice versa.
 
Since CHers dont seem to have the same abnormalities that cause pathological , more than normal addiction ( as seen in schizo ) the theory that CH makes people having more addictive trait was not standing very well, at least from my finding.
 
Secondly it was observed that schizophrenics smoke more during the active phase of their illness makes it more indicative that it is their illness that makes them smoke, this again was not observed in CH.  
 
Lastly, researches done on the abnormal/pathological nicotine addiction in schizo showed that this leads to an unusual reactions of the body to nicotine, such as the worsening of symptoms when nicotine is withdrawn. This was not observed in CHers.  
 
That was the basis of my comparison between the two.  
 
If someone can help by finding articles and studies that show CH in a person causes that person to become MORE addicted to whatever or specifically nicotine, than otherwise normally, it would be wonderful and it would shed a lot more light on the topic.  
 
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