Can somebody please explain or please post a link to easy to read articles defining the differences of Vasodilation and Vasoconstriction; and how each of these terms are relevant to CH's?

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constriction is smaller. Dilation means bigger.  Hope this is simple enough for you.

         potter

That was easy to understand, thanks Brew :) thanks Potter  :)

Now for the hard part, how are each of these terms relevant to CH's?

Brew...

Your animated response using lmgtfy.com is priceless!!! Well Done!!!

V/R, Batch...   Still  ;D

For decades the working theories about the cause of migraine and cluster centered around your question.

When Peter Goadsby's revolutionary brain studies hit the literature the shift has been to brain/nerve functioning as the cause of these disorders.

This does not deny the involvement of blood vessels but has shifted it to secondary role as a primary issue.
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Interesting to note that he is saying that the primary mode of action is NOT as a vasoconstrictor but on its effect on the central nervous system. Doesn't change our appreciation of this class of meds but suggests we need to change how we think about the nature of CH.
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Handb Exp Pharmacol. 2007;(177):129-43.   


Serotonin receptor ligands: treatments of acute migraine and cluster headache.

Goadsby PJ.

Institute of Neurology, Queen Square, London WC1N 3BG, UK. peterg@ion.ucl.ac.uk

Fuelled by the development of the serotonin 5-HT(1B/1D) receptor agonists, the triptans, the last 15 years has seen an explosion of interest in the treatment of acute migraine and cluster headache. Sumatriptan was the first of these agonists, and it launched a wave of therapeutic advances. These medicines are effective and safe. Triptans were developed as cranial vasoconstrictors to mimic the desirable effects of serotonin, while avoiding its side-effects. IT HAS SUBSEQUENTLY BEEN SHOWN THAT THE TRIPTANS' MAJOR ACTION IS NEURONAL, WITH BOTH PERIPHERAL AND CENTRAL TRIGEMINAL INHIBITORY EFFECTS, AS WELL AS ACTIONS IN THE THALAMUS AND AT CENTRAL MODULATORY SITES, SUCH AS THE PERIAQUEDUCTAL GREY MATTER. Further refinements may be possible as the 5-HT(1D) and 5-HT(1F) receptor agonists are explored. Serotonin receptor pharmacology has contributed much to the better management of patients with primary headache disorders.

PMID: 17087122 [PubMed]

Bob Johnson, you are always consistent with your informative and relevant articles, thank you :) 

LasVegas wrote on Mar 9^th, 2010 at 3:04pm:

Bob Johnson, you are always consistent with your informative and relevant articles, thank you :)

I second that. Thank You Bob!

Thank you, Bob.  :)

Quote:

When Peter Goadsby's revolutionary brain studies hit the literature the shift has been to brain/nerve functioning as the cause of these disorders. This does not deny the involvement of blood vessels but has shifted it to secondary role as a primary issue.

Well put. The cluster headache is initiated in the hypothalamus. It signals (among other things) the trigeminal nerve to get angry. At least some of the pain is related to vasodilation. Vasodilators are one way to treat the symptoms.

An interesting read and different slant on the pathophysiology of cluster headaches...  and the logic expressed appears to be clearly contrary to that of the good Dr. Goadsby... 

The slant diverges further in Ref 2 “how” versus “what” of a disease process... if you're really into heavy reading...

Cluster headache: Key pathophysiological issues
Vinod K Gupta, M.D.

Dear Editor,

Ferrari and colleagues find that menstruation, use of oral contraceptives, pregnancy and menopause had a much smaller influence on cluster headache attacks than in migraine.

[1] Although such data appear interesting, they are peripheral to the pathogenesis of the disorder; neither are these issues any more relevant to migraine pathophysiology. Fifteen key pathophysiological issues continue to be completely overlooked in migraine research; in this context, hormones, neuropeptides, magnesium, platelets, deep white matter lesions, neuronal ion channels and genetic linkages are rather peripheral concerns in primary headaches.

[2] Epidemiological data and associations are useful only if they provide clues to aetiology by leading to experiments that deepen our understanding of causal mechanisms.

[3] Unfortunately, this study [1] offers no mechanistic insight regarding cluster headache or any clue towards experiments that further shape our understanding. 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.


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

Published 2 March 2006

Some interesting food for thought, Batch. It is good to think outside the box. Otherwise, we may be trapped in a dead-end of our own construction.  Here are some responses to the main points raised.

1)– biological clocks are a good explanation for the duration of the headaches, and their regular frequency based on time of day and season of year.  These are neuronal in nature, although nerves take us to every other possibility: anatomical, chemical,  electrical, etc all come together when we say 'nerve'. 
2)Yes, the one-sided nature of the beast is consistent with an injury or anatomical asymmetry. But it could also be related to balance --- the fact that the headaches sometime shift sides in the absence of any obvious injury or anatomical change raises questions of its own.  Most people develop to be left-handed or right handed ... that is not about injury, it is reflection of nervous function.
3)Maybe the cluster type of headache simply has a different mechanism from migraine and is less likely to trigger vomiting.
4)Sounds reasonable at first glance, but not sure about the non-pulsatile nature. Most negative pulsing I have experienced is from vascular causes, sensitivity to changes in pressure with pulse. But that is not CH. 
5)Oxygen, triptans and nitroglycerin point to vascular mechanisms at work. That does not establish it as primarily vascular, as a typical patient is only sensitive to nitroglycerin and alcohol in a cycle... the sensitivity is switched on and off by something else.
6)No, verapamil's effectiveness does not prove a non-neuronal basis. Nerve cells may be sensitive to the effects of calcium channel blockade, and they may be less likely to go haywire when on verapmil.
7)Tissue creep? Maybe some healing process occurs in some people, and this leads to remission … collagen plasters over an injury around the trigeminal and years of pain free time result. Consistent with last years headaches - went out of several years remission at an unusual time of year after vomiting through my nose ... the acid bath may have ulcerated a branch of my trigeminal.


I think a model of circular causation is possible, where there is no single primary cause... several things may be needed to create a “circuit” that we call cluster headache. 

Hey Monty, 

Thanks for the comments...  I like this...

I offered up Dr. Gupta's letter merely as a different cut at the cluster headache pathophysiology so make no judgment other than to say it appears to carry some hefty logic...   but not in all cases as you've pointed out...

I agree a circular causation "circuit" model is possible...  although I find it easier to rationalize the model as a series of sequential homeostatic processes with feedback or loop back control elements traversing synaptic and vascular paths as the attack progresses from trigger into the end game phase. 

Bias or perturb one or more of these processes out of it's normal cycle with an external stimulus or block a feed back receptor and the cluster headache triggers, intensifies, stagnates, or aborts.

More to follow on this line of thinking...  I like where we're going...

Take care,

V/R, Batch

It's likely the vomit hit your sphenopalatine (Pterygopalatinum) ganglia...  that must have stung like heck...  it connects directly to the trigeminal nerve through the maxillary nerve (V2).  Lots of evidence it plays a role...

I've found that evaporative cooling of my sphenopalatine ganglia by freecycling 100% oxygen in the mouth and out the nose at 25 liters/minute has a moderating effect on cluster headache pain similar to a sphenopalatine ganglion block with topical lidocaine...   The numbing isn't as pronounced and it doesn't last as long... but it clearly takes the edge off the pain...

this is some great stuff guys  :)

Just found this yesterday.
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J Clin Neurosci. 2010 Mar 11.

What has functional neuroimaging done for primary headache ... and for the clinical neurologist?
Sprenger T, Goadsby PJ.

UCSF Headache Centre, Department of Neurology, University of California, 1701 Divisadero St, Suite 480, San Francisco, CA 94115, USA.

Our understanding of mechanisms involved in primary headache syndromes has been substantially advanced using functional neuroimaging.

THE DATA HAVE HELPED ESTABLISH THE NOW-PREVAILING VIEW OF PRIMARY HEADACHE SYNDROMES, SUCH AS MIGRAINE AND CLUSTER HEADACHE, AS BRAIN DISORDERS WITH NEUROVASCULAR MANIFESTATIONS, NOT AS DISORDERS OF BLOOD VESSELS.

PMID: 20227279 [PubMed]

Thanks Bob!

Well, thanks to you all for the discussion!