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LeLimey
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Hi y'all (See what a convention can do to you?!!)
Thought you might like to see this
http://news.bbc.co.uk/1/low/health/380497.stm
Its good to see CH getting alot of publicity over here. We have a TV interview here with our very own Val on BBC Wales tomorrow. I shall tape it and send copies of anyone would like to see it.
God I miss you lot!
edited cos I'm so thick I added the wrong link! Its Franks fault.. I didn't hit him hard enough.
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| « Last Edit: Jul 19th, 2005, 6:56pm by LeLimey » |
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Jimi
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Re: CH Article
« Reply #1 on: Jul 19th, 2005, 6:57pm » |
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It says I am not authorized to view it. Must have to be a Brit to see it. 
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Jimi
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Re: CH Article
« Reply #2 on: Jul 19th, 2005, 6:58pm » |
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well...........................I just tried it again and it let me view this time. maybe I didn't really do it before. maybe I just thought about doing it. I can't remember.
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LeLimey
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Re: CH Article
« Reply #3 on: Jul 19th, 2005, 7:00pm » |
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Here you go Jimi.. I cut and pasted it. I picked it up from the OUCH UK board
Headache's secrets revealed
Scientists have linked brain structure to brain function
A certain type of headache may be caused by structural abnormalities in the brain, researchers have discovered.
The finding could revolutionise approaches to all primary headaches, which had not been thought to be caused by factors in the physical structure of the brain.
But using a new scanning technique, doctors have established that cluster headaches are likely to be caused by excessive growth of grey cells in one part of the brain.
It is the section that governs the body clock, which could be responsible for the regularity of the headaches' appearances.
Male condition
Cluster headaches are characterised by a sudden excruciating pain on one side of the head around the eyes, temple or cheek, and can last for 15 minutes to 3 hours.
Affecting 0.1% of the population - mainly men - they recur over a period of weeks or months before disappearing, hence their name.
Professor Peter Goadsby, of the headache research unit at London's Institute of Neurology, published his team's discovery in the journal Nature Medicine.
He told BBC News Online that the finding revolutionised scientists' perception of headaches.
"It's like the first time somebody said the earth was round - you have to step back and reconsider," he said.
This was because whereas with secondary headaches - where there was a known structural cause such as a brain tumour or bleeding - primary headaches had been thought to be caused by chemical factors alone.
"The dogma is that primary headache, like cluster headaches and migraine, are due to abnormal brain function with completely normal brain structure.
"Our study shows this is simply not the case," he said.
Revolutionary discovery
In the past, high-resolution brain scans have shown no abnormalities in the brain structure of cluster headache sufferers.
But using the latest imaging techniques, Professor Goadsby and colleagues found an increase of grey matter in an area of the brain known as the hypothalamus on the side where the headache occurs.
Whereas standard high resolution scans take a picture of the brain that doctors can examine, the new technique takes pictures of many brains.
A computer then analyses the pictures down to the finest detail, making extremely subtle differences apparent.
Because the differences were seen both when the patients were studied while they had a headache and also in a headache-free state, changes are likely to be permanent.
Professor Goadsby said: "We also found that the area of the brain where these structural abnormalities were seen, the hypothalamus, is the same area of the brain where functional studies show that activity is abnormal during the headache state.
"This complete correlation of functional and structural abnormality is striking."
The hypothalamus is the part of the brain associated with circadian rhythms - the 24 hour rhythm of the human body.
"Our results demonstrate for the first time the precise location in the brain involved in cluster headaches and help to explain why this condition shows such striking seasonal variation and clock-like regularity," said Professor Goadsby.
"The findings have profound implications for understanding how the brain is affected in primary headaches."
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Charlie
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Re: CH Article
« Reply #4 on: Jul 19th, 2005, 7:07pm » |
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Thanks Helen.
There ya go.
I'm not the right one to comment on this so I'll let the other geeks do it.
Charlie
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E-Double
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Re: CH Article
« Reply #5 on: Jul 19th, 2005, 7:24pm » |
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Outstanding article.....You rock!
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Kris_in_SJ
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Re: CH Article
« Reply #6 on: Jul 19th, 2005, 9:01pm » |
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Good article, however ....
I find a certain amount of fault as Dr. Goadsby mentions this as a "male condition." Did I miss something? It sure seems to me that there are a significant number of female sufferers on this board. Myself among them, of course.
Kris
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Racer1_NC
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Re: CH Article
« Reply #7 on: Jul 19th, 2005, 9:11pm » |
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on Jul 19th, 2005, 9:01pm, Kris_in_SJ wrote:Good article, however ....
I find a certain amount of fault as Dr. Goadsby mentions this as a "male condition." Did I miss something? It sure seems to me that there are a significant number of female sufferers on this board. Myself among them, of course.
Kris |
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That bothers me as well......I can not accept that CH is not equally shared between men and women.
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E-Double
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Re: CH Article
« Reply #8 on: Jul 19th, 2005, 9:15pm » |
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on Jul 19th, 2005, 9:11pm, Racer1_NC wrote:
That bothers me as well......I can not accept that CH is not equally shared between men and women. |
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Come on Bill.......next you are gonna say that you get menstrual migraines
Seriously though, as discussed with the doc.....whether it is misdiagnosed or undiagnosed at high rates we will see the numbers shrinking as they do on this site for the overall population....Educating all is our job!
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Topical
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Re: CH Article
« Reply #9 on: Jul 19th, 2005, 9:59pm » |
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Very interesting article, thanks.
The article was publised in the BBC on June 29, 1999. I went to the magazine referenced and it was from July 1999.
I am looking around for more info on this and where it led.
Edit:
Here's a good read discussing the different types of headaches by Goadsby from 2002:
http://jnnp.bmjjournals.com/cgi/content/full/72/suppl_2/ii19
I think this is the latest work from April 2005:
"The clinical characteristics of headache in patients with pituitary tumours"
http://brain.oxfordjournals.org/cgi/content/abstract/128/8/1921
That man knows his stuff. I wish he was my doc. Thanks again Helen. What a tangled web our nerves weave.
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| « Last Edit: Jul 19th, 2005, 10:30pm by Topical » |
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Sean_C
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Thanks Hellen 
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BarbaraD
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Re: CH Article
« Reply #11 on: Jul 19th, 2005, 10:48pm » |
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He said "mainly" men --- women are only about 25% so it's still "mainly" men. I don't even get upset unless they said "all" men! Of course I'm a woman and just get meegraines.....
Hugs BD
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nani
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Re: CH Article
« Reply #13 on: Jul 19th, 2005, 10:57pm » |
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Saying "mainly men" may actually work to our advantage. More research funding goes into men's health issues than women's. Any attention to CH benefits us all.
Now, if we could only figure out how to make contraception a men's issue. 
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Cathi04
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Re: CH Article
« Reply #14 on: Jul 20th, 2005, 1:11am » |
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The pain in Spain rests main-ly in the men?
The pain in Spain rests main-ly in the men......
But who has the pain in Spain.......
mostly meeeen,
Mostly meeeen,
But 25 percent aren't theeem...........noot theeem...
nooot theeeeemmm........
The pain in Spain rests mainy in the mennn.75%....and the balance of that monstrous pain is in the wimmmmmain!!!!!!!!!!!!
(apologies to Eliza Doolittle.going back to my corner now)
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LeLimey
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Re: CH Article
« Reply #15 on: Jul 20th, 2005, 3:55am » |
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on Jul 19th, 2005, 9:01pm, Kris_in_SJ wrote:Good article, however ....
I find a certain amount of fault as Dr. Goadsby mentions this as a "male condition." Did I miss something? It sure seems to me that there are a significant number of female sufferers on this board. Myself among them, of course.
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That bit narked me too and I'm pretty sure he would have been misquoted, he has certainly never said anything like that elsewhere that I have seen.
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ben_uk
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Re: CH Article
« Reply #16 on: Jul 21st, 2005, 8:22am » |
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First – PET scan that determined activity in the SCN hypothalamus under Nitro bomb inducement:- Monday 3rd February 1997………lunch time  .
First Published:- http://www.thelancet.com/journals/lancet/article/PIIS0140673698024702/fu lltext
http://www.thelancet.com/journals/lancet/article/PIIS0140673698024702/ab stract
http://download.thelancet.com/pdfs/journals/0140-6736/PIIS01406736980247 02.pdf
Hypothalamic activation in cluster headache attacks
May A, Bahra A, Büchel C, Frackowiak RS, Goadsby PJ
The Lancet - Vol. 352, Issue 9124, 25 July 1998, Pages 275-278
Summary
Background
Cluster headache, one of the most severe pain syndromes in human beings, is usually described as a vascular headache. However, the striking circadian rhythmicity of this strictly half-sided pain syndrome cannot be readily explained by the vascular hypothesis. We aimed to assess changes in regional cerebral blood flow (rCBF) in patients with cluster headache.
Methods
We used positron emission tomography (PET) to assess the changes in rCBF, as an index of synaptic activity, during nitroglycerin-induced cluster headache attacks in nine patients who had chronic cluster headache. Eight patients who had cluster headache but were not in the bout acted as a control group.
Findings
In the acute pain state, activation was seen in the ipsilateral inferior hypothalamic grey matter, the contralateral ventroposterior thalamus, the anterior cingulate cortex, and bilaterally in the insulae. Activation in the hypothalamus was seen solely in the pain state and was not seen in patients who have cluster headache but were out of the bout.
Interpretation
Our findings establish central nervous system dysfunction in the region of the hypothalamus as the primum movens in the pathophysiology of cluster headache. We suggest that a radical reappraisal of this type of headache is needed and that it should in general terms, be regarded as a neurovascular headache, to give equal weight to the pathological and physiological mechanisms that are at work.
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ben_uk
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Re: CH Article
« Reply #17 on: Jul 21st, 2005, 8:23am » |
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Introduction
The pain of cluster headache is perhaps the most severe known to human beings. Women who have such headaches describe each attack as being worse than childbirth. The syndrome is clinically well defined1 and despite its recognition in published work for more than two centuries2 its pathophysiology is poorly understood.
The excruciatingly severe one-sided pain is likely to be mediated by activation of the first (ophthalmic) division of the trigeminal nerve, whereas the autonomic symptoms are a result of activation of the cranial parasympathetic outflow from the VIIth cranial nerve.3 The relapsing- remitting course,4 its seasonal variation,4 and the clockwise regularity5 are characteristic but unexplained features of the disorder.
The striking circadian rhythmicity of cluster headache has led to the suggestion of a central origin for its initiation.6,7 Substantially lowered concentrations of plasma testosterone during the cluster headache period in men provided the first evidence of hypothalamic involvement in cluster headache.8 This finding was further supported by a reduced response to thyrotropin-releasing hormone9 and a range of other circadian irregularities that have been reported in patients who have cluster headaches.10 Melatonin is a marker of the circadian system and a blunted nocturnal peak melatonin concentration and complete loss of circadian rhythm have been reported in patients who have cluster headache.10 The endogenous circadian rhythm is run by an oscillator in the suprachiasmatic nuclei in the ventral hypothalamus and reacts to temporal environmental cues of light conditions via a retino-hypothalamic pathway. The hypothalamus, or a closely related structure, is a candidate site for triggering the acute attack of cluster headache.
Positron emission tomography (PET) is probably the best technique for visualising in-vivo changes in regional cerebral blood flow (rCBF) in human beings. Modern high-resolution PET allows the detection of subtle changes in rCBF during defined behavioural tasks and provides an index of synaptic activity relating networks of regions to tested brain functions.11
Cluster headache attacks can be elicited with nitroglycerin during the active period without significant side effects.5 Nitroglycerin-provoked and spontaneous cluster attacks are comparable3,12 and nitroglycerin does not substantially alter rCBF.13 The headache can be rapidly and effectively aborted with sumatriptan. This approach was therefore used to detect brain regions with increased blood flow during nitroglycerin-induced cluster attacks, focusing our interest on the hypothalamic region.
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ben_uk
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Re: CH Article
« Reply #18 on: Jul 21st, 2005, 8:24am » |
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Methods and patients
Nine right-handed men (age 25–62 years, mean 43 years) with active chronic cluster headache, according to the Headache Classification Committee of the International Headache Society,1 were studied during an induced acute headache attack (study group). Acute cluster headache was provoked by inhalation of nitroglycerin (1•0–1•2 mg).5 All patients studied were not treated prophylactically for cluster headache and were otherwise healthy. Eight patients with a history of cluster headache but who were not having a headache bout (age 36–61 years, mean age 49 years) had a PET scan by the same study design (control group). None of the control patients had a cluster headache attack after nitroglycerin was applied. Informed consent was obtained from all patients and the study was approved by the Ethics Committee of the National Hospital for Neurology and Neurosurgery, London.
Design
During the active headache period each of the nine study patients had 12 or 13 consecutive scans at four times: baseline; after application of nitroglycerin; after onset of headache; and when headache-free, after treatment with subcutaneous sumatriptan (6 mg). Each of the eight controls had 12 consecutive scans by the same design. Since none of the patients in this group had a cluster headache attack after taking the nitroglycerin, we defined scans for the second and third condition according to the mean number of scans for these conditions in the study group. For each scan, patients rated their headache intensity with a visual analogue scale (0=no pain, 10=the most severe pain). Participants had their eyes closed during all scans.
Data acquisition and analysis
PET scans were done with an ECAT EXACT HR+ scanning system (CTI Siemens, Knoxsville, TN, USA) in three- dimensional mode with septa retraced. An antecubital vein cannula was used to administer the tracer, about 350 mBq of H215O. The activity was flushed into patients over 20 s at a rate of 10 mL/min. The data were acquired in one 90 s frame beginning 5 s before the peak of the head curve. The interval between scans was 8–15 min. Attenuation correction was done with a transmission scan done at the beginning of each study. Images were reconstructed by filtered-back projection into 63 images planes (separation 2•4 mm) and into a 128 by 128 pixel image matrix (pixel size 2•1×2•1 mm2). Statistical Parametric Mapping 97 (SPM'97 www.fil.ion.ucl.ac.uk/spm) was used for data analysis. Images were realigned with the first image as the reference and then coregistered with the patient's structural magnetic resonance imaging (MRI) image and finally spatially normalised into the space defined by the atlas of Talairach and Tournoux.14 The normalised images were smoothed with a Gaussian filter of 10 mm full width at half maximum. Statistical parametric maps were derived with pre-specified contrasts,15 to compare rCBF during headache versus rCBF during the non- headache phase after nitroglycerin application. We also addressed the question of significant rCBF differences in the study group relative to the control group with a group-by-condition interaction analysis.
Because headache is a strictly lateralised syndrome1 we mirrored PET and MRI scans in patients with right-sided headache in the sagittal plane to be able to analyse all patients in the same analysis. The uncorrected threshold of p < 0•001 was chosen because of a strong regional a-priori hypothesis based on the clinical and experimental data cited in the text.
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ben_uk
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Re: CH Article
« Reply #19 on: Jul 21st, 2005, 8:24am » |
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Results
Of the nine patients in the bout, five experienced a cluster headache attack on the left side and four patients on the right side after nitroglycerin spray. Typical concurrent autonomic symptoms such as ipsilateral miosis, lacrimation, and rhinorrhoea confirmed the presence of a classic cluster headache attack. All patients described the provoked attack as being similar to spontaneous attacks. In the nine patients who had attacks of acute cluster headache, significant activations in the acute attack compared with the headache-free state were found in the ipsilateral hypothalamic grey area, bilaterally in the anterior cingulate cortex, in the contralateral posterior thalamus, the ipsilateral basal ganglia, bilaterally in the insulae (figure 1 and 2), and in the cerebellar hemispheres (table). figure 1 shows that significant activation was detected next to the third ventricle slightly lateralised to the left and rostral to the aqueduct. The activation is ipsilateral to the pain side, lies in the diencephalon, and coincides, in the Talairach atlas,14 with the hypothalamic grey matter. figure 2 shows that significant activation was detected in the right frontal lobe (Brodman's area 10), bilaterally in the insula, in the cerebellum/vermis and in the hypothalamic grey matter. The activation in the hypothalamic grey area was seen only in the patients with a cluster headache attack but not in the control patients (p < 0•001).
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ben_uk
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Re: CH Article
« Reply #20 on: Jul 21st, 2005, 8:25am » |
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Discussion
We observed areas of activation in acute cluster headache that fall into two broad groups: areas known to be involved in pain processing or response to pain, such as cingulate and insula cortex and thalamus; and areas activated specifically in cluster headache but not in other causes of head pain, notably the hypothalamic grey areas. These data suggest that primary headache syndromes share some processing pathways but equally can be distinguished on a functional neuroanatomical basis by areas of activation specific to the clinical presentation.
Studies with PET have repeatedly given results that show activation of the anterior cingulate cortex on the sensation of somatic or visceral pain that are attributed to the emotional response to pain.13,16,17 Activations in the insula have been shown after application of heat,16,18 subacutaneous injections of ethanol,19 somatosensory stimulation,20 and during cluster headache.13 Given its anatomical connections, the insula has been suggested as a relay of sensory information into the limbic system and is known to play an important part in the regulation of autonomic responses.21 Painful stimuli are significantly effective in activating the anterior insula, a region closely associated with both somatosensory and limbic systems. Such connections may provide one route through which nociceptive input is integrated with memory to allow full appreciation of the meaning and dangers of painful stimuli. In the acute pain state the thalamus is a site where activations would most be expected. Activation of the contralateral thalamus as a result of pain is known from studies on animals22 and functional imaging studies in human beings.16,17 The acute pain in cluster headache, induced activation bilaterally in the cerebellar hemispheres and in the vermis. There seems to be no direct nociceptive input to the cerebellum,23 and there is no clinical evidence that cerebellar lesions or stimulation affect pain sensation in human beings.16 However, there are some PET studies that report an activation in this area during experimental pain.16,24
In contrast to migraine,25 no brain stem activation was found during the acute attack compared with the resting state. This finding is remarkable because migraine and cluster headache are often discussed as associated disorders and similar compounds, such as ergotamine and sumatriptan, are used in the acute treatment of both types of headache. 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 substantially as might be inferred from the different patterns of presentation and responses to preventive agents.26
Substantial activations ascribable to cluster headache were observed in the ipsilateral hypothalamic grey area when compared with the headache-free state. Just as it is striking that no brain-stem activation occurs, which is in contrast to acute migraine,25 we have seen no hypothalamic activation in experimental pain induced by capsaicin injection into the forehead.27 Injection into the forehead would activate first division (ophthalmic) afferents which traverse the trigeminal division responsible for pain activation in cluster headache. Thus two other types of first division trigeminal nerve pain, while sharing neuroanatomical pathways with cluster headache, do not give rise to hypothalamic activation. Moreover, in the eight control patients who did not experience a headache after taking nitroglycerin, rCBF in the region of the hypothalamic grey area was not increased. This finding implies that the activation we have observed is involved in the pain process in a permissive or triggering manner rather than simply as a response to first division nociception per se. Hypothalamic activation in traumatic nociception has been observed in the hypothalamus proper and is a different more rostral area than we report.19 Moreover, Hsieh and colleagues19 report changes contralateral to the pain, whereas we report changes that are ipsilateral and in the hypothalamic grey area in the region of the circadian pacemaker neurons which is, therefore, an anatomically distinct area on the opposite side of the brain. Given that this area is involved in circadian rhythm and sleep-wake cycling, our data establish an involvement of this area of the hypothalamus as a primum movens in the acute cluster attack.
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ben_uk
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Re: CH Article
« Reply #21 on: Jul 21st, 2005, 8:26am » |
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Cluster headache has been attributed to an inflammatory process in the cavernous sinus and tributary veins.28 Inflammation has been thought to obliterate venous outflow from the cavernous sinus on one side, thus injuring the traversing sympathetic fibres of the intracranial internal carotid artery and its branches. According to this theory, the active period ends when the inflammation is suppressed and the sympathetic fibres partially or fully recover. This theory is based on abnormal findings with orbital phlebography in patients with cluster headache,29 and the fact that nitroglycerin and other vasodilators can induce a cluster attack.5 However, given the circadian rhythmicity and unilaterality of the symptoms, a purely vasogenic cause cannot explain the entire picture of cluster headache.30 Moreover, the frequency and pattern of pathological findings at orbital phlebography in cervicogenic headache, migraine, and tension-type headache is similar to that in cluster headache.31 Given that we have found an increased signal in the region of the cavernous sinus in the patients with acute cluster headache in this study and after capsaicin injection to the forehead in another PET study,27 it seems likely that the vascular changes are an epiphenomenon of activation of the trigeminovascular system.32
A radical reappraisal of the pathophysiology of cluster headache is needed. Our data establish that cluster headache, far from being a primarily vascular disorder, is a condition the genesis of which is to be found in the central nervous system in pacemaker or circadian regions of the hypothalamic grey matter. Further, we suggest that both cluster headache and migraine might usefully be regarded are neurovascular headaches to include the neural contribution to these important clinical syndromes.
Contributors
All five investigators contributed to the design of the study and to the writing of the paper. Arne May was involved in planning, study coordination, and analysis. Anish Bahra was involved in recruiting the patients and scanning. Christian Büchel was involved in the statistical analysis. Richard Frackowiak and Peter Goadsby were involved in planning, study coordination, and review of the data.
Quote from my intro:- “Getting to know ya” board
Ingenious UK Sufferer « on: Mar 22nd, 2005, 2:45pm
“I was the first to undergo his pioneering experiment using PET. that determined activity in the SCN hypothalamus under Nitro bomb inducement.
Using the nav bar on the left, click on to "headache links" then under "cluster news" click on to "BBC story about Dr Peter J Goadsby". There under "Revolutionary discovery" you will see a PET brain scan image showing a hypothalamus glowing like a nuclear melt-down, that's me!”
Many thanks to Peter and his team for taking such good care of me, and many special thanks to Anish for taking such special care of me.
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Topical
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Re: CH Article
« Reply #22 on: Jul 21st, 2005, 9:00am » |
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Wow, we have a celebrity amongst us! So you are on a first name basis with Dr. Goadsby? *awe*
Very cool Ben!
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Jeepgun
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Re: CH Article
« Reply #23 on: Jul 21st, 2005, 9:18am » |
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Great stuff and very fascinating, Ben! 
My daughter wants to know if she can use your hypothalamus for a night light.
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| « Last Edit: Jul 21st, 2005, 9:19am by Jeepgun » |
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Her: ..... "WHAT is the MATTER with you!?"
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