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Toms headaches

(Member)
From: Northbridge
30 total posts
Not currently suffering :D
Tom has been on a very high dose of Melatonin which has stopped the CH's. If the dose is reduced the attacks return. He is on 3mg per night. I have done a lot of research on Melatonin and it's use for CH's and other headaches, some of it is attached below. My apologies if this is too much to read. However it is VERY exciting that something has finally helped. I hope it helps others. It is alos a drug that does not cause damage to the body as some of the other drugs for CH's do.
Martine
http://www.neurologyreviews.com/10_4April/Sleep_Headache.html
http://www.trueorigin.org/atp.asp
Adenosine is found in every part of the body, because it plays a role in the fundamental ATP-related energy metabolism, but it has special functions in the brain. There is a great deal of evidence that concentrations of brain adenosine are increased by various types of metabolic stress including anoxia and ischemia. The evidence also indicates that brain adenosine acts to protect the brain by suppressing neural activity and also by increasing blood flow through A2A and A2B receptors located on vascular smooth muscle. By counteracting adenosine, caffeine reduces resting cerebral blood flow between 22% and 30%. Caffeine also has a generally disinhibitory effect on neural activity. It has not been shown, however, how these effects cause increases in arousal and alertness.

Adenosine is released in the brain through a complex mechanism. There is evidence that adenosine functions as a synaptically released neurotransmitter in some cases, but stress-related adenosine increases appear to be produced mainly by extracellular metabolism of ATP. It is not likely that adenosine is the primary neurotransmitter for any group of neurons, but rather that it is released together with other transmitters by a number of neuron types. Unlike most neurotransmitters, adenosine does not seem to be packaged into vesicles that are released in a voltage-controlled manner, but the possibility of such a mechanism has not been completely ruled out.

Several classes of adenosine receptors have been described, with different anatomical distributions. A1 receptors are widely distributed, and act to inhibit calcium uptake. A2A receptors are heavily concentrated in the basal ganglia, an area that plays a critical role in behavior control, but can be found in other parts of the brain as well, in lower densities. There is evidence that A 2A receptors interact with the dopamine system, which is involved in reward and arousal. (A2A receptors can also be found on arterial walls and blood cell membranes.)

Beyond its general neuroprotective effects, there are reasons to believe that adenosine may be more specifically involved in control of the sleep-wake cycle. Robert McCarley and his colleagues have argued that accumulation of adenosine may be a primary cause of the sensation of sleepiness that follows prolonged mental activity, and that the effects may be mediated both by inhibition of wake-promoting neurons via A1 receptors, and activation of sleep-promoting neurons via indirect effects on A2A receptors. More recent studies have provided additional evidence for the importance of A2A, but not A1, receptors.

http://www.ncbi.nlm.nih.gov/pmc/articles/PMC2757148/
ATP is a good candidate for a signal that mediates the local coordination of individual circadian clocks in the SCN and perhaps in other brain regions.


http://www.ncbi.nlm.nih.gov/pmc/articles/PMC2819050/
The circadian rhythms in the pineal gland
The major function of the pineal gland is the synthesis and release of melatonin, a neurohormone, which is elevated at night and circulated throughout the body serving as a signal of time to integrate physiological functions with environmental lighting on a daily and seasonal basis (Bailey et al. 2009; for more recent reviews, please see Klein 2006; Macchi and Bruce 2004). In lower vertebrates, pinealocytes possess a photosensitive and autonomic circadian rhythm in melatonin secretion that persists in dissociated cell cultures (Robertson and Takahashi 1988a,b; Zatz and Mullen 1988a; Zatz et al. 1988). In fact, avian pinealocytes resemble retinal cone photoreceptors as they both have oil droplets, utilize opsin, arrestin, transducin, and cGMP-gated cation channels (CNGCs) for phototransduction, and display hyperpolarizing responses to brief pulses of light (Pu and Dowling 1981; Tamotsu and Morita 1986; Dryer and Henderson 1991). Interestingly, mammalian pinealocytes are not sensitive to light, and the circadian oscillation in pineal melatonin production in this case is under SCN control through a polysynaptic pathway that involves both central and peripheral neuronal structures (review in Maronde and Stehle 2007). Even though the mammalian pineal gland serves as a peripheral oscillator driven by the SCN, the machinery for the production of melatonin, including the expression of key enzymes AANAT and hydroxyindole-O-methyltransferase that synthesize melatonin, is under circadian control (Klein 2006; Maronde and Stehle 2007). Over 600 genes that are important for immunity, cell cycle and death, intracellular signaling molecules, transcription factors, and circadian rhythmicity are also under circadian regulation in the mammalian pineal gland (Bailey et al. 2009). However, the molecular mechanism underlying melatonin secretion from pinealocytes is still not well understood, and the circadian regulation of cell excitability or ion channel activity have only been documented in non-mammalian pinealocytes.


http://www.ch.ic.ac.uk/local/projects/s_thipayang/bio.html
Oxidative Stress
The degenerative processes associated with aging is a biologically complex and multifaceted phenomena. A current, but putative theory on aging associates the gradual accumuation of oxidative stress in neural tissue to accelerated neurodegenerative changes and age-related diseases. Oxidative stress is defined as the cellular damage caused by oxygen free radicals. The two types of oxygen free radicals, the superoxide anion and the hydroxyl radical are naturally produced by product of aerobic metabolism, the latter bding more biologically toxic. The reactive nature of free radicals stems from their unpaired valence electron that mediates oxidative toxicity, damaging nucleic acid, membrane lipids, proteins, and carbohydrates. Approximately 5% of celular oxygen is not used in the production of ATP but is reduced to reactive free radicals. An estimated 1011 free radicals/cell/day formed, inducing perhaps up to 105 oxidized DNA residues formed/cell/day. Furthermore, it is suggested that the progression of brain cell aging occurs when the balance between oxidative stress and antioxidative defense tips towards increased free radical production. Neural activity,especially the release of the accumulation of oxidative stress leads to the morphological and physiological destruction of neurons. A gradual deterioration of neurological tissue occurs represented by functional loss, such as slowed reactions, diminished memory, or tremour. This progressive degeneration is the priced the ody pays for utilixing oxygen. Increased free radical generation may also results from the additive exposure to toxins, UV light and stress or from the decrease in the bodies defense sysems to reduce oxidative stress, namely free radical scavengers, antioxidative enzymes, or meal chelating agents.


http://onlinelibrary.wiley.com/doi/10.1111/j.1600-079X.2006.00407.x
/full

More direct evidence that oxidative stress increases melatonin consumption in rats has been provided by Tan et al. [78]. They observed that rats loaded with melatonin and then exposed to ionized radiation (which generates •OH) significantly increased cyclic 3-hydroxymelatonin (C3-OHM) excretion in urine. The rapid drop in circulating melatonin under conditions of excessive stress can be considered a protective mechanism for organisms against highly damaging oxidants; in this sense, melatonin can be categorized as a first line of defensive molecule. In addition to direct prevention of tissue injury, the increased levels of melatonin metabolites such as N1-acetyl-N2-formyl-5-methoxykynuramine (AFMK) and N-acetyl-5-methoxykynuramine (AMK) upregulate antioxidant enzymes and downregulate the pro-oxidative and proinflammatory enzymes (see below). In many disease states which reportedly involve free radicals and oxidative stress, e.g. Alzheimer's disease, cancer and coronary heart disease, melatonin levels in these patients are significantly lower than those in healthy counterparts. It is not clear whether the low melatonin levels in these patients are the result of consumption due to the elevated free radical production or due to the lower production of melatonin.

The low bioavailability (average 18.9%) and large individual variation (average 17.7-fold) may well explain the different responses in subjects who take melatonin orally. Currently, the most popular melatonin formula commercially available is a 3 mg tablet. For some subjects, this dose when taken to benefit sleep may induce drowsiness the day after; for others, whose bioavailability is low, this dose may not be sufficient to treat insomnia or related disorders. To obtain the optimal effects of melatonin treatment, individualization of dose is suggested based on the serum or salivary melatonin levels after melatonin administration or adjusting the dose depending on the responses of the subjects.
Drug interactions also influence the bioavailability of melatonin. For example, co-administration of melatonin with CYP1A2 inhibitor, fluvoxamine (also a serotonin reuptake inhibitor), in healthy subjects, results in a 17-fold increase in melatonin blood levels [122]. These data also indirectly indicate a very low melatonin bioavailability in humans, probably
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saintpeter

(Member)
From:
606 total posts
Not currently suffering :D
Hi Martine and Tom.
Fantastic to see Tom's green icon It's especially great, as you say, it's from a not damaging medication.
Best wishes to you and Tom for a happy Christmas and holiday.

Cheers Peter.
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sunset21

(Member)
From: Melbourne/East Bentleigh
27 total posts
Not currently suffering :D
Hi Martine and Tom,

GREAT news to see Tom is getting pain free nights with Melatonin. I too am in my second week of my CH cycle after 2 year remission….

During this cycle I have been using the Melatonin of the shelf however was doing nothing so on Fri I saw my local GP and asked for a prescription – she did say it was the first time she has prescribed this and had to look it up in her medical book but I had no problems getting it from her after telling her I suffer from CH.

That night I took 2 x 2mg (you are only meet to take 1) before bed and had my first night without a hit – Sat, Sun and last night I did the same – however I did wake up after an hour with the first signs of the beast coming so I went straight on to my O2 tank sitting on my back deck (E tank) for 10min and it killed the hit. I went straight back to sleep after that and did not wake up until the morning.

So far so good with O2 and Melatonin this cycle……..however early days - Also not shadows during the day.
icon
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Shell

(Member)
From: Echuca
123 total posts
Currently suffering :(
Hi Martine and Tom,

That's Fantastic news! iconiconiconicon
I'm so glad you have found some relief at last.
Hope you have a great Christmas and New year!

Thanks for your research into this, you have provided some great information here that I'm sure will be beneficial to many. My best wishes to you both.

Hi Sunset21,

So glad you have found the correct Melatonin now, the product from health food stores is not effective for CH, It is recommended to start with 10mg 30 minutes before bed time. Some go as high as 15 mg to get through the night. Helps to avoid the wake up calls. Give it 7-10 days to see if it helps you, so I'm so glad that you are persevering with it. I hope that this can be an effective tool in fighting the beast for you.

Regards Shelliconicon
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sunset21

(Member)
From: Melbourne/East Bentleigh
27 total posts
Not currently suffering :D
Hi Shell,

Yes only been taking 4 to 6mg before bed and waking up a few times with hits but the 02 has help get ride of them.

Will be taking 10mg tonight to see how that goes - the only thing is there is only 2mg in each tablet - which means 5 tablets per night and there only 21 tablet in a pack - I do have 2 more repeats.

I might need to see my Nero instead of my GP to get a compond chemist to mix me up a batch of 10mg per tablet.

Will keep you posted.

Cheers

Mat
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Dusker

(Member)
From:
765 total posts
Currently suffering :(
How wonderful to see Tom is GREEN!!!
Thank you for all that great information!

What a wonderful Christmas gift for you all.
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Toms headaches

(Member)
From: Northbridge
30 total posts
Not currently suffering :D
Just coming back to the site now. Tom was pain free until mid Dec and then when into a terrible patch. We then added amitriptaline ( spelling) into the combination. As long as Tom has twelve hours sleep this seems to work. He has been pain/attack free for 3 weeks.
Melatonin needs to be made up at a compounding chemist and taken in its pure form in order to work. Tom takes 3mg and he is only 8 anything less does not work.
Good lick to any one trying it out.
Martine.
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Dusker

(Member)
From:
765 total posts
Currently suffering :(
Hello Martine
I was wondering how Tom was going.
Sorry to hear that he had a bad patch, but now back up and and into it again.
He must be a strong little fellow.
Heather
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Ben

(Member)
From:
324 total posts
Currently suffering :(
HI Martine and Tom,
I was born in 1975, making me 35 years old now. I had my first headache investigation in 1979 when I was 4. I was a screaming child that no-one knew what to do with. I sought many treatments whilst growing up. It took until 1998 for me to first hear the term "Cluster Headache" 19 years after first presenting with the problem.
Times were different back then, nobody knew what was wrong, let alone a CH diagnosis. I have spent most of my life with Doctors and specialists saying "You are too young for CH". Tom proves otherwise and vindicates my position to some extent.

However, despite my childhood experiences, I take no personal satisfaction in seeing someone so young afflicted with CH.

It is a tragedy for me to see someone else so young affected by this disease.
It breaks my heart. If his life turns out anything like mine, it will not be nice.

It is great to see a diagnosis so early in Tom's life. At least he will grow up with support from family and knowledge of his condition, rather than having a cloud of suspicion and doubt hanging over his head, as I always did.

Medicine has moved along a lot since 1979, so have treatment options for CH.
There is also a lot of evidence to support the theory that Tom's CH will disappear at any stage. Through puberty, hormonal changes and growth spurts. CH can spontaneously disappear back from whence it came.

Fingers crossed this happens for Tom. It can take away your childhood having CH so young. For me it was a devastating blow to my personal development from which I have never fully recovered.

When I was this young Soluble Aspirin 900mg (Aspro Clear) was my abortive drug and my saviour. Maybe 600mg (2 tablets) would be more appropriate at his age and bodyweight.
It's worth a try.

I wish him well.

Cheers, Ben.
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