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Everything posted by alleyoop

  1. I guess I am at the mercy of the scholarship committee. I don't have the funds to book early. The same is true with air fares. When will the scholarships be awarded? Thanks in advance, Bobb
  2. Austin was the venue for the Second Annual CB Conference, and one of my all time favorites! The BBQ and music scene are unparalleled!! Hopefully, I will find a way to be there again. Fun, Fun, Fun!!! bobb
  3. One that I didn't see mentioned that I took for four years was clomiphene citrate (Clomid). I do believe that it helped me go from chronic to episodic, but there are side effects. Dr. Todd Rozen wrote a paper a few years back after using it on a chronic CH patient. alley
  4. Potter, I would think that you realize by now that the "General Board" is public. We do not leave posts on the public boards that talk about busting. We have two private boards for those posts: "Share Your Busting Stories" and "Clusterbuster Files". Those two boards are where any posts talking about anything busting related are to be found. It was me who told spiny to move the post, so you're barking up the wrong tree. If you want the thread moved and pinned on the "Share Your Busting Stories" board, I will be glad to do so. But for obvious reasons, we will not leave it on the "General Board". Bobb
  5. Thanks J for reposting this. Sherri, in Dec, 2003, I applied for SSDI for my chronic CH. I was turned down, appealed, turned down again, appealed and after 3 1/2 yrs finally got a hearing in front of an ALJ, who ruled "fully favorable" on the spot. I had originally gone with one of the nationally advertised SSDI attorneys. After the second denial, I was dropped by this attorneys' office. I retained a local attorney who specialized in SSDI. That would be my recommendation to you. The local attorneys know most of the ALJs that you may draw, and if they have a reputation for only taking on solid cases, then that is a big plus. Hope this helps. alley
  6. Thanks Batch and Leslie!! Since I too, am feeling that old feeling like I'm about to go into cycle after 18 mos PF, I will be going to town tomorrow for some benadryl. bobb
  7. Maybe we should consider the possibility of holding the 2016 CB Conference at the La Bomba Shack in honor of Mark? Just a thought, although it is probably an impracticable one. R.I.P. Pinky.
  8. After not hearing from you for so long, it is indeed gratifying to know that you're still with us Fab. This board just lost one of our oldest and dearest members (Pink Shark Mark), which goes to show we never know when our number will come up. Be well Fab and please follow orders -- well maybe you can sneak by nurse Griselda every once in a while. Wishing you improving health and much happiness, Bob Bowling
  9. Sending healing prayers your way Fab.
  10. http://www.motherjones.com/politics/1995/09/migraine-killer
  11. http://www.motherjones.com/politics/1995/09/migraine-killer
  12. Sounds like the logical choice to me Pete. If you want, I'll make it a 'sticky'. Thanks again for your advocacy my friend.
  13. Batch, I can't thank you enough for the contributions you are making to these boards. Bob Bowling 8-)
  14. 1) Um...sometimes...from what I remember that info can seem like a huge load of legal fine print boilerplate warnings to comply with laws here in the US, or just a case of lawsuit averse lawyers going hog wild trying to cover every base and create work for themselves, but whatever the case, I'm a bit out of the pharmaceutical loop....thank gawsh....since adopting busting instead of toxic pharma for CH. 2) Yes, sometimes to the nth degree 3) Back when on pharma, I looked at the risks, weighed them against the specter of unrelieved CH attacks, and if the risks were particularly ominous/dangerous.....I would say screw it and still go ahead and risk it anyway. Examples: At high cycle I was injecting five 6mg imitrex shots a day (back before I knew 3mg was a plenty strong dose), right when media reports about coma and death from imitrex were peaking (mid/late 90's). I was charging up a helluva credit card bill at the Tijuana farmacias I would cross the border to visit for imitrex, available there without prescription. Or taking sustained high doses of prednisone despite reading it could cause me to need to be on dialysis for the rest of my life (I don't know if I had even read that right, but now I know too many CH'ers who've needed hip replacements courtesy prednisone, and it sure walloped my immune system after tapering off of it, a known side effect that still treats me to repercussions 26 years later). So my drug risks offered mixed results. I don't know if I'll get off scott free without any imitrex heart issues catching up to me many years after my imitrex abuse. I do have to say imitrex saved my arse for a couple cycles back when busting and 100% high flow O2 weren't known options. Yes I did experience more attacks per day - just as I do if aborting with O2. Here's the thing about that though: I still made it through an entire approx. 11 week cycle without a single attack ever going full blown. And I was never aware of a single side effect from imitrex, which makes me lucky, as that sure isn't the case with everyone. I'm mainly critical of imitrex because of what I've seen others experience, especially the spate of recent reports of SERIOUS heart issues, but not from my own experience. I think the fact that we can be so desperate to quell the beast that we'll take scarily risky amounts of prescription dugs is a good reason for all CH'ers to be well informed about the busting alternative. Great post Jeebs! 8-)
  15. Modern Drug Discovery March/April 1999 Modern Drug Discovery, 1999, 2 (2), 20-21, 23-24, 28, 31. Copyright © 1999 by the American Chemical Society. Ergot, a potent neurotoxin and vasoconstrictor found in a fungus that grows on rye, was one of the first effective migraine medications and has been a springboard for further migraine drug development. BY CAROL HART "A great plague of swollen blisters consumed the people by a loathsome rot so that their limbs were loosened and fell off before death." Thus one 9th century writer described an outbreak of "St. Anthony's Fire", or ergotism, caused by ingesting toxic amounts of the alkaloids produced by Claviceps purpurea, a fungus that infests rye. Gangrene with burning pain in the extremities was one of two common presentations of ergot poisoning, which could also produce convulsions, hallucinations, severe psychosis, and death. St. Anthony was the patron saint of those stricken, and the Order of St. Anthony provided care for these patients. Outbreaks of "dancing mania" that occurred between the 13th and 16th centuries have sometimes been attributed to ergotism, and one appealing, if unprovable, theory proposes that the women accused of witchcraft in the Salem trials of 1692 were suffering from ergot-induced psychosis and convulsions. Ergot poisoning was not identified as the cause of St. Anthony's Fire until the 17th century. Cold damp growing conditions, common in France and Germany, promoted fungal growth. Repeated epidemics occurred throughout the Middle Ages, when whole populations were affected by bread made from contaminated rye. The last reported outbreak, which caused more than 200 cases and 4 deaths, occurred in 1951 in Pont St. Esprit, France. During the Middle Ages, midwives discovered the first medical application for ergot: A small dose could be used to hasten labor or prevent postpartum bleeding. Late in the 19th century, liquid extracts of ergot were used in Germany and the United States to treat "vascular headache" such as migraine (see sidebar, What makes a headache a migraine?) (1). TO SIDEBAR: What makes a headache a migraine? The ergot family Extracted from the dried C. purpurea, ergot contains numerous neurotoxic and vasoconstrictive alkaloids. The vasoconstrictive properties account for both the gangrenous form of ergot poisoning and ergot's medical applications in preventing postpartum hemorrhage and treating migraine headache. Since the potency and effects of naturally occurring ergot are unpredictable, turn-of-the-century chemists set about identifying and synthesizing the medically useful alkaloids found in ergot. Ergot proved to be a treasure chest--and a Pandora's box--of useful and fascinating chemical entities. Images of migraine history... In 1918, Arthur Stoll isolated ergotamine, which was introduced by Sandoz (now Novartis) under the trade name Gynergen in 1921 and marketed as a safer and more reliable form of the medieval midwife's nostrum. Controlled trials in the 1930s showed it to be effective in relieving migraine headache. Also during the 1930s, two U.S. chemists succeeded in identifying the common nucleus of the ergot drugs, which they named lysergic acid. With this information, it became feasible to synthesize the ergot compounds, a project undertaken by Albert Hofmann in Stoll's laboratory at Sandoz, among others (2). In 1935, Sandoz chemists succeeded in synthesizing ergonovine, which was developed as methylergonovine (Methergine) and widely used to control postpartum hemorrhage. Further efforts to isolate the various alkaloids occurring naturally in ergot led to the development of a preparation of ergoloid mesylates (Hydergine) for treating dementia. In 1943, Hofmann synthesized dihydroergotamine (DHE), marketed for the treatment of blood pressure and later shown to be highly effective for migraine. Migraine drugs In the course of Hofmann's trial-and-error synthesis of lysergic acid derivatives, the 25th compound, lysergic acid diethylamide (LSD-25), failed to show any therapeutic promise in early testing on animals. In 1943, five years after it was first synthesized and tested, Hofmann decided to synthesize LSD-25 again for further testing. While completing the synthesis, he was overcome by strange sensations, which later developed into mild euphoria accompanied by pleasant visual hallucinations. Surmising that he had somehow absorbed or ingested some of his newly synthesized compound, Hofmann proceeded to test the substance on himself by taking what he believed to be a minuscule dose--0.25 mg--and was rapidly plunged into what can only be described as a very bad trip. Like the natural ergot from which it was derived, LSD proved to be too potent, risky, and unpredictable to have a medical application. In the course of exploring the ergot family, Sandoz chemists went on to discover yet another important antimigraine drug, methysergide (Sansert). Used for daily preventive therapy rather than abortive treatment of migraine, methysergide is a serotonin antagonist, whereas ergotamine is a serotonin agonist. Interestingly, "unworldly feelings" or hallucinations are among methysergide's possible side effects (3). The ergot drugs are structurally related to the biogenic amines, serotonin, norepinephrine, and dopamine and interact with multiple receptors in these systems (1). The same is true for all the major psychedelic drugs. Two of the four rings in LSD's chemical structure are identical to the ring structure in serotonin, and the side chain attached to serotonin's ring structure is identical to another part of the LSD molecule (4). Because of their structural similarities with the neurotransmitters, ergotamine and DHE exert wide-ranging effects on physiologic processes mediated by the adrenergic, dopaminergic, and serotonergic receptor systems, particularly the latter (1). They are serotonin 1A, 1B, 1D, and 1F receptor agonists; they also block the release of two important vasoactive neuropeptides currently thought to be involved in migraine, substance P and calcitonin gene-related peptide (CGRP) (1). Ergotamine and DHE Ergotamine is not an analgesic and is ineffective for common tension head aches. Its vasoconstrictive effects have long been presumed to explain its efficacy for migraine, but the proposed mechanism of action of the ergot alkaloids has changed as understanding of migraine pathophysiology has evolved. Its main limitation is the relatively high incidence of side effects, which, according to different studies, range from 17 to 41%, compared with nonsteroidal anti-inflammatory drugs, for which the incidence of side effects is 5 to 28%. Nausea and vomiting predominate among the side effects observed following ergotamine ingestion, potentially exacerbating the nausea and vomiting commonly associated with migraine. Drowsiness, tiredness, or fatigue are also common, rendering it less useful for treating migraine attacks in the workplace. Overuse is associated with development of a chronic drug rebound headache (a headache pattern similar to tension headache superimposed on the migraine, which continues to occur) and risk of ergotism (5). DHE improved on ergotamine by reducing some of its more troublesome side effects. DHE avoids much of the hypertensive and emetic effects of ergotamine and also appears to be free from risk of drug rebound headaches (1). Because DHE is much less vasoconstrictive than ergotamine, it has been argued that its antimigraine action may have some other basis, such as an anti-inflammatory effect on blood vessels. Although the efficacy of DHE for migraine was first reported in 1945, it was little used in the United States until the 1980s. Even then, DHE was primarily an emergency treatment for intractable migraine, since few patients were comfortable with self-administered injections. In December 1997, a nasal spray formulation called Migranal was approved by the FDA. All of the ergots retain the potential to produce vasospastic reactions, potentially causing myocardial or peripheral ischemia (deficiency in the blood supply to an organ or tissue), and are contraindicated for severe coronary artery disease, peripheral vascular disease such as Raynaud's disease, or uncontrolled hypertension. Methysergide is capable of causing fibrotic complications (scar tissue that forms on the heart or lungs or in the gut); other ergot drugs have been suspected of having this potential as well. Sumatriptan: A new kind of serotonin agonist Pharmaceutical companies had largely ignored migraine as a diagnosis, despite the size of the potential market: There are an estimated 23 million sufferers in the United States alone (see sidebar, The burden of migraine). The new era in antimigraine drugs began in 1973 with efforts to synthesize a more selective serotonin agonist, following up on numerous observations implicating serotonin (a potent vasoconstrictor and a pain modulator) in the generation of a migraine attack (6). Glaxo Wellcome introduced the first of the new serotonin agonists, sumatriptan (Imitrex), in 1991. TO SIDEBAR: The burden of migraine Sumatriptan has agonist effects at two serotonin (5-HT) receptors, 5-HT1B and 5-HT1D, with weaker effects at other 5-HT1 receptors. Sumatriptan is about fivefold more potent at 5-HT1D receptors than at 5-HT1A receptors, in contrast to DHE, which is about 10-fold more potent at 5-HT1A than 5-HT1D receptors (7). Sumatriptan relieves not only the pain of migraine but also the associated symptoms of nausea, vomiting, light sensitivity (photophobia), and sound sensitivity (phonophobia)(8). Many patients are able to continue to work or return to work after sumatriptan treatment, which often is not possible with ergotamine because of its sedating or nauseating effects. However, up to 40% of patients experience headache recurrence within the same migraine attack a few hours after initial treatment with sumatriptan (8). In a trial comparing subcutaneous DHE and sumatriptan, the latter showed higher response rates at 1 hour (78% vs 57%) and 2 hours (85% vs 73%), but the rate of headache recurrence within 24 hours was 2.5 times greater with sumatriptan (8). The "me too" triptans Drug developers began to look for new antimigraine agents to repeat, and hopefully improve upon, the success of sumatriptan in what has proven to be a billion-dollar-and-growing market. Three new triptans entered the U.S. market in late 1997 and 1998--zolmitriptan (Zomig, Zeneca Pharmaceuticals), naratriptan (Amerge, Glaxo Wellcome), and rizatriptan (Maxalt, Merck & Co). Three more are in clinical trials or pending FDA approvalóeletriptan (Relpax and Pfizer), frovatriptan (Vanguard Medica), and almotriptan (Almirall-Prodespharma/ Phar macia and Upjohn). These second-generation triptans attempt to improve on sumatriptan's record by offering a shorter tmax, longer half-life, greater oral bioavailability, improved CNS penetration, or reduced cardiac effects (9). Clinical-trial data suggest that the differences among the various triptans are subtle rather than dramatic. While some patients who found sumatriptan ineffective or difficult to tolerate may do well with one of the newer triptans, the overall efficacy rates for all of these orally administered agents hover around 65% (9). Sumatriptan and the other triptans produce "triptan sensations", side effects which can include tingling, numbing, anxiety, heaviness or tightness in the chest and throat, and sensations of warmth, burning, cold, or pressure (8). These effects do not appear to be cardiac in origin, but they have not been fully explained. As with the ergot drugs, the triptans are contraindicated or prescribed with caution for those with uncontrolled blood pressure, coronary artery disease, or peripheral vascular disease. Pathophysiology of migraine As with many other disorders, drug development and understanding of disease etiology have progressed together. The efficacy of the ergot drugs was long attributed to their potent vasoconstrictive effects, since migraine was believed to result from dilation of the cranial blood vessels in response to some irritating stimulus. This theory corresponded well to the throbbing character of the pain and to the fact that vasodilating substances (such as alcohol or tyramines in foods) sometimes triggered headaches, while vasoconstricting agents (caffeine and ergotamine) could relieve them. Vasodilation may account for much of the pain of migraine headache, but the attack is now believed to be generated within the CNS. In a 1995 Nature Medicine report, Weiller and colleagues described PET scans made of nine migraineurs (people with migraines) during attacks. Increased blood flow was observed in the brain stem during the migraine, supporting the theory of a "migraine generator" in the region of the raphe nucleus, which is the center of the brain serotonin system. Sumatriptan taken during the attack relieved the headache but did not affect the brain stem activity, which may suggest an explanation for the high rate of headache recurrence seen with this agent (10). The serotonin connection Several clinical and experimental observations confirm that the serotonin system has a major role in producing or maintaining a migraine attack. Serotonin-releasing agents such as reserpine can induce a migraine attack, whereas serotonin administered intravenously is effective in relieving migraine, although with unacceptable side effects (11). There is a 30% decrease in platelet 5-HT during migraine without aura (11). Increased urinary secretion of serotonin's main metabolite, 5-hydroxyindoleacetic acid, is seen during migraine attacks (6). As a neurotransmitter, serotonin is a modulator of mood, sleep, sexual behavior, feeding behavior, and pain awareness. In humans, 90% of the body's serotonin is found in the gastrointestinal tract, with the remainder occurring in platelets and the CNS. Seven classes of serotonin receptor have been identified. The 5HT1-type receptors are inhibitory, and 5HT2-type receptors are excitatory. Migraine abortive agents are 5-HT1 agonists, but effective preventive treatments, including methysergide and amitriptyline, are 5-HT2 antagonists (1). Ergots show some 5-HT2 antagonist activity in addition to their 5-HT1D agonist effects (7). As 5-HT1B/1D agonists, the triptans are known to act directly on 5-HT1B receptors in smooth muscle, but they also appear to act at serotonin receptors on the peripheral trigeminal nerves to decrease sensory nerve activation. They also cause constriction of dilated cranial blood vessels by activation of a 5-HT1-like receptor found in these vessels that is believed to be identical to 5-HT1D (see sidebar, Neurogenic inflammation) (3). TO SIDEBAR: Neurogenic inflammation A dopamine connection? Some evidence suggests that the dopamine system is also involved and that a state of dopaminergic hypersensitivity exists in migraine (13). Nausea with or without vomiting is experienced by more than 80% of migraineurs, suggesting that changes in dopamine activity in the brain stem may occur early in the course of an attack. Gastric motility is reduced in most migraine attacks even if nausea is not present, which may suggest that dopaminergic hyperactivity in the gastrointestinal tract is a feature of migraine (13). Dopamine antagonists such as metoclopramide (Reglan) and prochlorperazine (Compazine) are regularly used in the treatment of migraine. Their efficacy has been attributed to their antiemetic action, not to any specific effects on migraine, but they may be achieving their effects by antagonizing D2 receptors that are activated during the migraine attack (13). In several small studies and case reports, D2 antagonists have been remarkably effective in relieving migraine headache, as well as migraine-related nausea or vomiting. Intravenous haloperidol (Haldol) relieved migraine in six out of six patients, for example, and efficacy rates of 82 to 88% were reported for intravenous prochlorperazine in two small randomized double-blind trials (13). Calcium channel defects Most recently, the genetic evidence for familial hemiplegic migraine (see sidebar, Who gets migraines, and why?) suggests mutations of calcium channel genes may be responsible for this rare migraine variant. Drawing upon gene association studies for common migraine, it has been suggested that migraine may be a "channelopathy" arising from mutations in genes involved in gating calcium and potassium channels that alter the threshold for CNS excitability (14). TO SIDEBAR: Who gets migraine, and why? Other directions in drug development The proposition that migraine is a neuroinflammatory process has provoked new directions in drug development. To date, none has shown much promise in improving on the safety and efficacy of the ergots and triptans. Lanepitant, a neurokinin antagonist, has failed to show efficacy, but this failure may relate to poor absorption of the oral drug during a migraine attack (less than 10% of that observed in fasting volunteers) (12). Another neurokinin antagonist, RPR100 893-201, was also ineffective, but again, plasma concentrations for the oral formulation may have been inadequate (12). Bosantan, an endothelin antagonist, given to patients intravenously, also has proven ineffective (12). Ganaloxone is a member of a class of neurosteroids called epalons that modulate GABAA receptors in the CNS. Developed to treat epilepsy and migraine, it showed promising antimigraine effects in Phase II studies using a liquid formulation (12). However, the tablet formulation developed for further studies produced disappointing results, and the antimigraine trials were dropped, although there is still the possibility that ganaloxone may be studied as a migraine preventive therapy. Drug researchers continue to pursue the serotonin connection in the hopes of developing a still more specific antimigraine drug that would be free of cardiac effects. Eli Lilly is reportedly close to beginning Phase III trials for a new agent that targets the 5-HT1F receptor and that may have a much more favorable side effect profile than the current triptans that target 5-HT1B/1D receptors. The vasodilation theory of migraine also continues to provoke new research. Nitric oxide is a potent vasodilator and also a modulator of pain awareness. Nitroglycerin, which releases nitric oxide, invariably brings on a migraine attack when given to a migraine-prone individual. Nitric oxide releasers also trigger the release of CGRP from perivascular nerve endings in animals (12). A nitric oxide synthetase inhibitor was reported effective in a small double-blind study and is likely to receive further study (12). Finally, CGRP antagonists may be another promising direction for future migraine drug development. While the triptans have greatly expanded the treatment options for this common, often debilitating disorder, more effective management of migraine may await further exploration of the complex actions of the ergot drugs, which act on every system so far proposed to explain migraine. References 1. Silberstein, S. D., The pharmacology of ergotamine and dihydroergotamine. Headache 1997, 37(Suppl. 1), S15-S25. 2. Hofmann, A. LSD, My Problem Child, McGraw-Hill: New York, 1981. 3. Mosby's GenRx, 8th ed.; Mosby-Year Book: 1998. 4. Snyder, S. H. Drugs and the Brain, Scientific American Library: New York, 1986. 5. Meyler, W. J. Side effects of ergotamine. Cephalalgia 1996, 16, 5-10. 6. Goadsby, P. J. Current concepts of the pathophysiology of migraine. Neurologic Clinics 1997, 15(1), 27-42. 7. Peroutka, S. J. The pharmacology of current anti-migraine drugs. Headache 1990, 30(1 Suppl.), 4-16. 8. Mathew, N. T. Serotonin 1D (5-HT1D) agonists and other agents in acute migraine. Neurologic Clinics 1997, 15(1), 61-83. 9. Lipton, R. B. The triptans and beyond. In Program for the 1998 American Association for the Study of Headache, Scottsdale Symposium; AASH: Scottsdale, AZ, 1998; addendum to agenda. 10. Weiller, C. et al. Brain stem activation in spontaneous human migraine attacks. Nature Med. 1995, 1, 655-660. 11. Ferrari, M. D.; Saxena, P. R. On serotonin and migraine: A clinical and pharmacological review. Cephalalgia 1993, 13, 150-164. 12. Silberstein, S. D. Migraine: Acute treatment. In 40th Annual American Association for the Study of Headache Meeting Program; AASH: San Francisco, CA, 1998. 13. Peroutka, S. J. Dopamine and migraine. Neurology 1997, 49, 650-656. 14. Gardner, K.; et al. A new locus for hemiplegic migraine maps to chromosome 1q31. Neurology 1997, 49(5), 1231- 1238. 15. Stewart, W. F. et al. Prevalence of migraine headache in the United States. JAMA 1992, 267(1), 64-69. Carol Hart is a science writer based in Narberth, PA (twoharts@interserv.com; http://nasw.org/users/twoharts/).
  16. #1 Not really, since I feel that they are more of disclaimers written in by pharmaceutical attorneys. #2 Definitely. Every time I am prescribed a new drug, I research it and the side effects on the most reliable sites I can find BEFORE filling the script. #3 I always try to heed the warnings, especially as they pertain to my particular health problems and look for any interactions that may be in play with whatever else I am taking, be it prescribed or otherwise. Thanks MG for reemphasizing this! I too, think that we need to pay more attention to this. Great post!!! [smiley=thumbup.gif] [smiley=thumbup.gif] [smiley=thumbup.gif]
  17. After hearing from several of you suggesting making this thread a "sticky", it is done. I feel that it is that important. BB
  18. While we're on the subject of sumatriptan, I wanted to bring up the fact that we are seeing a number of peeps that have been having cardiology problems with this drug. It seems that the majority (correct me if I'm wrong) of these cases involve overuse of imitrex. At any rate it has become alarming, and I am not the only one to notice this. I'm sure that THMH will chime in, as he has had first hand experience with this. I am not trying to demonize sumatriptans in any way, just think we should as a forum be more aware of the risks. As NightCrawler implies, it is very doubtful that the medical community will be on top of this. Carry on......... BB
  19. Genetic aspects of cluster headache. Authors Sjöstrand C1. Author information Journal Expert Rev Neurother. 2009 Mar;9(3):359-68. doi: 10.1586/14737175.9.3.359. Affiliation Abstract Cluster headache (CH), a primary neurovascular headache syndrome, is characterized by recurrent, unilateral, short-lasting attacks of excruciating pain in the temporal and/or orbital region. The pain is considered one of the most severe pain conditions known to humans. Compared with the general population, first-degree relatives of probands with CH have a significantly increased risk of the same disorder. However, there seems to be no clear mode of inheritance, suggesting that both genetic and environmental factors are of importance, with the pathophysiology being multifactorial. Despite the genetic influence of the disease, a low prevalence and small pedigrees complicate the feasibility of genetic studies. To date, only genetic studies with limited sample sizes have been performed, but results have indicated an association with the HCRTR2 gene, which is involved in the regulation of chronobiological rhythms. Collaborative multicenter studies on large clinically well-defined materials are needed to reach a better understanding of the complex genetic background of CH. PMID 19271945 [PubMed - indexed for MEDLINE] http://www.ncbi.nlm.nih.gov/m/pubmed/19271945/?i=3&from=%2F20425202%2Frelated
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