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Everything posted by CHfather

  1. Tony, maybe this is what you're looking for???? https://clusterbusters.org/forums/topic/681-1-the-clusterbuster-method-a-quick-rundown/?tab=comments#comment-8322 (Asking this question to anyone who happens to be reading this thread: This document contains this statement about tryptamines: "For aborting attacks, they rival oxygen in safety and effectiveness." This puzzles me. Is this true, but no one does it anymore except on rare occasions (maybe because of the five-day "shutting the door" principle/rule)? From the time I have been here (~10 years), I really don't recall anything being pushed about using them to abort, and they don't seem to effectively do that a lot of the time. Maybe as a SPUT?) Tony, IF this is what you are looking for, it's the first of the 13-part series provided by tommyd back in 2010. You can see all of them in the ClusterBuster Files section. A lot of them are out of date. If you are looking for a summary of busting to share, I think the document under the "New Users - Read Here First" banner at the top of each page is probably as good as we have.
  2. Tony, do you mean the 2006 article by Sewell, Halpern, and Pope, "Response of Cluster Headache to Psilocybin and LSD"? If so, I have it. But I can't attach it here because I have apparently already used up my allotted attachment capacity. Tried to paste it, but the formatting all falls apart, as you can see below. Left in here in case you want to try to wade through the mess. If you PM me an email address, I can send it that way. (It used to be easily located at the main CB page, but that seems quite jumbled now.) Response of cluster headache to psilocybin and LSD Abstract—The authors interviewed 53 cluster headache patients who had used psilocybin or lysergic acid diethylamide (LSD) to treat their condition. Twenty-two of 26 psilocybin users reported that psilocybin aborted attacks; 25 of 48 psilocybin users and 7 of 8 LSD users reported cluster period termination; 18 of 19 psilocybin users and 4 of 5 LSD users reported remission period extension. Research on the effects of psilocybin and LSD on cluster headache may be warranted. NEUROLOGY 2006;66:1920–1922 R. Andrew Sewell, MD; John H. Halpern, MD; and Harrison G. Pope, Jr., MD Cluster headache, often considered the most painful of all types of headache,1 affects predominantly men (0.4% vs 0.08% of women) and typically begins after age 20 years. The disorder is categorized as either episodic, occurring for 1-week to 1-year periods, in- terspersed with pain-free remission periods, or chronic, in which the headaches occur constantly for more than a year with no remission longer than 1 month.2 Ten percent of episodic cluster headaches ultimately evolve into the chronic form, and these are termed secondary chronic. In standard descrip- tions of cluster headache, an attack refers to the actual paroxysm of pain, a cluster period refers to a period of time when attacks occur regularly, and a remission period refers to a prolonged attack-free in- terval.3 Oxygen and sumatriptan are the mainstays of acute abortive treatment, whereas verapamil, lith- ium, corticosteroids, and other neuromodulators can suppress attacks during cluster periods. No medica- tions are known to terminate cluster periods or ex- tend remission periods. The effects of the ergot alkaloid derivative lysergic acid diethylamide (LSD) and the related indolalkylamine psilocybin on cluster headache have not previously been described and may include such properties. Case series. We were contacted by a 34-year-old man, diag- nosed with episodic cluster headache at age 16 years, who re- ported a complete remission of his cluster periods when he repeatedly used LSD on a recreational basis between ages 22 and 24 years. Cluster periods resumed once he stopped. Based on this experience, he attempted to treat his cluster headache by ingest- ing psilocybin-containing mushrooms every 3 months and again achieved lasting remission. On three occasions when he missed his scheduled dose, a cluster period reoccurred. Intrigued by this history, we located—through cluster head- ache support groups and an Internet-based survey—several hun- dred people with cluster headache who reported use of psilocybin- containing mushrooms or LSD specifically to treat their disorder, and we administered a standardized questionnaire (available from the authors). The consent form and study were approved by the McLean Hospital institutional review board. We restricted our analysis to the 53 individuals who 1) agreed to be contacted for evaluation by telephone or e-mail and 2) met International Classi- fication of Headache Disorders-2 criteria for cluster headache and allowed us to obtain copies of medical records documenting a diagnosis of cluster headache by an MD or DO. If the medical records did not support the diagnosis, the subject was excluded from further analysis. The final sample included subjects from across the United States as well as Great Britain, The Nether- lands, and South Africa. We found no significant differences be- tween men and women on demographic indices or headache features (table 1). Notably, 31 (58%) of the 53 individuals reported that they had never used psilocybin or LSD except to treat their cluster headache, and a further 13 (25%) had used these drugs for recreational purposes only in the remote past during adolescence. Results are summarized in table 2 and listed in complete form in table E-1 (on the Neurology Web site at www.neurology.org). Of the 32 subjects with episodic cluster headache, 19 had used sub- lingual psilocybin during cluster attacks; 17 found psilocybin to be effective in aborting attacks (defined as ending the attack within 20 minutes). Only one subject had used sublingual LSD for an acute attack, reporting it to be effective. Twenty-nine subjects had used psilocybin prophylactically during a cluster period; 15 (52%) reported that it was effective (defined as causing total cessation of attacks), and a further 12 (41%) reported partial efficacy (defined as attacks decreasing in intensity or frequency but not ceasing). Five of six LSD users reported cluster period termination. Twenty subjects ingested psilocybin during a remission period; 19 re- ported an extension of their remission period, in that their next expected cluster period was delayed or prevented entirely. Four of five subjects reported similar remission extension with LSD. Of the 21 subjects with chronic cluster headache, 5 of 7 re- ported that psilocybin aborted a cluster attack; 10 of 20 reported that psilocybin induced a complete termination of cluster attacks; and a further 8 reported partial efficacy. Of two chronic cluster headache patients who ingested LSD, both at subhallucinogenic doses, one reported no attacks for 10 days, and the other reported none for 2 months. Interestingly, 22 (42%) of the 53 subjects reported partial or complete efficacy (as defined above) from sub- hallucinogenic doses of psilocybin or LSD. Discussion. Our results are interesting for three reasons. First, no other medication, to our knowl- edge, has been reported to terminate a cluster pe- riod. Second, unlike other ergot-based medications, which must be taken daily, a single dose of LSD was described as sufficient to induce remission of a clus- Additional material related to this article can be found on the Neurology Web site. Go to www.neurology.org and scroll down the Table of Con- tents for the June 27 issue to find the title link for this article. From the Biological Psychiatry Laboratory (J.H.H., H.G.P.) and Clinical Research Laboratory (R.A.S.), Alcohol and Drug Abuse Research Center, McLean Hospital/Harvard Medical School, Belmont, MA. Funding sources include MAPS of Sarasota, FL (J.H.H., H.G.P.), and NIDA, NIH T32-DA07252 (R.A.S.). No funding source had any role in study design; collection, analysis, or interpretation of data; writing the report; or submis- sion of the manuscript. Disclosure: The authors report no conflicts of interest. Received December 20, 2005. Accepted in final form March 10, 2006. Address correspondence and reprint requests to Dr. R. Andrew Sewell, Oaks Building, ADARC, McLean Hospital, 115 Mill St., Belmont, MA 02478; e-mail: asewell@mclean.harvard.edu 1920 Copyright © 2006 by AA Enterprises, Inc. Table 1 Cluster headache characteristics by sex and subtype Headache features Headache type n Age, y Episodic Attack duration, min Attacks/day at peak Cluster period duration, wk Remission period duration, wk Men 26 45 (8) 97 (66) 5.5 (3.7) 13 (10) 11 (10) Women 6 45 (11) 66 (34) 6.2 (3.0) 15 (10) 9 (5) Total 32 45 (8) 91 (60) 5.6 (3.5) 13 (10) 11 (9) 1° Chronic NA NA Men 6 48 (8) 79 (57) 9.8 (7.4) Women 1 38 (NA) 90 (NA) 8.0 (NA) Total 7 47 (8) 81 (53) 9.6 (6.8) 2° Chronic NA NA Men 10 45 (6) 105 (70) 6.9 (3.0) Women 4 46 (10) 139 (64) 7.5 (1.0) Total 14 45 (7) 115 (68) 7.1 (2.5) Data are presented as mean (SD). 1° = primary; 2° = secondary; NA = not applicable. ter period, and psilocybin rarely required more than three doses. Third, given the apparent efficacy of subhallucinogenic doses, these drugs might benefit cluster headache by a mechanism unrelated to their psychoactive effects. Table 2 Reported efficacy of principal reported treatments for cluster attacks, cluster periods, and remission extension Partially Several limitations of this study should be consid- ered. First, it is subject to recall bias, because it relies primarily on participants’ retrospective re- ports. However, 6 participants (11%) provided de- tailed headache diaries that corroborated their recall. In addition, 3 (6%) of the 53 participants tried psilocybin for the first time subsequent to consenting to participate in the study but before being ques- tioned; 2 reported complete efficacy and 1 reported partial efficacy—a prospective response rate consis- Medication Acute treatment Total, n Effective, n (%) effective, n (%) Ineffective, n (%) tent with our retrospective findings. A second consideration is the possibility of selec- tion bias, in that individuals with a good outcome Oxygen 47 24 (52) 19 (40) 4 (9) Triptans 45 33 (73) 8 (18) 4 (9) Psilocybin 26 22 (85) 0 (0) 4 (15) LSD 2 1 (50) 0 (0) 1 (50) Prophylactic Propanolol 22 0 (0) 2 (9) 20 (91) Lithium 20 1 (5) 8 (40) 11 (55) Amitriptyline 25 0 (0) 4 (16) 21 (84) Verapamil 38 2 (5) 22 (58) 14 (37) Prednisone 36 15 (45) 5 (14) 15 (42) Psilocybin 48 25 (52) 18 (37) 3 (6) LSD 8 7 (88) 0 (0) 1 (12) Remission extension Psilocybin 22 (31) 20 (91) NA 2 (9) LSD 5 (7) 4 (80) NA 1 (20) Nine additional individuals had taken psilocybin and two addi- tional had taken lysergic acid diethylamide (LSD) purposefully for remission extension but were not yet due for another cluster period at the time of our evaluation; hence, for them, efficacy could not be scored. may have been more likely to participate. Recruit- ment over the Internet also selects for younger, more educated, and more motivated subjects,4 likely lead- ing to increased reported efficacy. Third, participants were not blind to their treat- ment, raising the possibility of a placebo response. However, cluster headache is known to respond poorly to placebo; controlled trials have shown a placebo re- sponse of 0% to prophylactic medications such as vera- pamil,5 capsaicin,6 and melatonin,7 and less than 20% to abortive medications such as sumatriptan.8 There- fore, it seems unlikely that we would have found more than 50 cases of apparent response to psilocybin or LSD through placebo effects alone. Our observations must be regarded as prelimi- nary, in that they are unblinded, uncontrolled, and subject to additional limitations as described above. Therefore, our findings almost certainly overesti- mate the response of cluster headache to psilocybin and LSD and should not be misconstrued as an en- dorsement of the use of illegal substances for the self-treatment of cluster headache. However, given the high reported efficacy for this notoriously refrac- June (2 of 2) 2006 NEUROLOGY 66 1921 tory condition, it is difficult to dismiss this series of cases as entirely artifactual. Further research is warranted. Acknowledgment The authors thank Nancy K. Mello, PhD, and Kimberley Lindsey, PhD, for their comments on an earlier version of this manuscript, and Robert Wold, Earth and Fire Erowid, for assistance with data collection. References 1. Dodick DW, Rozen TD, Goadsby PJ, Silberstein SD. Cluster headache. Cephalalgia 2000;20:787–803. 2. Headache Classification Subcommittee of the International Headache Society. The International Classification of Headache Disorders. Cepha- lalgia 2004;24 (suppl 1):44–48. 3. Ekbom K. Some remarks on the terminology of cluster headache. Ceph- alalgia 1988;8:59–60. 4. Etter JF, Perneger TV. A comparison of cigarette smokers recruited through the Internet or by mail. Int J Epidemiol 2001;30:521–525. 5. Leone M, D’Amico D, Frediani F, et al. Verapamil in the prophylaxis of episodic cluster headache: a double-blind study versus placebo. Neurol- ogy 2000;54:1382–1385. 6. Marks DR, Rapoport A, Padla D, et al. A double-blind placebo-controlled trial of intranasal capsaicin for cluster headache. Cephalalgia 1993;13: 114–116. 7. Leone M, D’Amico D, Moschiano F, Fraschini F, Bussone G. Melatonin versus placebo in the prophylaxis of cluster headache: a double-blind pilot study with parallel groups. Cephalalgia 1996;16:494–496. 8. van Vliet JA, Bahra A, Martin V, et al. Intranasal sumatriptan in cluster headache: randomized placebo-controlled double-blind study. Neurology 2003;60:630–633. CME
  3. I don't know a lot about methlypred, so I can only say that those dosages sound low, and I feel certain they're much too frequent. Here's what one expert says about dosage and use: "Corticosteroids in the form of prednisone 1 mg/Kg up to 60 mg for four days tapering the dose over three weeks is a well accepted short-term preventive approach. It often stops the cluster period, and should be used no more than once a year to avoid aseptic necrosis." https://clusterbusters.org/wp-content/uploads/2014/03/GoadsbyClusterTreatment.pd I don't know of a medical O2 tank that is 2000 liters, but that's a big one (M size, I guess), which is good. I've written a bunch about O2 use at this file (same as I linked before), so maybe you can take a look there and see whether you have further questions. https://clusterbusters.org/forums/topic/6213-basic-non-busting-information/ 10/15 lpm might be fine, or it might not be enough. Your mask might be fine (with some modifications), or you might want to try upgrading to the "Cluster O2 kit." Your breathing strategy might be fine, or you might want to try something different. All addressed in there. I'd also note (quoting from there): "Some people have observed that for some reason when the O2 level in their tank is “low,” the O2 doesn’t work as effectively for aborting, or might not work at all. “Low” in some cases can be as much as a third of a tank remaining. Something to be aware of." Batch has also posted data about how it can take a while at first for O2 use to become fully effective, so that might be a "normal" O2 issue you're having. Another tip for using O2 that might or might not be in there is to look down toward your feet as you use it. Don't ask me . . . but many people find that it helps. With a proper system and techniques, you ought to be getting aborts in less than 10 minutes. Also in that doc are some things people can do when they don't have O2. There are a bunch of them, with caffeine or energy drinks/shots the most common. Also, Benadryl, melatonin, "brain freeze," and some other possibilities. I just don't know what you want to do with the baby in there. I really don't know why the Maxalt and Cambia have those CH exceptions so prominently stated. One of these days I might look into that. You can also look things up using the search bar at the top right each page. Just a good thing to know about.
  4. My gosh, that's a whole lot of powerful stuff you're taking. You have a headache doctor who specializes in working with pregnant women, so I am very reluctant to overstate anything. And you don't say how often you are using the various abortives and possible preventives, so I can only tell you some things we might say to someone on those meds. 1. Most people with CH don't need 6mg of sumatriptan to stop an attack. 2mg is usually enough; I would say that for sure 3mg is enough 90-plus percent of the time. There are ways to get to 2 or 3mg. One is to take apart the 6mg injector. doses. https://clusterbusters.org/forums/topic/2446-extending-imitrex/ Others are to use the 3 or 4mg injector for migraine, whose name I always forget, or to get vials and syringes prescribed and measure your own. The less of this you take, the better off you are (more on this below). 2. Here's what the Mayo Clinic says about rizatriptan (Maxalt): "Rizatriptan is used to treat acute migraine headaches in adults and children 6 years of age and older. It is not used to prevent migraine headaches and is not used for cluster headaches." I think some people have had relief from CH with this drug, but it isn't first line. 3. Here's what a neutral website says about Cambia: "Cambia is used to treat a migraine headache attacks, with or without aura, in adults 18 years of age and older. It is not used to prevent migraine headaches. Do not use Cambia to treat a cluster headache." https://www.drugs.com/cambia.html I guess I'd at least want to ask the doc about this and the Maxalt. 4. Depending on how often you are using them, you seem to be taking a whole lot of triptans (including the pills), and (again, depending on how often you are using them) it wouldn't be surprising to me if you're having more and worse attacks from triptan overuse. 5. If you're having any kind of overuse condition -- plus: two cycles of steroids (methylpred) in how long? one a year is recommended -- that could help explain why the O2 isn't working. 6. It would be good to know more about your O2 setup. There are other possible explanations for it working/not working. What size and number tanks of O2 do you have? How high does your regulator go? Are you sure you have a non-rebreather mask? 7. You should very seriously consider Batch's vitamin d3 regimen, which has helped hundreds. With regard to helping people with the regimen, his generosity is exceptional. I'm sure he will have considered its application with women who are pregnant. https://vitamindwiki.com/Cluster+headaches+substantially+reduced+by+10%2C000+IU+of+Vitamin+D+in+80+percent+of+people 8. I'd suggest you might look over this file. https://clusterbusters.org/forums/topic/6213-basic-non-busting-information/ 9. For all practical purposes, I don't see a real preventive in your list of meds. (Typically, that would be something like verapamil.) Your doctor might see some of what you are taking as preventives, and there might be reasons not to prescribe other ones. The d3 regimen is a very effective preventive, but it takes time to reach full effectiveness.
  5. If you put the word reishi into the search bar at the top right of any page, I believe you'll find some experiences, including a woman who said she had found relief from her CH with reishi mushrooms. I don't know what there is about lion's mane, but I remember a guy who kept trying new things and would often have success followed by disappointment. I think he took lion's mane during one of those experimental periods.
  6. We're sorry that you have to be here, but glad that you are here!
  7. Batch is the fellow you're thinking of. It's a shortened version of his last name. So glad you've found good docs and are getting good relief. (Technically, you aren't chronic until you have attacks for a year with only a short period without attacks during that time.) You might find some useful ideas in this file: https://clusterbusters.org/forums/topic/6213-basic-non-busting-information/
  8. This file will give you an overview of how CH is treated. It includes a brief description of the busting protocol (the same description of busting that is under the blue banner on each page, "New Users ..."). https://clusterbusters.org/forums/topic/6213-basic-non-busting-information/ As Vipul says, oxygen and the D3 regimen are things you should be doing. There are other things described in that file that might also help you (Benadryl, caffeine, higher doses of melatonin, "brain freeze"). Most of us here are not persuaded that microdosing is an effective way to treat CH -- you probably have to get to some threshold dose for it to be effective. I don't think that the Mirtazipine is likely to have brought on your attacks, but others might have a more informed opinion about that. Some antidepressants will block the effects of busting, but I don't know about Mirtazipine. It might not seem much like a happy birthday, but I can say that finding this site with its generous and helpful people is a happy thing for you in the longer run.
  9. I think it would be good for you to read this file. Some things you can do right now (start D3 regimen, for sure); others might need prescription. You might have to fight with a doctor for oxygen, even though it is the #1 recommended abortive. Be ready. https://clusterbusters.org/forums/topic/6213-basic-non-busting-information/
  10. Splitting injections: https://clusterbusters.org/forums/topic/2446-extending-imitrex/ Or, ask for a prescription for vials and syringes so you can measure out your own dose. There's a lot of caffeine in energy shots (the smaller things like 5-Hour Energy). Not as much in the standard bigger drinks (RedBull). You would probably do fine just brewing some coffee and keeping it in the fridge.
  11. FWIW, I know of a person with CH who has resolved all major attacks through busting, but, like you, has mild to intense shadow pain every day. No question that what he has is CH, not migraine.
  12. Batch is the man for D. He is emphatic about his preference: >>The most significant change occurred in July of 2018 with the switch from the oil-based liquid softgel vitamin D3 formulations to the Bio-Tech D3-50 50,000 IU water soluble vitamin D3. Several of us found it faster acting with a higher bioequivalence in elevating serum 25(OH)D3 than the same dose of the oil-based liquid softgel vitamin D3 formulations. << More here: https://clusterbusters.org/forums/topic/6807-new-to-this-forum-–-cast-iron-until-hit-by-ch/?tab=comments#comment-67520
  13. This recommended doctor list is old, and there's nothing specifically listed for Dayton, but you could check in the Ohio section: https://clusterbusters.org/wp-content/uploads/2014/10/OUCH-DOCS-US-07-22-14-NC-OR.pdf I know THE Ohio State University has a headache clinic.
  14. I guess we kind of knew this, but it's still sad to me to see it confirmed. https://www.docguide.com/phase-3-randomized-placebo-controlled-study-galcanezumab-patients-chronic-cluster-headache-results-3?tsid=5 Phase 3 randomized, placebo-controlled study of galcanezumab in patients with chronic cluster headache: Results from 3-month double-blind treatment; Dodick D, Goadsby P, Lucas C, Jensen R, Bardos J, Martinez J, Zhou C, Aurora S, Yang J, Conley R, Oakes T; Cephalalgia 333102420905321 (Feb 2020) OBJECTIVE To report efficacy and safety of galcanezumab in adults with chronic cluster headache. BACKGROUND Galcanezumab is a humanized monoclonal antibody that binds to calcitonin gene-related peptide and inhibits its biological activity. METHODS This study comprised a prospective baseline period, a 12-week double-blind, placebo-controlled treatment period, and a 52-week open-label period. Up to six protocol-specified concomitant preventive medications were allowed if patients were on a stable dose for 2 months prior to the prospective baseline period. Patients were randomized 1:1 to monthly subcutaneous galcanezumab (300 mg) or placebo. The primary endpoint was overall mean change from baseline in weekly attack frequency with galcanezumab compared to placebo. Key secondary endpoints were ≥50% response rate and percentage of patients meeting sustained response. Results from the double-blind treatment period are reported. RESULTS A total of 237 patients were randomized and treated (120 placebo; 117 galcanezumab). At baseline, the mean age was 45 years and 63% were using ≥1 preventive drug. The primary endpoint was not met; mean change in weekly attack frequency was -4.6 placebo versus -5.4 galcanezumab ( p  = 0.334). Key secondary endpoints also were not met. Injection site-related treatment-emergent adverse events were more common in the galcanezumab than the placebo group, with significantly more injection site erythema. CONCLUSION Treatment with galcanezumab 300 mg did not achieve its primary and key secondary endpoints. This study underscores the potential distinct biology of cCH as well as the significant unmet need for safe, effective, and well-tolerated preventive treatment. The safety profile of galcanezumab in cCH is consistent with that observed in trials of episodic CH and migraine.
  15. Lenny, were you able to buy this reg straight from the company, with no prescription or other authorization?
  16. Good for you for making it happen, Luis!! At 15 lpm, the E tank has about 45 minutes worth of O2. Closer to 35 minutes, realistically. So now might be a good time to try to get a bigger tank, or more E tanks.
  17. Luis, You might want to look over the discussion of oxygen here: https://clusterbusters.org/forums/topic/6213-basic-non-busting-information/ The guy in this youtube video does a good demonstration of a standard breathing strategy, starting at 3:18. http:// https://www.youtube.com/watch?v=PtFHRIQN17s&t=127s Your mask will not look like his (he is using the one that is made particularly for people with CH), but yours should have a bag on it that fills as you are breathing out and empties as you breathe in. Many people with CH find that it helps them stop the attack faster if they quickly drink some caffeine or an "energy shot" such as 5-Hour Energy as they are starting on the O2.
  18. I have a question. It says here, "The diagnostic criteria of episodic and chronic cluster headache (cCH) were recently modified." Does anyone know what the modification was? https://www.docguide.com/episodic-and-chronic-cluster-headache-differences-family-history-traumatic-head-injury-and-chronoris?tsid=5 Episodic and Chronic Cluster Headache: Differences in Family History, Traumatic Head Injury, and Chronorisk; Barloese M, Beske R, Petersen A, Haddock B, Lund N, Jensen R; Headache (Dec 2019) OBJECTIVE AND BACKGROUND The diagnostic criteria of episodic and chronic cluster headache (cCH) were recently modified, yet pathophysiological differences between the two are still unclear. The aim of this cross-sectional study is to identify and characterize other differences between episodic and cCH. METHODS Data from a retrospective, questionnaire- and interview-based study were analyzed with a focus on associated factors including traumatic head injury (THI), familial history, and change of phenotype. Attack patterns were analyzed using Gaussian and spectral modeling. RESULTS 400 patients and 200 controls participated. A positive family history was more prevalent in chronic than episodic cluster headache (eCH) (34/146 (23%) vs 33/253 (13%), respectively, P = .008). A history of THI was more common in patients than controls (173/400 (43%) vs 51/200 (26%), respectively, P < .0001) and in chronic compared to eCH (77/146 (53%) vs 96/253 (37%), respectively, P = .004). Patients with a positive family history had a unique diurnal attack pattern with twice the risk of nocturnal attacks as patients who did not report family history. Patients reporting phenotype change had a chronobiological fingerprint similar to the phenotype they had experienced a transition into. A higher attack frequency in chronic patients was the only difference in symptom manifestation across all analyzed subgroups of patients. CONCLUSIONS cCH is associated with a positive family history and THI. In familial CH, a peak in nocturnal chronorisk may implicate genes involved in diurnal-, sleep- and homeostatic regulation. The stereoty
  19. This study is further evidence for a theory that has been developing for a while. It is that in people with CH the brain's pain perception mechanisms, which are associated with the hypothalamus, are messed up ("abnormal functioning of the pain control circuitry"). https://www.docguide.com/altered-hypothalamic-region-covariance-migraine-and-cluster-headache-structural-mri-study?tsid=5 Altered Hypothalamic Region Covariance in Migraine and Cluster Headache: A Structural MRI Study; Chong C, Aguilar M, Schwedt T; Headache (Jan 2020) OBJECTIVES The hypothalamus plays a key role in both migraine and cluster headache (CH). As brain region-to-region structural correlations are believed to reflect structural and functional brain connectivity patterns, we assessed the structural covariance patterns between the volume of the hypothalamic region and vertex-by-vertex measurements of cortical thickness in patients with migraine and in those with CH relative to healthy controls (HC). METHODS T1-weighted images were acquired on a 3T MRI scanner for a total of 59 subjects including 18 patients with CH (age: mean = 43.8, SD = 12.4), 19 with migraine (age: mean = 40.1, SD = 12.2), and 22 HCs (age: mean = 39.1, SD = 8.2). Imaging was collected between attacks (migraineurs) and during out-of-bout phases (CH). Data were post-processed using FreeSurfer version 6.0 and within-group correlations between hypothalamic region volume with cortical thickness were explored using a whole-brain vertex-wise linear model approach. Between-group differences in correlation slopes between hypothalamic region volume and vertex-by-vertex measurements of cortical thickness were interrogated using post-hoc comparisons. RESULTS There were no significant between-group differences (migraine vs CH; migraine vs HC; or CH vs HC) for age, sex, total brain volume or volume of the left or right hypothalamic region. For each group, there were significant positive correlations (P < .01) between right and left hypothalamic region volumes with cortical thickness measurements. HC had significant positive correlations between hypothalamic region volume and cortical thickness over large portions of the superior and rostral medial frontal, orbitofrontal cortex and rostral anterior cingulate, and smaller clusters in the superior and middle temporal, posterior cingulate, fusiform, and precentral cortex. Post-hoc analysis showed significant differences in covariance patterns in those with migraine and CH relative to HC, with both migraine patients and CH having weaker structural covariance of hypothalamic region volume with frontal and temporal cortical thickness. CONCLUSION Recent evidence suggests hypothalamic region connectivity to frontal and temporal areas to be relevant for regulating pain perception. Thus, the diminished structural covariance in migraineurs and CH might suggest abnormal functioning of the pain control circuitry and contribute to mechanisms underlying central sensitization and chronification of pain.
  20. I think 200mcg = 8,000IU. Great results! You are strongly urged to take all the cofactors listed in the full D3 regimen, though, or you could start to have some issues from too much D.
  21. Cluster S, I would suggest that you and your husband take a look at this document so you have a full sense of all of his options: https://clusterbusters.org/forums/topic/6213-basic-non-busting-information/
  22. Maybe for some people caffeine is a trigger. For most people it's an effective abortive. Those pills might or might not be helping you, Talia, but the caffeine in them is probably trying to help.
  23. Prednisone, Emgality, and D3 to prevent, and a triptan to abort. As long as there aren't any adverse interactions among those things, and since you acknowledge that you won't learn much about what's helping and what isn't, and as long as you know that if you have a future cycle O2 is fundamental, I don't see any holes. If your triptan injector is 6mg, you will want to think about splitting your doses, since most people can abort an attack with 2mg or 3 at most. Maybe you have a 3 or 4mg injector. If not, here's info on splitting: https://clusterbusters.org/forums/topic/2446-extending-imitrex/ Since your docs seem to be enlightened, you might see whether they'll prescribe it in vials so you can measure out your own doses.
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