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Joyisnow77

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Posts posted by Joyisnow77

  1. I overheard at a conference that the inventor tried to find a use of its invention for quite a while before zooming in on CH and read that it is working on some of us but is pretty much a hit or miss. IMO there is so many things that could help the vagal nerve before trying the « zapper ».

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  2. Support from friends and family, enjoying the moment whenever i can (trying blocking anxio/depression), watching comedy shows and movies, walks in nature, self-compassion, music, grattitude that i’m more knowledgeable now than ever about the condition and some kind of hope that one day a cure will come our way. 

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  3. It is hard for me to explain but usually I feel two short and quick hits on the right side of my brain (my ch side) with a weird feeling of distanciation like i've been knocked off. It last about 15 seconds but I know that it is there. One or two days later it is there in full mode... so I have one day to bust it!  

  4. Alterations of structural connectivity in episodic cluster headache: A graph theoretical analysis ( https://www.sciencedirect.com/science/article/pii/S0967586818315170 ). Study seems pretty legit.. 

    Conclusion: "We demonstrate that the structural volumes - look at the article - and connectivity in patients with cluster headache are significantly different from those in healthy controls, especially revealing hub re-organization. These alterations are implicated in the pathogenesis of cluster headache and suggest that cluster headache is a network disease."

    I am no neurologist, but is this a first time that structural brain volumetry points to pathogenesis? If so, are those structures affected are "damaged" by any substance or behaviour? Ex: lack of sleep, nicotine, alcohol, etc? Is this why as well that triptamines are helping by "reconnecting" the brain? 

     

  5. The new theory still needs to be tested ... but implies that cigarettes might create CH and happens when testosterone is low... (my understanding). 

     

    The hypothesis theory will include several principles: (1) the need of double lifetime tobacco exposure, (2) that cadmium is possibly the primary agent in cigarette smoke that leads to hypothalamic‐pituitary‐gonadal axis toxicity promoting cluster headache, (3) that the estrogenization of the brain and its specific sexually dimorphic nuclei is necessary to develop cluster headache with tobacco exposure, and (4) that the chronic effects of smoking and its toxic metabolites including cadmium and nicotine on the cortex are contributing to the morphometric and orexin alterations that have been previously attributed to the primary headache disorder itself.

    Linking Cigarette Smoking/Tobacco Exposure and Cluster Headache: A Pathogenesis Theory (https://onlinelibrary.wiley.com/doi/abs/10.1111/head.13338)

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  6. Vitamin D deficiency in patients with cluster headache: a preliminary study (https://thejournalofheadacheandpain.biomedcentral.com/articles/10.1186/s10194-018-0886-7

    Results: There was no significant difference among the patients with cluster headache, migraineurs, and controls. (...)  In the 14 patients with seasonal periodicity, patients with periodicity of winter to spring had a trend of lower serum 25(OH)D concentrations than those with periodicity of summer to autumn. 


    Any episodics Winter and Summer on vit D feels improvement while on the regimen? I feel that vitamine D effects testosterone level so any increase could help?... Thoughts? 

  7. Swedish population study founds that onset on episodic for smokers and drinkers were less intense and early; http://journals.sagepub.com/doi/abs/10.1177/0333102417731773

     

    Conclusion;

    A majority (66.7%) of the patients reported that attacks appear at certain time intervals. In addition, cluster headache patients who were current tobacco users or had a history of tobacco consumption had a later age of disease onset (31.7 years) compared to non-tobacco users (28.5 years). The Cluster Headache Severity Scale score was higher in the patient group reporting sporadic or no alcohol intake than in the groups reporting an alcohol consumption of three to four standard units per week or more. Maximum severity cluster headache patients were characterised by higher age at disease onset, greater use of prophylactic medication, reduced hours of sleep, and lower alcohol consumption compared to the non-cluster headache maximum severity group.

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