Cluster Headache Clinical Phenotypes: Tobacco Nonexposed (Never Smoker and No Parental Secondary Smoke Exposure as a Child) versus Tobacco‐Exposed: Results from the United States Cluster Headache Survey

Rozen, Todd D.

doi:10.1111/head.13295

Cited by 40 publications

(72 citation statements)

References 35 publications

(97 reference statements)

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“…The clinical CH phenotype in tobacco smokers appears to be more severe, based on attack frequency, cycle duration, and headache‐related disability. Tobacco exposure is associated with a chronic state of CH . Some patients have smoked to manage pain attacks (eg, to distract from the pain) while others decreased their consumption to avoid exacerbation .…”

Section: Discussionmentioning

confidence: 74%

Cluster Headache in Subjects With Substance Use Disorder: A Case Series and a Review of the Literature

et al. 2019

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Objective To describe a case series of 7 patients presenting cluster headache (CH) criteria and a substance use disorder, reported to a French Addictovigilance center. Then, to assess clinical, pharmacological, and neurobiological linkages between substance use and CH onset. Background CH patients are presenting a higher prevalence of comorbidities, among which the use of psychoactive substances, licit or illicit, have been explored by a few authors. Recently, 3 cases of CH in patients seen in the hospital‐based addiction care center have been reported to the Toulouse addictovigilance center. Methods Other cases have been identified in the same tertiary hospital after a collaborative investigation done with the departments of neurology and psychiatry and included in the case series. A narrative review was performed to assess the potential of psychoactive substance consumption to induce or facilitate CH. Results From 2016 to 2018, 6 males and 1 female aged between 26 and 54 years old, presenting CH criteria and a substance use disorder, were included in our case series. Among substances used, there are: (1) daily use of tobacco and alcohol in 5/7 subjects; (2) daily or almost daily use of cocaine in 5/7 subjects; (3) regular use of cannabis before attacks beginning in 4/7 subjects; and (4) opioids, as a substitutive medication or abused, in 5/7 subjects. The intranasal route administration is reported by all the subjects and precedes the beginning of attacks for 5/7 subjects. Conclusions We have found a CH prevalence of 0.9% in our studied population, while it is estimated at 0.1% in the general population. The coexistence of cluster headache and addiction behaviors reflects possible common neurobiological pathways, which would include the hypothalamus. Research could be conducted on the potential of hypothalamic therapeutic targets.

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Section: Discussionmentioning

confidence: 74%

Cluster Headache in Subjects With Substance Use Disorder: A Case Series and a Review of the Literature

et al. 2019

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“…81,82 When acrolein is applied to the nasal mucosa in rats it will enhance meningeal blood flow via TRPA1 channel activation and the release of CGRP. 17 Thus, males predominated in the tobacco exposed subgroup whiles females predominated in the tobacco nonexposed subgroup and as the presentation of the subgroups differed clinically their underlying pathology may also be disparate. This may neuroanatomically link the central hypothalamic pathway alterations from cigarette toxin exposure with the more peripheral trigeminalautonomic complex pathway alterations that would be required for a tobacco/CH pathogenesis theory.…”

Section: Cadmium Hypothesis In Summarymentioning

confidence: 99%

“…There are multiple studies suggesting a relationship between cigarette smoking and CH. 17 The tobacco exposed subgroup had a later age of onset of CH and a fixed diurnal and seasonal cycle pattern, suggesting a syndrome resulting from the delayed effects of toxin exposure over time that resulted in damage to the hypothalamus/ suprachiasmatic nucleus, the presumed generator or modulator of CH. That, in those CH patients who never smoked, the majority were exposed to cigarette smoke as a child via secondary smoke exposure by one or both parents suggests an almost requirement for tobacco exposure to develop CH in most sufferers.…”

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confidence: 98%

“…1). 17 In addition, 85% of the smokers had a double (and possibly triple) exposure history with secondary smoke exposure as a child from one or both parents who smoked. In the United States as of 2016, around 15% of the population were current smokers (males 17%, females 13%) while cluster headache prevalence is only about 0.1% world-wide.…”

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confidence: 99%

“…-Cigarette smoking is not rare, thus why do more smokers not develop CH? It is important to note that from the United States Cluster Headache survey data the tobacco exposed subtype were significantly more likely to have a history of head trauma, excessive caffeine use, and have a history of alcohol abuse versus the tobacconon-exposed subtype, suggesting these additional risk factors are also possibly required for the development of CH along with double lifetime tobacco exposure 17 (Fig. 18 The author suggests that an individual smoking history is important to developing CH but secondary smoke exposure as a child is also a needed requirement to initiate this primary headache syndrome.…”

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confidence: 99%

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Linking Cigarette Smoking/Tobacco Exposure and Cluster Headache: A Pathogenesis Theory

Rozen

2018

Headache

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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.

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Family History of Cluster Headache

et al. 2020

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IMPORTANCE Genetic and environmental factors are thought to contribute to cluster headache, and cluster headache can affect multiple members of a family. A thorough understanding of its inheritance is critical to understanding the pathogenesis of this debilitating disease.OBJECTIVE To systematically review family history rates and inheritance patterns of cluster headache.EVIDENCE REVIEW A systematic review was performed in PubMed, Embase, and Cochrane Library. Search criteria were created by a librarian. Articles published between 1985 and 2016, after the publication date of a large review in 1985, were analyzed independently by 2 neurologists to identify family history rates and pedigrees. Pedigrees were analyzed by a genetic counselor. FINDINGS A total of 1995 studies were found (1988 through the search criteria and 7 through other means). Forty articles met inclusion criteria: 22 large cohort studies, 1 twin-based study, and 17 case reports or small case series. Across the 22 large cohort studies, the positive family history rate of cluster headache varied between 0% and 22%, with a median of 8.2%. The largest 5 studies, of 1134, 785, 693, 609, and 500 probands each, had a positive family history in 18.0% (numerator not provided), 5.1% (40 of 785 cases), 10.0% (numerator not provided), 2.0% (12 of 609 cases), and 11.2% (56 of 500 cases), respectively. No meta-analysis was performed, given differences in methodologies. Separately, 1 twin-based study examined 37 twin pairs and reported a concordance rate of 5.4% (2 pairs). Finally, 67 pedigrees were identified. Most pedigrees (46 of 67 [69%]) were consistent with an autosomal dominant pattern, but 19 of 67 (28%) were consistent with an autosomal recessive inheritance pattern; 10 pedigrees of probable or atypical cluster headache were identified, and all were consistent with an autosomal dominant inheritance pattern. The sex ratio for cluster headache in identified pedigrees was 1.39 (103:74) in affected men and boys compared with affected women and girls, which is lower than that of the general cluster headache population. CONCLUSIONS AND RELEVANCECluster headache is an inherited disorder in a subset of families and is associated with multiple hereditary patterns. There is an unexpectedly high preponderance of women and girls with familial cluster headache; genetic subanalyses limited to female participants are necessary to further explore this observation, because these data are otherwise masked by the higher numbers of male participants with cluster headache. Overall, this systematic review supports the notion that familial cluster headache is likely the result of multiple susceptibility genes as well as environmental factors.

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Cluster Headache Clinical Phenotypes: Tobacco Nonexposed (Never Smoker and No Parental Secondary Smoke Exposure as a Child) versus Tobacco‐Exposed: Results from the United States Cluster Headache Survey

Cited by 40 publications

References 35 publications

Cluster Headache in Subjects With Substance Use Disorder: A Case Series and a Review of the Literature

Cluster Headache in Subjects With Substance Use Disorder: A Case Series and a Review of the Literature

Linking Cigarette Smoking/Tobacco Exposure and Cluster Headache: A Pathogenesis Theory

Family History of Cluster Headache

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