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Background: Headaches associated with physical exertion include headache precipitated by coughing or other Valsalva maneuvers, headache brought on by prolonged physical exercise, sexual headaches and cardiac cephalalgia. Objective: To review and update the clinical characteristics, etiologies, pathophysiology and management of these headaches related to exertion. Methods: In depth review of the publications, both in PubMed and in the main textbooks, of the different headaches induced by physical exercise. Results: Cough, exercise and sexual headaches can be primary or secondary; therefore, complementary studies are mandatory to rule out structural lesions. However, clinical characteristics, such as an old age and response to indomethacin for cough headache or being a young male and response to beta-blockers for exercise and sexual headaches, plus a normal examination are suggestive of a primary etiology. Etiology for secondary varieties, as posterior fossa lesions for cough headache or vascular malformations for exercise and sexual headaches, are also different. Finally, headache as a distant manifestation of myocardial ischemia, also known as "cardiac cephalalgia", appears at exertion in around two-thirds of cases and typically lasts less than 30 minutes and is relieved by nitroglycerine. Conclusions: Primary and secondary cough headache can usually be suspected based on clinical characteristics and separated from exercise and sexual headaches, which share many aspects. Cardiac cephalalgia is not necessarily an exertional headache and should be considered in adult patients with short lasting headaches and patent vascular risk factors. [ABSTRACT FROM AUTHOR]

Background: One of the advantages of CGRP monoclonal antibodies is their excellent safety and tolerability. However, postmarketing surveillance, is essential to detect potential rare emergent adverse events. Objectives: To report two patients who developed restless legs syndrome symptoms after treatment with CGRP antibodies. Methods and results: Two women with chronic refractory migraine, with no significant medical antecedents, developed typical restless legs syndrome symptoms 1.5 and 4 months after starting erenumab 140 mg, respectively. In case 1 symptoms resolved when erenumab was stopped for two months but reappeared on galcanezumab. In both patients migraine attacks had dramatically decreased and no iron deficiency was found. Conclusions: Even though caution is needed before establishing a causal relationship, these cases suggest that restless legs-like symptoms might be an emergent adverse event of CGRP antibodies, regardless of the mechanism of action. We propose that plastic changes in CGRP sensory fibers, which are very abundant in legs, induced by CGRP monoclonal antibodies could be the reason for restless legs syndrome development. [ABSTRACT FROM AUTHOR]

This letter, published in the journal Cephalalgia, is a response to a review paper on exertional headaches. The authors acknowledge that they did not mention lumbar puncture as a treatment option for primary cough headache in their update. They express skepticism about the value of this invasive procedure, citing the lack of certainty in diagnosing primary cough headache before the MRI era and the potential for low intracranial pressure to cause cough headache. They also discuss the relationship between primary sex headache and exertional headache, noting that some patients experience both types of headaches while others only have one or the other. The authors agree with the need for further data to better understand these headache types. [Extracted from the article]

Background and Objective: Unlike migraine and migraine with aura, little information exists regarding chronic migraine (CM) as a risk factor for cardiovascular disease. In this study we aim to determine whether an association between CM and endothelial dysfunction exists.Methods: Individuals 18 years and older diagnosed with episodic migraine (EM) and CM according to ICHD criteria were studied. After an overnight fast and abstinence from vasoactive drugs, ultrasound studies were performed and blood samples taken from patients and matched controls according to internationally agreed on protocols.Results: A total of 113 individuals were enrolled (35 CM, 37 EM, 41 controls). CM patients had a lower percentage of flow-mediated vasodilation (FMD; difference of means = 5.03%; p = 1.0E-6) and breath-holding index (BHI; difference of means 0.754; p = 2.0E-6), as well as increased carotid intima media thickness (cIMT; difference of means = 0.128 mm; p = 7.0E-5) than controls. The EM patients and controls comparison found similar, but less pronounced, differences: decreased BHI (p = 0.031), and increased cIMT (p = 0.028). Fibrinogen (r = 0.277; p = 0.006), C-reactive protein (r = 0.288; p = 0.003), and erythrocyte rate sedimentation (r = 0.298; p = 0.002) also correlated with cIMT, and inversely with BHImV and FMD.Conclusions: Migraine is associated with systemic and cerebral endothelial dysfunction demonstrated by ultrasound studies and biological markers. The degree of these changes was strongly associated with the severity of migraine. Our data indicate that migraine may be a cerebral disorder with systemic endothelial damage. [ABSTRACT FROM AUTHOR]

Introduction: Effectiveness of candesartan in migraine prevention is supported by two randomized controlled trials. We aimed to assess the effectiveness, tolerability, and response predictors of candesartan in the preventive treatment of migraine. Methods: Observational, multicenter, prospective cohort study. The 50%, 75% and 30% responder rates, between weeks 8–12 and 20–24, were compared with the baseline. Treatment emergent adverse effects were systematically evaluated. Response predictors were estimated by multivariate regression models. Results: Eighty-six patients were included, 79.1% females, aged 39.5 (inter-quartile range [IQR] 26.3–50.3), with chronic migraine (43.0%), medication overuse headache (55.8%) and a median of two (inter-quartile range: 0.75–3) prior preventive treatments. At baseline patients had 14 (10–24) headache and 8 (5–11) migraine days per month. The 30%, 50% and 75% responder rates were 40%, 34.9% and 15.1% between weeks 8–12, and 48.8%, 36%, and 18.6% between weeks 20–24. Adverse effects were reported by 30 (34.9%) and 13 (15.1%) patients between weeks 0–12 and 12–24, leading to discontinuation in 15 (17.4%) patients. Chronic migraine, depression, headache days per month, medication overuse headache, and daily headache at baseline predicted the response between weeks 20–24. Conclusion: Candesartan effectiveness and tolerability in migraine prevention was in line with the clinical trials' efficacy. Trial registration: The study protocol is registered in ClinicalTrials.gov (NCT04138316). [ABSTRACT FROM AUTHOR]

Background: Some studies have suggested an association between migraine and inflammatory bowel disease. We determined migraine prevalence in a cohort of patients with inflammatory bowel disease. Methods: Patients with inflammatory bowel disease aged 18–65 years were interviewed using an ad hoc headache questionnaire. Those who admitted a history of headache in the last year answered the three questions of the ID-Migraine questionnaire. Those who answered "yes" to the three of them were classified as "definite" and those who answered "yes" to two were classified as "probable" migraine. Results: We interviewed 283 patients with inflammatory bowel disease. Of these, 176 (62.2%) had headache. Fifty-nine (20.8%; 95% CI 16.3–26.0%) met migraine criteria either definite (n = 33; 11.7%; 95% CI 8.2–16.0%) or probable (n = 26; 9.2%; 95% CI 6.1–13.2). When divided by gender, 12 men (9.6%; 95% CI 5.1–16.2%) and 47 women (29.8%; 95% CI 22.8–37.5%) met migraine criteria. The prevalence of migraine was increased in inflammatory bowel disease patients from the current cohort (20.8%) versus that reported for our general population for the same age group (12.6%; p < 0.0001). These differences remained significant in female inflammatory bowel disease patients (29.8% versus 17.2% in our general population; p < 0.0001), but not in males (9.6% in inflammatory bowel disease vs 8.0%; p = 0.30). Seventeen patients with inflammatory bowel disease (6.0%; 95% CI 3.54–9.44%) fulfilled chronic migraine criteria. There were no differences in migraine prevalence by inflammatory bowel disease subtypes. Conclusion: Migraine prevalence, including chronic migraine, seems to be increased in patients with inflammatory bowel disease. The fact that this association was stronger for women suggests an influence of sex-related factors. [ABSTRACT FROM AUTHOR]