Headache最新文献

Objective: We assessed whether the effectiveness of monoclonal antibodies (mAbs) targeting the calcitonin gene-related peptide (CGRP) pathway changes according to the duration of chronic migraine (CM) over 12 months.

Background: In most patients, CM is a progressive disease starting with episodic migraine. Longer CM duration might be associated with more difficult treatment, probably because the mechanisms underlying chronicization are strengthened. Therefore, early treatment of CM could lead to better outcomes compared with later treatment.

Methods: This cohort study included individuals with CM treated with anti-CGRP mAbs in two tertiary headache centers from April 2019 to May 2023. The primary outcome included a change in monthly migraine days (MMDs) from baseline to the third trimester of treatment, 10-12 months. Secondary outcomes established whether response to anti-CGRP mAbs has a more rapid onset in individuals with shorter CM duration compared with longer duration; they included change in MMDs, monthly headache days (MHDs), and days and number of intakes of acute medication during each trimester compared to baseline. Additional outcomes included persisting MMDs, MHDs, and days and number of intakes of acute medication during each trimester of treatment. Patients were compared across tertiles of the overall CM duration.

Results: The study included 335 individuals with CM, with a median (interquartile range [IQR]) age of 48 (39-57) years; 270 (80.6%) were women. Patients in the highest tertile of CM duration (aged 18-60 years) were older than patients in the lower duration tertiles (0-7 years and 8-18 years, respectively), with a median (IQR) age of 56 (48-64) years compared with 42 (31-50) years, and 48 (39-56)years, respectively (p = 0.025); however, this difference was likely due to a correlation between age and disease duration. The change in MMDs from baseline to the last trimester of treatment (10-12 months) was comparable across tertiles of CM duration (median [IQR] -12 [-18 to -5] days, -12 [-17 to -6] days, and -12 [-18 to -4] days; p = 0.946). No difference emerged in secondary outcomes, suggesting a similar time to onset of anti-CGRP mAbs effect across all tertiles of CM duration.

Conclusions: Our data showed that anti-CGRP mAbs are effective and have a rapid onset of action in CM regardless of disease duration.

Objective: This study utilized the theoretical framework of the "fear avoidance model" (FAM) and investigated the role of fear of attack in pain-related disability. To this end, a measurement specific to cluster headache (CH) was used to investigate whether fear of attacks, alongside attack frequency, is a significant predictor of pain-related disability in CH.

Background: Cluster headache substantially impacts daily functioning, yet empirical research exploring specific contributing factors is limited.

Methods: A cross-sectional online survey was undertaken in patients with CH, gathering sociodemographic, clinical data, and responses on the Cluster Headache Scale and the Depression, Anxiety and Stress Scale.

Results: Analysis of data from 640 patients (chronic CH: 287/640 [44.8%]; female: 264/640 [41.3%]; male: 373/640 [58.3%]; gender diverse: three of 640 [0.5%]; age range: 18-86 years; mean [standard deviation] Cluster Headache Scales subscale disability score: 36.9 [9.8]; out of 869 respondents) revealed that both attack frequency and fear of attacks significantly predicted pain-related disability (p < 0.001, percentage of variance explained: R² = 0.24). More variance was explained by fear of attacks (R² = 0.22) than by attack frequency (R² = 0.02). This relationship remained significant even when controlling for depression and anxiety, which were also identified as independent predictors of pain-related disability (p < 0.001, R² = 0.44).

Conclusion: This study emphasizes the relevance of psychological factors in CH-related disability. Fear of attacks was found to be an independent predictor, while attack frequency was of minor relevance. Empirical investigation of the FAM in CH could improve the understanding of the mechanisms underlying disability and contribute to the development of CH-specific interventions.

Objective: To review the most common types of primary and secondary headaches that are associated with Sjogren's disease (SjD).

Background: Sjogren's disease is a chronic systemic autoimmune disease that typically presents with xerophthalmia, xerostomia, and arthralgias. Sensory and motor neuropathies are commonly reported neurological complications with SjD. Primary and secondary headaches are also frequent neurological complications associated with SjD, which may be under-recognized.

Methods: In this study, researchers conducted a literature review through the platforms of PubMed and Google Scholar with the keywords: (1) Sjogren's syndrome, (2) Sjogren's disease, (3) headache, (4) migraine, (5) tension-type headache, (6) aseptic meningitis, (7) cerebral venous sinus thrombosis, and (8) idiopathic intracranial hypertension. Included articles involved a study population of patients with both SjD and headache. There were no exclusion criteria. A total of 54 articles were identified, and 31 articles were utilized for study analysis.

Results: In patients with SjD, headaches were a frequently reported neurological complaint. The most common types of primary headaches associated with SjD were found to be migraine and tension-type headache. Patients with SjD were more likely to report severe, debilitating headaches compared to the general population. Furthermore, patients with SjD have been found to experience dangerous types of secondary headaches, including aseptic meningitis and cerebral venous sinus thrombosis.

Conclusions: Headaches are a common neurological complication in patients with SjD. Current literature suggests that there is an increased risk of both primary and secondary headaches in individuals with SjD compared to the general population and that headaches may occur throughout the clinical course of the disease. There are also reports of patients who experience the onset of primary and secondary headaches prior to the diagnosis of SjD. SjD has been linked to dangerous, life-threatening conditions that cause headaches, which require urgent recognition and treatment. Therefore, it is important to have a higher index of suspicion for patients who present with headaches and clinical symptoms of SjD, such as xerophthalmia and xerostomia. Utilizing a detailed history, physical examination, and neuroimaging can assist clinicians to recognize and diagnose types of headaches in patients with SjD to prevent dangerous complications.

Objective: To investigate the association of periodontitis and clinical periodontal parameters with migraine as well as mortality among people with migraine disease.

Background: Periodontitis has been shown to increase the systemic inflammatory burden thereby promoting various systemic health outcomes; however, the evidence regarding the relationship between periodontitis and migraine is scarce.

Methods: A cross-sectional study was performed, and it included 13,108 participants from the National Health and Nutrition Examination Survey (1999-2004). Weighted logistic regression analysis was used to evaluate the association between periodontitis/clinical periodontal parameters and migraine. Mediation analysis was performed to explore the potential mediating role of inflammatory response. A cohort study including 1909 participants with migraine disease was further conducted to assess the associations between periodontitis/clinical periodontal parameters and mortality from all causes, cardiovascular disease (CVD), and cancer in participants with migraine disease using Cox proportional hazards models. Death outcomes were ascertained by linkage to National Death Index records through December 31, 2018.

Results: Periodontitis was positively associated with migraine (odds ratio [OR] 1.29, 95% confidence interval [CI] 1.01-1.65). Each 1-unit rise in attachment loss and pocket depth was linked to a 17.5% (OR 1.18, 95% CI 1.08-1.29) and 28.1% (OR 1.28, 95% CI 1.08-1.51) increase in migraine risk, respectively. Mediation analyses revealed that leukocyte, monocyte, and lymphocyte counts mediated 17.9%, 7.3%, and 20.1%, respectively, of the association between periodontitis and migraine. During a median follow-up of 17.7 years among 1909 participants with migraine disease, periodontitis was associated with greater all-cause mortality (hazard ratio 1.82, 95% CI 1.25-2.66), but was not significantly associated with mortality from CVD or cancer among participants with migraine disease. Similar association patterns were also observed for attachment loss and pocket depth.

Conclusions: This study provides evidence that periodontitis and clinical periodontal parameters were significantly associated with migraine as well as all-cause mortality in people with migraine disease. These findings underscore the importance of considering periodontal health in the prevention and management strategies for migraine disease.

Objective: To evaluate the effectiveness of first switching between monoclonal antibodies (mAbs) targeting calcitonin gene-related peptide (CGRP) or its receptor in the treatment of migraine.

Background: Although mAbs targeting CGRP or its receptor have emerged as a leading treatment for migraine prevention, a proportion of patients do not respond. While switching between these antibodies is a common clinical practice in such cases, the effectiveness remains a subject of study.

Methods: We conducted a retrospective cohort study at a tertiary headache center, analyzing data from clinical records of patients treated with anti-CGRP mAbs from January 2020 to March 2024. Baseline was defined as the monthly headache days (MHDs) in the 3 months prior to the start of the second mAb. The primary endpoint was the change in MHDs at month 3 and month 6 following the switch. Additionally, we evaluated response rates in both periods. Subgroup analyses were conducted based on changes in mechanism of action. Finally, we assessed the influence of the number of doses of the first mAb and the inter-treatment interval.

Results: Out of 1244 initially identified patients, 185 were included in the month-3 analysis and 123 in the month-6 evaluation. The median MHDs decreased from 27.0 (interquartile range [IQR] 16.1, 30.0; range 5.0, 30.7) at baseline to 21.0 (IQR 10.0, 30.0; range 0.0, 30.0; p < 0.001) at month 3, and to 20.0 (IQR 10.0, 30.0; range 0.0, 31.0; p < 0.001) at month 6. Subgroup analyses revealed no significant differences in MHDs between maintaining the same target or changing it (baseline: 28.0 [IQR 16.2, 30.0; range 5.0, 31.0] vs. 27.0 [IQR 6.0, 31.0; range 6.0, 31.0]; month 3: 23.0 [IQR 10.0, 30.0; range 0.0, 31.0] vs. 19.0 [IQR 11.0, 30.0; range 1.0, 31.0], p = 0.144; month 6: 24.0 [IQR 11.0, 30.0; range 0.0, 31.0] vs. 17.0 [IQR 10.0, 30.0; range 3.0, 31.0], p = 0.170). There was no association between a ≥50% reduction in MHDs and the number of previous doses of the first mAb (odds ratio [OR] 1.0; 95% confidence interval [CI] 1.0, 1.1; p = 0.189) or the inter-treatment interval (OR 1.0; 95% CI 0.9, 1.1; p = 0.914).

Conclusion: Switching between anti-CGRP mAbs resulted in a reduction in MHDs, with no significant differences based on the mechanism of action. Factors such as the number of doses of the first mAb and the inter-treatment interval did not appear to predict a ≥50% reduction in MHDs at month 3. Our findings support the viability of switching as an effective treatment option for patients with migraine who do not respond to initial mAb therapy.

Objective: To evaluate factors associated with new-onset migraine (NOM) after transcatheter atrial septal defect (ASD) closure and predictors of unremitting NOM. The pathogenic role of migraine biomarkers such as calcitonin gene-related peptide (CGRP) and neuropeptide Y (NPY) were also assessed.

Background: New-onset migraine has been observed after transcatheter ASD closure. Neuropeptides like CGRP and NPY stored both in the brain and heart are implicated in migraine pathophysiology. The potential role of those migraine biomarkers in NOM, as well as the risk factors and long-term outcomes of NOM, remain largely unknown.

Methods: We enrolled patients without previous migraine who underwent successful transcatheter ASD closure between 2001 and 2013. The parameters of transthoracic echocardiography, and plasma CGRP and NPY levels measured by enzyme-linked immunosorbent assay, were collected prospectively before and after ASD closure, and compared between patients with NOM and those without. Predictors of NOM were assessed. Telephone interviews were performed in 2022 to assess migraine status. Clinical and procedural characteristics were compared between patients with unremitting migraine and those with transient migraine that remitted within 1 year.

Results: Of the 212 patients (median age, 21 years; 75.9% female), 43 (20.3%) had NOM. Potential predictors of NOM included a young age (adjusted odds ratio [aOR] 0.98, 95% confidence interval [CI] 0.96-0.99; p = 0.040), large ASD size (aOR 1.07, 95% CI 1.01-1.14; p = 0.022), and transient residual shunting after closure (aOR 2.78, 95% CI 1.05-7.36; p = 0.039). Post-closure plasma CGRP levels, but not NPY levels, were significantly higher than pre-closure levels (47.9 vs. 38.0 pg/mL, p = 0.023) among patients with NOM. Of the 27 patients with migraine who reported their migraine status at a median 14-year follow-up, 13 (48.1%) had unremitting migraine. Patients with unremitting migraine were more likely to have a smaller device-to-ASD size ratio (1.21 vs. 1.33, p = 0.039) and a larger pulmonary flow-to-systemic flow ratio (2.9 vs. 2.3, p = 0.012) than those with transient migraine.

Conclusions: Calcitonin gene-related peptide may play a pathogenic role in NOM after transcatheter ASD closure. A young age, large ASD size, and transient residual shunting potentially predict migraine occurrence after ASD closure. NOM not reaching remission for years may result from a significant shunt before closure.

Objective: The relationship between migraine and Parkinson's disease (PD) remains controversial. We aimed to investigate the causal and genetic associations between migraine and PD.

Methods: Genetic data for migraine [any migraine (AM), migraine without aura (MO), and migraine with aura (MA)] and PD were sourced from the latest genome-wide meta-analyses conducted by the International Headache Genetics Consortium and the International Parkinson's Disease Genomics Consortium, respectively. Various analyses were performed to evaluate the potential causal associations and explore genetic correlations between these conditions.

Results: The analyses indicated that AM (odds ratio [OR] 1.02, 95% confidence interval [CI] 0.91-1.14; p = 0.785), MO (OR 0.94, 95% CI 0.84-1.07; p = 0.358), and MA (OR 1.01, 95% CI 0.95-1.06; p = 0.846) were not significantly associated with the risk of PD. Similarly, reverse analyses also demonstrated no significant causality between PD and the risks of migraine or its subtypes. After adjusting for coronary heart disease, AM (OR 0.99, 95% CI 0.90-1.10; p = 0.897), MO (OR 0.94, 95% CI 0.86-1.03; p = 0.207), and MA (OR 1.00, 95% CI 0.93-1.07; p = 0.902) remained unrelated to PD risk. Likewise, PD was found to be unassociated with AM (OR 0.96, 95% CI 0.92-1.02; p = 0.168), MO (OR 0.95, 95% CI 0.86-1.05; p = 0.287), and MA (OR 1.02, 95% CI 0.93-1.13; p = 0.669). These null findings persisted even when adjusting for hypertension. Apart from above causal inference results, no significant genetic correlation was found between AM (r_g = -0.06, p = 0.127), MA (r_g = -0.05, p = 0.516), or MO (r_g = -0.06, p = 0.492) and PD, and no correlations were observed across specific genomic regions. Additionally, no shared heritability was observed between PD and migraine, or its subtypes, in tissue expression.

Conclusion: Our study suggests that there is no significant causal association or genetic correlation between migraine and PD from a genetic perspective.