Headache最新文献

Objective: We set out to examine detailed phenotypic data from our clinic for associations of vertigo in chronic migraine.

Background: Vertigo is a non-canonical, common symptom of migraine. Little is known about its associations with other symptoms within the migraine phenotype. There is significant methodological heterogeneity and therefore inadequate overall evidence about the potential differences in efficacy of any migraine treatments in patients with problematic vertigo associated with migraine, compared to those without vertigo. Enhancing understanding of migraine-related vertigo could help guide treatment and inform on mechanisms of vestibular migraine, a poorly understood diagnostic entity.

Methods: Chronic migraine extended phenotypes of patients seen within the adult headache service at King's College Hospital Tertiary Headache Service between January 2014 and December 2021 (n = 589) were extracted from the first documented clinic consultation letter retrospectively. For those with information about vertigo (n = 562), potential associations of interest for the presence of vertigo (gender, allodynia, aura, photophobia, phonophobia and osmophobia, baseline headache frequency, number of premonitory symptoms, presence of cranial autonomic symptoms, and age) were analyzed using a regression model (IBM SPSS v 29). Missing data were excluded (final n = 435).

Results: The total sample size for analysis in the regression model was n = 435, after excluding missing data (n = 126) and outliers (n = 1). Patients were 16-92 years old (median, 47; interquartile range, 37-55), and the majority (83.4%) were female. Vertigo associated with migraine was present in 275 of 562 (49%) patients. Within the regression model, the presence of aura (odds ratio, 2.13; 95% confidence interval, 1.4-3.23, P < 0.001) and allodynia (odds ratio, 2.74; 95% confidence interval, 1.76-4.26, P < 0.001) were positively associated with vertigo.

Conclusions: Vertigo in chronic migraine is common and may be associated with a more enriched phenotype independent of baseline headache frequency. Future treatment strategies should be evaluated for their effects on this often under-recognized yet disabling symptom.

Objective: The aim of this case series is to describe a clinical phenotype of midfacial pain and suggest its potential as a candidate for future iterations of headache and facial pain classifications.

Background: Patients with facial pain that is located in the middle part of the face often consult otorhinolaryngologic, neurologic, or pain specialists. In the past, a diagnosis of midfacial pain was suggested if other causes were excluded.

Methods: This case series is based on a retrospective analysis of patients consulted in two headache and facial pain centers. The patients were selected if the pain was located in the zygomatic, infraorbital, or nasal region, and rhinosinusitis and other primary or secondary facial pain syndromes were excluded during a comprehensive diagnostic process.

Results: Twelve patients in the 18-74 years age group (median, 40.5 years; interquartile range [IQR], 18.3; 4 of 12 [33%] patients were women), from two tertiary headache and facial pain centers in Warsaw and Hamburg were included in the case series based on consultations conducted between January 1, 2024, and December 31, 2024. Patients reported 20-30 (median, 30; IQR, 2.8; mean = 28.1; standard deviation, 3.2) monthly facial pain days of mostly moderate intensity (range from 1 to 9; median, 5; IQR, 2.125; mean = 5.2; SD, 1.9) on Numeric Rating Scale. Pain was described as dull, pressing, or tension-like and was bilateral in 10 of 12 (83%) patients. Seven of 12 (58%) patients described pain occurring simultaneously in regions innervated by the first (nasal region) and second branch (infraorbital) of the trigeminal nerve.

Conclusions: This study provides preliminary evidence for a distinct phenotype of idiopathic midfacial pain that is not caused by rhinosinusitis, stomatognathic disorders, or facial manifestations of primary headaches. Our data call for prospective studies on this type of idiopathic facial pain for future International Classification of Headache Disorders and International Classification of Orofacial Pain editions.

Objective: This study aimed to evaluate the choroid plexus volume in patients with spontaneous intracranial hypotension (SIH), including the lateral, third, and fourth ventricles, and explore its potential relationship with clinical characteristics.

Background: SIH is caused by cerebrospinal fluid (CSF) leaks. The choroid plexus is predominantly responsible for CSF production and has been implicated in altered CSF dynamics in various neurological conditions.

Methods: This retrospective case control study included 25 patients with SIH who were diagnosed between 2022 and 2024 from a single tertiary center. In addition, 25 age- and sex-matched healthy controls were included. Choroid plexus volumes were manually segmented from 3D contrast-enhanced magnetization-prepared rapid acquisition gradient echo MRI sequences using 3D Slicer. The total intracranial volume was also calculated. Clinical data, including the Bern score and Headache Impact Test-6 score, were collected from patients with SIH. Group differences in choroid plexus volumes were assessed using a generalized linear mixed model for the lateral ventricles and multivariable linear regression for the third and fourth ventricles, adjusting for age, sex, body mass index, and total intracranial volume. Associations with clinical variables were evaluated using univariable linear regression.

Results: After adjusting for covariates, the choroid plexus volume in the lateral ventricles was significantly higher in patients with SIH compared to that in healthy controls (unstandardized regression coefficient = 201.81 mm³, p = 0.016). However, no significant differences were observed in the choroid plexus volumes of the third (p = 0.617) and fourth ventricles (p = 0.314). Additionally, choroid plexus volume was not associated with disease duration (p = 0.292), Bern score (p = 0.580), and Headache Impact Test-6 score (p = 0.539) in patients with SIH.

Conclusion: The lateral ventricular choroid plexus is enlarged in patients with SIH, which may represent a compensatory response to CSF hypovolemia.

Background: Migraine and glaucoma represent substantial public health concerns. Previous epidemiological studies on their direct association have yielded inconsistent findings, though shared pathophysiological mechanisms are proposed. This large, population-based cohort study aimed to explore the migraine-glaucoma association, assessing glaucoma prevalence, clinical presentation, and disease severity markers in patients with migraine compared to nonmigraine controls.

Methods: This retrospective cohort study, conducted in southern Israel using data from Clalit Health Services and Soroka University Medical Center, used medical records from 2000 to 2023. Adult patients with migraine (identified by ICD-9 codes/triptan claims) were matched with nonmigraine controls. The primary outcome was ophthalmologist-diagnosed glaucoma (ICD-9 code, ≥1 intraocular pressure measurement). We evaluated the association between migraine and glaucoma risk using adjusted models and compared the time to glaucoma diagnosis between groups. In the glaucoma subcohort, we compared clinical outcomes, treatment patterns, and time to first surgical intervention between migraine and nonmigraine groups.

Results: The cohort included 83,758 individuals (30,733 migraine, 53,025 controls). Patients with migraine had lower glaucoma diagnosis-free survival (p < 0.001) and a 31% higher relative risk of glaucoma diagnosis (adjusted relative risk = 1.31; 95% confidence interval, 1.15-1.48; p < 0.001). In the glaucoma subcohort (n = 2306), patients with migraine had earlier and more frequent ophthalmic surveillance (p < 0.001). These patients also showed lower use of topical hypotensive medications (p = 0.058) and a lower hazard of glaucoma surgery (adjusted hazard ratio = 0.66; 95% confidence interval, 0.43-1.00; p = 0.047).

Conclusions: This population-based study provides evidence for an association between migraine and an increased risk of glaucoma. Although increased ophthalmologic surveillance among patients with migraine likely contributes to earlier diagnosis and detection of milder cases, shared biological mechanisms may also play a role. Furthermore, patients with migraine and glaucoma demonstrated lower medication use and fewer surgical interventions, potentially indicating a less severe disease course.

Objective: This study aimed to summarize and analyze the current literature related to calcitonin gene-related peptide (CGRP), the vestibular system, and vestibular migraine.

Background: CGRP is a neuropeptide that has been implicated in the pathophysiology of migraine. Vestibular migraine (VM) is a subtype of migraine that causes recurring episodes of vestibular symptoms like vertigo and is often associated with migrainous symptoms. Although the pathophysiology of VM is not completely understood, CGRP expression in the central and peripheral vestibular systems has suggested that it may also play a role in this closely related disease.

Methods: We performed a synthesis of current literature regarding the neuroanatomy of CGRP and the vestibular system and how CGRP stimulation and blockade affect vestibular function. Data was included from human and animal experiments indexed on PubMed.

Results: CGRP expression in rodents was found in the vestibular cerebellum, vestibular nuclei, and in lateral olivocochlear efferent neurons. αCGRP-null (-/-) mice have a decreased gain of the vestibular-ocular reflex as well as impaired balance testing. CGRP infusion in rodents causes phonophobia, motion sickness, and imbalance. In vasodilator-induced migraine models, CGRP expression was increased in central vestibular structures, with associated vestibular dysfunction and motion sensitivity. In humans, monoclonal antibodies targeting the CGRP pathway can reduce dizziness from vestibular migraine.

Conclusion: CGRP is expressed in the central and peripheral audiovestibular system and is implicated in the pathophysiology of VM. Preliminary results have shown promise for the treatment of VM with CGRP-targeted therapies although more high-level placebo-controlled data is needed especially for orally administered gepants. Further study is required to better understand how CGRP influences vestibular function and its role in vestibular migraine.

Background: The transient receptor potential melastatin 3 (TRPM3) ion channel has been implicated in sensory modulation and pain transmission and may contribute to migraine pathophysiology through calcitonin gene-related peptide (CGRP) release in the trigeminovascular system. This study aimed to investigate TRPM3 activation and its role in CGRP release, vasodilatory responses, and migraine-relevant behaviors using preclinical models.

Methods: Male and female Sprague-Dawley rats were used to evaluate CGRP release from trigeminal ganglia (TG) and dura mater following stimulation with the TRPM3 agonist CIM0216. CGRP levels were quantified using ELISA. Myograph studies assessed vasodilation in the middle cerebral artery (MCA) and middle meningeal artery. Immunohistochemistry was used to examine TRPM3 and CGRP localization in TG, dura mater, MCA, and human dura mater. Potential behavioral responses to subcutaneous CIM0216 administration were assessed via mechanical sensitivity tests. Calcium responses to CIM0216 were investigated on CGRP neurons in the TG of transgenic female mice.

Results: TRPM3 channel activation with CIM0216 triggered CGRP release from TG at 100 μM, with indications of enhanced release in female tissues. Immunohistochemistry confirmed colocalization of the TRPM3 channel and CGRP in TG neurons. Additionally, TRPM3 expression was detected in arterial structures, indicating potential involvement in vascular regulation. Although CIM0216 induced CGRP release ex vivo, subcutaneous CIM0216 administration was unable to induce allodynia-like symptoms in rats. Application of CIM0216 induced an increase of cytosolic calcium in trigeminal CGRP neurons.

Conclusions: TRPM3 activation triggers CGRP release and vasodilatation. The findings that TRPM3 induced CGRP release support further investigation of TRPM3 as a therapeutic target for migraine.

Methods: We conducted a systematic review and meta-analysis following Preferred Reporting Items for Systematic Reviews and Meta-Analyses guidelines, retrieving data from PubMed, Elsevier, Web of Science, and Cochrane Central Register of Controlled Trials . Primary outcomes included changes from baseline in acute headache medication days and monthly migraine days (MMD). Secondary outcomes comprised the incidence of adverse events (AEs), common AEs, and the proportion of patients achieving a ≥ 50% reduction in MMDs.

Results: Five randomized controlled trials including 875 patients (mean age of 42.7 years) were analyzed. Erenumab treatment was associated with significant reductions in acute headache medication days (mean difference = -1.72; 95% confidence interval [CI]: -2.81 to -0.62; p = 0.002) and MMDs (mean difference = -1.88; 95% CI: -2.68 to -1.07; p < 0.001). Whereas erenumab increased the risk of common AEs such as constipation (risk ratio [RR] = 1.43; 95% CI: 1.17 to 1.76; I² = 14%), the overall incidence of AEs was not significantly different compared to placebo (RR = 1.02; 95% CI: 0.92 to 1.14; I² = 57%). A higher proportion of patients achieved a ≥50% reduction in MMDs after 3 months in the erenumab group (RR = 1.49; 95% CI: 1.26 to 1.77; I² = 22%).

Conclusion: Erenumab appears effective in reducing migraine frequency and symptomatic medication use among patients with chronic migraine MOH, with an acceptable tolerability profile.