Headache最新文献

A 38-year-old woman with temporomandibular joint dysfunction (TMJD) and chronic migraine presented with refractory TMJD-related pain. Conservative treatments and prior injections provided only short-term relief. To achieve longer lasting pain reduction, an ultrasound-guided V3 nerve block was performed, targeting the mandibular nerve with a 4-mL injection of 1% lidocaine. The patient experienced immediate pain relief and sustained improvement. Encouraged by results on the right side, she underwent the same procedure on the left, achieving identical relief. Despite unchanged migraine frequency, TMJD pain resolution significantly enhanced her quality of life, demonstrating the efficacy of ultrasound-guided V3 nerve blocks.

Background: Patients with obesity often experience stigma in healthcare, which may lead to underdiagnosis or undertreatment. In the context of pain management, and migraine specifically, patients with obesity are more likely to receive both opioid and non-opioid analgesics. However, little is known about their use of preventive treatments.

Methods: We conducted a large retrospective cohort study using propensity score matching for sex and age, utilizing data from the Clalit Health Services database in Israel. The study compared newly diagnosed patients with migraine with and without obesity, identified between June 2020 and June 2023. The comparison focused on prescriptions for migraine-specific acute medication (triptans) and preventive migraine treatments.

Results: Our final analysis included 11,934 patients with migraine and obesity and 11,934 without obesity. Patients with obesity were more likely to have cardiovascular risk factors and psychiatric comorbidities. Patients with obesity were also more likely to receive acute treatment with triptans (adjusted odds ratio [aOR] 1.17, 95% confidence interval [CI] [1.11-1.23]), and preventive treatments such as topiramate (aOR 1.66, 95% CI [1.38-1.99]), gabapentinoids (aOR 1.30, 95% CI [1.13-1.50]), and duloxetine (aOR 1.42, 95% CI [1.18-1.70]), adjusting for comorbidities.

Conclusion: Our findings do not support the notion that patient with migraine and obesity are undertreated; instead, they show a modest increase in prescriptions for acute and some of the preventive medications.

Cluster headache (CH) is a disabling primary headache disorder with limited therapeutic options. Calcitonin gene-related peptide (CGRP) is known to be involved in CH pathophysiology; however, except for galcanezumab (300 mg) in episodic CH, anti-CGRP monoclonal antibodies did not reduce CH attacks in randomized clinical trials. Atogepant is an oral, small-molecule, CGRP receptor antagonist, which is approved for the preventive treatment of migraine. Here, we describe four case reports of CH (two episodic CH and two chronic CH), unresponsive to previous prophylactic treatments, who responded to daily atogepant (60 mg). Chronic CH cases were refractory to subcutaneous galcanezumab. In one case, a reduction to atogepant (30 mg daily) resulted in recurrence of headache attacks, which subsided on reintroduction of the initial dose. No serious adverse effects were reported. Despite the limited number of cases and the open retrospective design, our case series suggests atogepant as a possible prophylactic treatment for CH. Further research on CGRP signaling in CH and the implementation of well-designed clinical trials are necessary.

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.

Objective: This article reviews the differences and similarities between persistent postural-perceptual dizziness (PPPD) and vestibular migraine.

Background: PPPD is considered a chronic functional vestibular disorder characterized by persistent dizziness, unsteadiness, nonspinning vertigo, and often exacerbated by upright posture, movement, or complex visual stimuli. Frequently misdiagnosed, PPPD shares overlapping features with vestibular migraine (VM), a common cause of episodic vertigo.

Methods: A literature search was conducted covering articles published from January 2000 to March 2025 with a special focus on recent publications that discuss both PPPD and VM.

Results: Although some propose that PPPD is a chronic form of VM, its historical classification as a functional disorder, distinct from the neurological basis of migraine, may suggest otherwise. This review explores PPPD's diagnostic criteria, pathophysiology, and the differential diagnosis of VM, emphasizing the importance of identifying migraine symptoms to guide treatment. Evidence supports migraine prevention and specifically flunarizine as a primary preventive treatment for VM, with emerging data on calcitonin gene-related peptide-targeted treatments showing promise. For PPPD, however, vestibular rehabilitation therapy is a cornerstone treatment.

Conclusion: A multidisciplinary approach addressing both conditions is critical for optimal patient outcomes. Studies on comorbid migraine treatment in patients with PPPD are warranted and may reveal distinct phenotypes within the same disease spectrum.

Background: Vestibular migraine (VM) is a common migraine subtype characterized by recurrent vestibular symptoms. Despite its prevalence, evidence-based treatment guidelines are lacking. Vestibular rehabilitation (VR) has been proven effective in many vestibular disorders, but its role in managing VM has not been well established. This systematic review aimed to summarize and pool the evidence on the effectiveness of VR for VM using standardized outcome measures, primarily focusing on patient-reported dizziness-related quality-of-life assessments.

Methods: We systematically searched MEDLINE, Embase, Cochrane Library, and Scopus from inception to March 2025 for studies evaluating self-reported and physical outcome measures of VR in patients with VM. Meta-analysis of mean change in Dizziness Handicap Inventory (DHI) scores was performed. Risk of bias was assessed using the Cochrane RoB 2 tool for the randomized controlled trials and the ROBINS-I tool for observational studies.

Results: Seven studies comprising 413 patients (mean age, 45.4; 76% female) with VM treated with VR were included. The effect of vestibular rehabilitation on DHI scores showed a pooled mean difference of -29.3 (95% confidence interval [CI], -40.2 to -18.3), more than the clinically important difference of 18 points. Although, our meta-analysis had high heterogeneity (Cochran's Q p value <0.001, I² = 94.7%).

Conclusion: VR demonstrated a reduction in DHI scores, meeting the clinically significant difference of 18 indicating clinical improvement. However, the considerable heterogeneity limits the generalizability of these results and highlights the need for further standardized randomized controlled trials with subgroup analyses to better determine the specific benefits and optimal protocols of VR in managing VM.