Headache最新文献

Background: Despite optimized therapy, up to 30% of patients with trigeminal neuralgia (TN) experience treatment failure. To date, there is limited and low-quality data available on rescue strategies for this subset of patients. This study describes clinical outcomes associated with intravenous (IV) magnesium sulfate and methocarbamol, with or without adjunctive antiseizure medications (ASMs), in the management of acute, refractory TN pain crises.

Methods: This was a single-center, retrospective cohort study conducted at the Cleveland Clinic Headache and Facial Pain Section from January 2015 to 2024. We analyzed adults (≥18 years) with treatment-refractory TN who received a standardized 3-day infusion regimen of magnesium sulfate and methocarbamol, with or without IV ASMs (levetiracetam, lacosamide, or valproic acid). Each encounter represented a distinct TN pain crisis treated with 3 consecutive days of infusion therapy. Infusions were administered specifically during acute exacerbations of pain that occurred despite ongoing or previously attempted maintenance treatment. Pain intensity was assessed using the 11-point numerical rating scale before and after each infusion day. The primary outcome was the proportion of encounters achieving a ≥50% reduction in NRS score from day 1 preinfusion to day 3 postinfusion.

Results: A total of 170 patients were included. The patient encounters analyzed in this study had an overall mean age of 57.0 years and consisted mostly of females (n = 130, 76.5%). A ≥50% reduction in pain score was achieved in 86.9% of encounters. The largest reduction occurred on day 1, with diminishing but continued improvements on days 2 and 3. Adjunctive IV ASMs were not associated with improved response compared to the magnesium and methocarbamol alone (72.4% vs. 75.8%, respectively; p = 0.740). Pain Disability Index scores also improved among patients with follow-up data.

Conclusion: A 3-day IV infusion protocol combining magnesium sulfate and methocarbamol, with or without adjunctive ASMs, was associated with rapid, meaningful pain relief in most patients with acute TN pain crises. Larger, prospective studies are warranted to further investigate and confirm the effectiveness of this IV treatment strategy for managing this challenging neurological condition.

Objective: This study evaluated cranial magnetic resonance imaging (MRI) signs in patients with post-dural puncture headache (PDPH) using an established assessment score developed for spontaneous intracranial hypotension (Bern score). We hypothesize that patients with chronic PDPH do not have typical imaging features of intracranial hypotension.

Background: PDPH is a well-known complication following an intentional or unintentional lumbar dural puncture with positional headache, neck stiffness, and hearing disturbances usually resolving within 14 days. However, the chronic course of PDPH is poorly represented in the third version of the International Classification of Headache Disorders (ICHD-3). Moreover, data on the role of cranial MRI in this cohort are lacking, but could facilitate care and management of chronic PDPH.

Methods: In this post hoc retrospective case series based on a chart review, we identified 86 consecutive patients from a tertiary medical care center in Freiburg, Germany between 01/2018 and 10/2024 with chronic PDPH, defined as persisting symptoms for >14 days post puncture and/or persisting after one or more epidural blood patches (EBP). Inclusion criteria were history of lumbar puncture (LP) or unintended dural puncture (UDP) and contrast enhanced cranial MRI for assessment of Bern score in all patients. Presence of epidural lumbar fluid was evaluated using heavily T2-weighted MRI or computed tomography (CT) myelography, whenever available (83/86 patients). Data were reviewed independently and blinded by two radiologists.

Results: Eighty-six patients with chronic PDPH (66 females; mean age of 38.8 ± 11.2 SD years) were included with LP as primary cause in 72% (n=62) and UDP while peridural (synonymous epidural) anesthesia (PDA) in 28% (n = 24). Median symptom duration was 220.0 (interquartile range [IQR] 94.0-474.0) days. Overall median Bern score was 2.0 (IQR 1.0-3.0) with no significant differences between LP versus PDA (p = 0.379). Local epidural fluid was present in 9/83 (11%) cases with adequate imaging and accompanied by higher median Bern scores (5.0 vs. 2.0; p = 0.026). Prior EBP was linked to lower median Bern scores (1.0 vs. 3.5; p < 0.001).

Conclusion: Patients with chronic PDPH predominantly present a low Bern score and rarely exhibit spinal epidural fluid. If present, spinal epidural fluid is accompanied by higher Bern score. Our findings highlight the unreliability of current MRI diagnostics to detect patients with chronic PDPH, which must not lead to a mitigation of the diagnosis or a refusal of treatment. Further research on MRI markers is needed here.

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.

Objective: The aim of this study was to synthesize a unifying disease model for idiopathic intracranial hypertension (IIH) based on the current literature.

Background: IIH is a complex neurological condition defined by abnormally elevated intracranial pressure in the absence of an identifiable etiology. Although various causal mechanisms are thought to contribute to the development of IIH pathophysiology, how they interrelate remains poorly understood.

Methods: Here, we synthesize emerging evidence indicating that cerebrospinal fluid (CSF) and interstitial fluid (ISF) dyshomeostasis drive IIH pathology and how alterations in neurofluid regulation are associated with transverse sinus stenosis, brain volume, and the cerebral glymphatic system.

Results: We propose a unified disease model where obesity-mediated metabolic dysfunction results in impaired glymphatic clearance with consequential accumulation of brain ISF with resultant increased brain volume. This subsequently results in extramural compression of the dural venous sinuses. Dural venous stenosis causes venous hypertension with further veno-glymphatic congestion and a positive feedback loop on impaired glymphatic drainage, which further perpetuates interstitial fluid stasis and increased brain volume with increased intracranial pressure.

Conclusions: The presented unifying disease model integrates various observations and suspected drivers of the condition into a cohesive framework of IIH pathogenesis that may be used for future investigations and clinical conceptualization.