Basilar artery curvature is associated with migraine with aura in the Northern Manhattan Study

https://doi.org/10.1016/j.jns.2021.120073Get rights and content

Highlights

  • Migraine with aura is associated with increased basilar artery curvature.

  • Curvature determined by horizontal deviation of midpoint at three levels.

  • Strength of association was not affected by traditional vascular risk factors.

Abstract

Introduction

Genetic and imaging studies demonstrate a link between vascular morphology and migraine with aura (MA). We examined the relationship between basilar artery (BA) curvature and MA in a population-based cohort of stroke-free participants.

Methods

This cross-sectional study included participants from the MRI substudy of the Northern Manhattan Study. Participants had structured migraine assessments at enrollment and underwent brain MR angiography. BA curvature was defined as the sum of the total BA horizontal deviation from midline at the distal tip, mid-pons, and vertebrobasilar junction, and was the primary independent variable in logistic regression analyses. BA measurements were obtained blinded to migraine status. We compared groups of all migraine vs no migraine, migraine without aura (MwoA) vs no migraine, and MA vs no migraine.

Results

Of 880 participants, 146 had MwoA and 32 had MA. Average BA curvatures were 15.2 ± 8.9 mm in non-migraineurs, 15.8 ± 9.3 mm in MwoA, and 18.5 ± 11.4 mm in MA. In an adjusted model, greater BA curvature was associated with MA (OR 1.042 per mm, 95% CI 1.006–1.080) but not with MwoA (OR 1.014 per mm, 95% CI 0.993–1.035), when compared to non-migraineurs.

Conclusions

Greater BA curvature was associated with MA. Given aura typically originates from the occipital cortex, understanding the physiopathology of this association may provide clues to migraine's underlying mechanisms and relationship with stroke.

Introduction

Accumulating evidence suggests a genetic link between migraine pathogenesis and vascular-related pathways. From 37 identified probable causal genes of migraine, the majority of their functional pathways are related to circulatory system development, artery development, and artery morphogenesis [1]. Structurally, migraine may be associated with cerebrovascular abnormalities including an incomplete Circle of Willis [2], white matter changes [3], and infarct-like lesions [4]. Alterations in vascular morphology may therefore play a role migraine and might also modulate the known association between ischemic stroke risk and migraine [5]. Investigators have also proposed endothelial dysfunction, microemboli, and neurometabolic imbalances as potential mechanisms for triggering cortical spreading depression (CSD) in migrainous aura, providing additional possible mechanisms linking migraine and stroke [[6], [7], [8]].

Migraine likely results from the interplay among different parts of the brain, including the occipital cortex in visual aura symptoms, the brainstem in autonomic dysfunction, and the pons in migraine generation [9]. Further, many imaging studies show increased prevalence of posterior circulation hyperintensities and infarct-like lesions [4,10]. Given possible predisposition to abnormalities in the posterior circulation territory, the vertebrobasilar system is of particular interest. In the majority of normal individuals, the basilar artery (BA) courses straight in the midline or paramedian position [11]. Anatomic deviations and vessel curvature in the vertebrobasilar system convey important influences on vertebrobasilar hemodynamics which may have implications in atherosclerosis and plaque formation [12]. Both BA dolichoectasia (abnormal elongation and dilation) and tortuosity (abnormal twists and turns) can be pathologic entities and have been linked to ischemic stroke [13,14]. Therefore, BA curvature, which refers to any BA course that deviates from midline, may also share a relationship with migraine pathophysiology. Investigators previously showed in a post-hoc analysis of the Anatomy and Cerebral Hemodynamic Evaluation of Migraine (ACHE-M) study that basilar artery curvature may be associated with MA [15]. To further investigate a potential relationship between basilar artery structure and migraine, we sought to compare basilar artery lateral displacement between migraine without aura (MwoA), MA, and migraine-free subjects among stroke-free participants from the Northern Manhattan Study (NOMAS), a large, urban, multi-ethnic prospective population-based study. We hypothesized that increased basilar artery curvature measured by lateral displacement is associated with MA.

Section snippets

Methods

This study included subjects from NOMAS, which is an ongoing, prospective, population-based study of stroke incidence and vascular risk factors in an urban, multi-ethnic population based in the Northern Manhattan area [16]. In brief, NOMAS used random digit dialing with dual-frame sampling to enroll 3298 clinically stroke-free participants who had resided in the Northern Manhattan area for at least 3 months with a telephone. In 2003, standardized MRI protocols were introduced in NOMAS and

Sample characteristics

This cross-sectional study included a sub-sample from NOMAS of 880 participants who had brain MRA and BA lateral displacement measurements, of whom 178 (20.2%) had any type of migraine. There were 146 participants (82.0% of all migraines) who had MwoA and 32 (18.0% of all migraines) who had MA. Compared to those not included who did not have BA lateral displacement measurements, the included subsample had similar age (70.7 vs 70.5 years), race-ethnicity (white: 13.9 vs 16.6%, black: 17.9 vs

Discussion

In this sample from NOMAS, we found that increased BA curvature, measured by lateral displacement throughout the course of the BA, was associated with MA. Our results showed that for every millimeter of lateral basilar artery displacement, there was a 4% greater odds of MA. The ACHE-M study previously showed in a post-hoc case-control analysis that BA displacement was associated with MA in a young cohort (average age in third decade of life) [15]. The present study from NOMAS adds to the

Sources of funding

NOMAS is funded by the National Institutes of Neurologic Disorders and Stroke, Grant #R37 NS029993. Dr. Yang was funded by the National Institutes of Neurologic Disorders and Stroke, Grant #T32NS007153-38.

Disclosures

None.

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