ABSTRACT
BACKGROUND: While migraine, particularly migraine with aura, is a recognized risk factor for ischemic stroke, the association of migraine with silent brain infarction is a matter of debate, as studies on this topic have yielded conflicting results. METHODS: A systematic review of the literature was conducted of studies reporting migraine and silent brain infarction, assessed by magnetic resonance imaging, between January 1980 and April 2022, by consulting Medline and Embase databases. Studies with a control group were included in a meta-analysis of population-based studies. An exploratory meta-analysis of both population-based and clinical-based studies was further performed to test the association between migraine with aura and silent brain infarction. RESULTS: A total of 2,408 articles were identified, among which 24 were included in the systematic review and 10 in the meta-analysis. The meta-analysis of population-based studies showed no association of migraine with silent brain infarction (odds ratio (OR)=1.32 [95% CI 0.92;1.90], P=0.13) and migraine with aura with silent brain infarction (OR=1.56 [0.74;3.30], P=0.24). However, in the exploratory meta-analysis of population-based and clinical-based studies, migraine with aura was significantly associated with silent brain infarction (OR=1.91 [1.02;3.59], P=0.04) and to silent cerebellar infarcts (OR=2.57 [1.01;6.56], P=0.05). CONCLUSION: In this updated systematic review and meta-analysis of population-based studies, migraine and migraine with aura were not associated with silent brain infarction.
ABSTRACT
Large artery intracranial stenosis (ICS) is a common finding in stroke patients, but is much less prevalent in Western countries than in Asia and in young adults than in the elderly. We investigated the prevalence and causes of ICS among French young adults with ischaemic stroke. Clinical and radiological data of patients aged 18-54 years treated consecutively for acute ischaemic stroke in the anterior circulation at a tertiary stroke centre were analysed retrospectively. Patients with>50% ICS were identified. ICS was evaluated using TOF-MRA, vessel wall-MRI, digital subtraction angiography and CT-angiography. A total of 316 patients were included. ICS was diagnosed in 29 patients, resulting in a prevalence of 9.2% (95% CI, 6.2 to 13.3). The leading cause of ICS was atherosclerosis (n=13), ahead of moyamoya disease (n=4), dissection (n=2), vasculitis (n=2), and reversible cerebral vasoconstriction syndrome (n=1). The cause of ICAS could not be determined in 7 patients. ICS was found in nearly one in 10 ischaemic strokes among French young adults. Atherosclerosis was the leading cause of ICS. The cause of ICS could not be determined in almost a quarter of the patients.
Subject(s)
Brain Ischemia , Intracranial Arteriosclerosis , Ischemic Stroke , Stroke , Adolescent , Adult , Aged , Arteries , Brain Ischemia/complications , Brain Ischemia/diagnostic imaging , Brain Ischemia/epidemiology , Constriction, Pathologic/complications , Constriction, Pathologic/epidemiology , Humans , Intracranial Arteriosclerosis/complications , Intracranial Arteriosclerosis/diagnostic imaging , Intracranial Arteriosclerosis/epidemiology , Magnetic Resonance Angiography/methods , Middle Aged , Retrospective Studies , Risk Factors , Stroke/diagnostic imaging , Stroke/epidemiology , Stroke/etiology , Young AdultABSTRACT
Migraine is characterized by symptoms related to cortical hyperexcitability such as photophobia, phonophobia, osmophobia and allodynia. One-third of migraineurs experience aura, whose neurophysiological substrate is thought to be cortical spreading depression (CSD). Functional magnetic resonance imaging (MRI) has shown the migraine aura to be characterized by cerebral hyperactivity/hyperperfusion followed by hypometabolism/hypoperfusion spreading along the occipital cortex with the same spatiotemporal organization as the experimentally triggered CSD. The link between migraine aura and headache remains undetermined. Neuroimaging studies have failed to show a leakage of the blood-brain barrier, which was suspected to occur during CSD and to cause the stimulation of trigeminal nociceptive receptors. However, recent studies have highlighted the involvement of neuroglial inflammation and other studies have suggested that a common central network plays a role in the link between CSD and migraine pain. Finally, MRI has made it possible to study the contribution of metabolites such as glutamic acid, γ-amino-butyric acid and sodium in the pathophysiology of hyperexcitability in migraine.
