Prolonged acute migraine with aura and reversible brain MRI abnormalities after liquid sclerotherapy
© Zouitina et al.; licensee Springer. 2014
Received: 5 May 2014
Accepted: 14 June 2014
Published: 19 June 2014
Transient visual disturbances constitute the most commonly reported neurological side effect during and immediately after sclerotherapy. A few studies, based on clinical and diffusion-weighted MRI assessments, have suggested that these transient neurological symptoms correspond to migraine with aura. Recently, it has been reported that brain magnetic resonance imaging can reveal transient T2*-weighted abnormalities during the acute phase of migraine with aura. We reported a 36-year-old man who presented with transient neurological symptoms and concomitant T2*-weighted abnormalities on brain magnetic resonance imaging immediately after liquid sclerotherapy. We hypothesize that the reversible nature of the patient’s T2*-weighted abnormalities may indicate a relationship with the post-sclerotherapy migraine with aura attack.
KeywordsMigraine Migraine aura Sclerotherapy Magnetic resonance imaging Gradient-echo T2*-weighted imaging
Transient visual disturbances constitute the most commonly reported neurological side effect during and immediately after sclerotherapy, with an incidence of 1.4%s . Furthermore, foam sclerotherapy appears to be associated with a higher incidence of transient visual disturbances than liquid sclerotherapy . Research has suggested that these transient neurological symptoms (which are more frequent in patients with patent foramen ovale (PFO) and/or a history of migraine) correspond to migraine with aura (MA) [3–5].
Here, we report on a patient who presented with transient neurological symptoms and concomitant T2*-weighted abnormalities on MRI immediately after liquid sclerotherapy. We hypothesize that the reversible nature of the patient’s T2*-weighted abnormalities may indicate a relationship with the post-sclerotherapy MA attack.
In migraine with aura, visual disturbances may comprise additional features (such as flickering lights and spots), or the loss of features (such as hemianopia and loss of vision) and may be associated with sensory disturbance and speech impairment (depending on the extent of cortical spreading depression (CSD) [1, 11]. These complications appear to be more frequent after foam sclerotherapy than after liquid sclerotherapy . Although the degree to which the injected volume of sclerotic agent contributes to the development of neurological side effects is subject to debate, it appears reasonable to decrease the volume when (i) neurological symptoms occurs after sclerotherapy and (ii) another sclerotherapy session is required . Recent clinical and brain MRI studies have shown that these transient neurological symptoms (which are more frequent in patients with PFO) correspond to MA rather than to transient ischemic events [5, 12].
Migraine with aura occurs in about one third of migraine sufferers . It is clinically defined by at least two recurrent episodes of fully reversible symptoms (the most frequent of which are visual disturbances, sensory disturbances and speech and/or language impairment). The aura symptom spreads gradually over a period of 5 minutes and (for each individual aura) lasts between 5 and 60 minutes (although this upper limit was set arbitrarily). Indeed, it has been reported that aura lasts for more than one hour in up to 37% of patients . This epidemiological reality has been recently taken into consideration in the third edition of the International Classification of Headache Disorders, in which aura lasting more than an hour but less than a week (in the absence of radiologically confirmed brain ischemia) was defined as “probable migraine with aura (prolonged aura)” . These atypical clinical presentations always warrant a thorough work-up, since cerebrovascular disease must be always considered . As such, brain MRI is usually required to carefully screen for the underlying cause during the acute phase. Recently, transient T2*-weighted imaging abnormalities on brain MRI have been reported during the acute phase of MA [6–8]. The occurrence of these transient T2*-weighted imaging abnormalities after sclerotherapy lends support to the hypothesis whereby endothelin release and microembolization trigger CSD . The two most likely explanations for these T2* findings relate to (i) increased oxygen consumption and a subsequent increase in the intravenous deoxyhaemoglobin concentration  and (ii) venous dilatation following the release of vasoactive factors (such as endothelin). In murine models, systemic levels of endothelin-1 (ET-1, one of the most potent vasoconstrictors and a CSD inducer) are significantly elevated one and five minutes after the initiation of foam sclerothapy . Furthermore, Lemos et al.'s study of a population of Portuguese patients revealed a possible role for the endothelin receptor type A in migraine without aura . Nevertheless, the prevalence and significance of these phenomena merit further investigation.
In conclusion, the present observation suggests that the transient nature of the T2*-weighted imaging abnormalities is associated with a CSD caused by migraine aura after sclerotherapy.
Written informed consent was obtained from the patient for publication of this Case report and any accompanying images. A copy of the written consent is available for review by the Editor-in-Chief of this Journal.
We thank David Fraser PhD for providing medical writing services on behalf of Amiens University Hospital.
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