Simultaneous bilateral visual auras: A case report

Migrainous auras arouse particular interest among researchers due to their presentation, the presence of focal neurological symptoms, and their reversibility. Aura phenomena have been carefully studied both from clinical, biochemical and neuroradiological perspectives, allowing a satisfactory pathogenetic interpretation of the mechanisms (1). The diagnostic clinical criteria of three typical auras are included in the International Classification of Headache Disorders 3 beta version (ICHD-3 beta) (2). Among them, visual auras are by far the most common, being frequently the sole aura phenomenon, although other focal neurological symptoms, such as paresthesia or aphasia, can occur. The availability of accurate diagnostic criteria helps in differentiating migraine with aura (MA) from other neurological disease, including epileptic seizures, cerebral ischemia, or any condition that presents with focal neurological symptoms (ICDH-3 beta) (2). A 45-year-old woman suffering from migraines – both MA, and without aura (MO) (2) – for decades presented to our outpatient centre. Headache attacks that fulfilled the ICHD 3 beta criteria for the diagnosis of MO started at the age of 23, with an average frequency of 2–3 attacks per month; given the good response to symptomatic treatments (triptans), a prophylactic therapy was not considered. In addition, from the age of 29, she began to suffer from attacks fulfilling the ICHD 3 beta diagnosis of MA, with an average frequency of 4–5 episodes per year. MA frequency remained stable until 6 months before the observation. From that time, the patient presented an increased rate of MA attacks to 2–3 per month, and with concomitant modification of her usual typical visual aura. In about half of the attacks, in addition to the usual scintillating scotoma progressively expanding to the left field of view of both eyes and disappearing within 20–40 min, she described a blurred right field of view with different clinical characteristics and described it as like looking “through a wet glass”. These two phenomena occurred and progressed simultaneously, with a slight difference in duration, being a few minutes longer for the blurred vision. No other aura symptoms were reported. The headache following the different aura phenomena maintained the same characteristics, and met the ICHD 3 beta criteria for MO (2). Interestingly, crises with both visual alterations constantly presented with scintillating scotoma on the left visual field and the blurred vision on the right, while crises with a single phenomenon regularly presented scintillating scotoma with alternative visual field side involvement in different attacks. The blurred vision never occurred as an isolated manifestation of visual aura. Visual disturbances during MA attacks were described as very disabling, preventing the patient from undertaking any activities, and were regularly associated with anxiety and fear. Gadolinium-enhanced cerebral MRI and angio-MRI, hemocoagulative screening, Doppler vessels ultrasound, transcranial Doppler with bubble test, EEG and echocardiography did not show any noteworthy alterations. Prophylactic therapy with flunarizine 5 mg, 5 days/week for 4 months was started. Subsequently, the frequency of MA attacks reduced to one every 2–3 months (follow-up: 1 year). Since the introduction of the therapy, the two different auras presented concomitantly on only two occasions. Cortical spreading depression (CSD), which consists of a transient neuronal hyperactivity followed by a depolarization that spreads across the cortex at a speed of 2 mm/min, is considered the neurophysiological phenomenon underlying migraine aura (1). Recent prospective studies investigated auras with regards to the clinical features, duration, and frequency; although these surveys allowed for a better clinical characterization of auras (3–4), the proposal to modify and extend some aura features could complicate the differential diagnosis with other neurological conditions (5). These studies, in fact, highlight phenotypes that do not fit with the classical parameters of typical auras, as an increase in duration that exceeds one hour in about 15% of the attacks has been proposed. Thus, according to the results of these surveys, the occurrence of a sensory or aphasic aura in the absence of the visual one would not be considered as a particularly rare and suspicious event, contrary to what has been considered until now (6). Despite these new and accurate clinical descriptions, which confirmed some peculiar characteristics of auras, to the best of our knowledge a concurrent and simultaneous onset of two distinct types of visual aura, likely due to two distinct CSDs originating in the occipital cortex of each hemisphere, has never been previously reported. The presentation of a mono or bilateral aura could be due to intercurrent sporadic circumstances that lead to an increase in the cortex excitability (7) up to the threshold necessary to trigger a single aura. Functional neuroimaging investigation during complex visual aura could clarify this pathogenetic hypothesis. Albeit the subject of study for a long time and in a deep manner, MA never ceases to present new and fascinating aspects that call for further and more accurate clinical and neuroradiological studies.

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