Basilar Artery Migraine: Transcranial Doppler EEG and SPECT From the Aura Phase to the End

Abstract

Transcranial Doppler, electroencephalography, and single photon emission computed tomography were performed in a case of basilar migraine during the different phases of the attack. In the aura phase, the patient had bilateral blindness and ataxia. Doppler ultrasound studies showed a reduction in the mean flow velocity of the posterior cerebral arteries, electroencephalography showed slow activity confined to the posterior regions, and single photon emission computed tomography, an area of hypoperfusion in the right parietal and occipital regions. During the headache phase, when the neurological examination was normal, transcranial Doppler showed an increase in the mean flow velocity of both posterior cerebral arteries and the electroencephalogram revealed an increase: in the slow activity over the occipital regions. When the pain subsided, the electroencephalogram showed a progressive reduction of the slow abnormalities and transcranial Doppler was reported as normal. After a week, single photon emission computed tomography and cranial magnetic resonance imaging were normal. After a month, a follow-up electroencephalogram was also normal. All these findings indicated a transient focal reduction of cerebral blood flow during the aura phase. Transcranial Doppler (TCD) is an effective technique for the study of cerebral blood flow (CBF) in patients with migraine. The available data refer to the pain phase and the intericta period. 1,2 The possibility of documenting the CBF variation starting with the aura phase is a rare event limited to cases with prolonged aura. 3 In this case, the data suggest a decrease of CBF in the cortical area responsible for the neurological manifestations during the aura phase.Determinations of regional cerebral blood flow (rCBF) with Xenon-133 during migraine with aura have already demonstrated initial focal hypoperfusion followed by hyperemia. 4 More recently, the use of technetium Tc 99m hexamethyl propylenamine oxime (Tc 99m HMPAO) single photon emission computed tomography (SPECT) in patients with migraine without aura has failed to show evidence of CBF focal alterations. 5 A relative rCBF reduction during migraine attacks might account for the different electroencephalographic abnormalities described in these patients, the meaning of which is uncertain.We performed an EEG, TCD, and cerebral SPECT using Tc 99m HMPAO, during all phases of a basilar migraine attack in order to correlate the focal electroencephalographic abnormalities with the dynamic alterations of the rCBF.In view of the neurological deficit in the aura phase, we evaluated the TCD parameters with respect to the posterior cerebral arteries (PCAs) and compared them with those of the middle cerebral arteries (MCAs). The normal values for mean flow velocity (MFV) suggested by the Italian Society of Neurosonology 6 (PCA 51 to 26 cm/ sec, MCA 76 to 44 cm/sec, pulsatility index [PI] 0.99 to 0.69 cm/sec) were taken into account. CASE HISTORYA 25-year-old woman was hospitalized with complaints of positive scotomata and bilater...

Structural and Functional Neuroimaging in Migraine: Insights From 3 Decades of Research

“…22,110 Single-photon emission computed tomography Activation in the primary visual area of the occipital cortex. 23 migraine aura can also appear in migraine attacks without aura. 22 Of note, in most reported cases examined with SPECT (a semiquantitative blood flow technique), aura symptoms corresponded to areas of cerebral hypoperfusion.…”

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The pathophysiology of migraine: year 2005

“…CSD is a wave of neuronal and glial depolarisation, followed by long-lasting suppression of neural activity, and it can be evoked in mammals with lissencephalic [63,64] or folded cortex [65]. Human neuroimaging such as planar Xenon [66][67][68][69], single photon emission tomography [68,[70][71][72][73][74] positron-emission tomography [75,76], magnetoencephalography [77,78] and MRI [79][80][81] support the hypothesis that CSD underlies migraine [82]. However many subjects never experience symptoms of typical visual auras in studies showing spreading hypoperfusion [75] or blood oxygenation level-dependent (BOLD) signal changes [79], and the initial hyperaemia characteristics of CSD were not directly demonstrated in human cortex.…”

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