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Aphasic Migraineous Aura With Left Parietal Hypoperfusion: A Case Report

J. Linn, T. Freilinger, D. Morhard, H. Brueckmann, A. Straube
Published 2007 · Medicine

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Migraine aura typically consists of transient neurological deficits such as visual disturbances, unilateral sensory or motor deficits, or dysphasic symptoms that develop normally within minutes and last up to an hour (1). Its most likely neurophysiological correlate is a phenomenon called cortical spreading depression (CSD). During CSD a wave of neuronal and glial depolarization propagates across the cerebral cortex at 2–3 mm per minute (2, 3). It is followed by a long-lasting suppression of neuronal activity. The change in extracellular ion concentrations associated with CSD might trigger trigeminal afferences, which in turn activate the trigeminovascular system, the final pathway that evokes the typical pain of migraine (4). Since neuronal activity is strongly coupled to brain perfusion, CSD is associated with characteristic cerebral blood flow changes. The initial short phase of hyperperfusion is followed by a strong reduction of cerebral blood flow (2, 5–8). Most patients with migraine aura have been scanned either during a spontaneous visual aura or during an experimentally evoked visual aura. To our knowledge, this is the first report on the performance of perfusion magnetic resonance imaging (MRI) on a patient with spontaneous aphasic aura which showed local hypoperfusion in the left inferior parietal lobe.
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