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P. N. Shams, G. T. Plant; Migrainous Visual Aura Due to Focal Cerebral Lesions. Can the Diagnosis Be Made on the Semiology of Attacks? Nine Case Reports and Review of the Literature. Invest. Ophthalmol. Vis. Sci. 2009;50(13):4042.
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To identify clinical features which could differentiate between the visual auras of idiopathic migraine and those due to structural cortical lesions which also fulfill the diagnostic criteria for idiopathic migraine with visual aura, as defined by The International Classification of Headache Disorders.
Prospective observational study including nine cases of migraine-like visual aura due to focal cerebral lesions seen in the practice of one neuro-ophthalmologist at Moorfields Eye Hospital and The National Hospital for Neurology and Neurosurgery London between 1986 and 2008. A further 31 cases from the literature were identified by searches of PubMed from 1966 until March 2008.
Five key clinical features are outlined in detail to help to identify which patients with migraine-like visual auras require further investigation; 1) Onset of visual aura for the first time in fourth or fifth decade of life; 2) Duration of the visual aura less than 5 minutes; 3) Increase in frequency or change in the pattern of longstanding visual auras; 4) Visual auras recurring in the same location in the visual field; 5) Unexplained visual field defect (VFD) and/or persistent VFD following a typical visual aura.
Photopsia and the slow propagation of scintillating scotoma across the visual field are strongly associated with the visual aura of idiopathic migraine. Our cases support the observation that visual auras fulfilling the diagnostic criteria for idiopathic migraine, can arise from acquired cortical lesions. Despite the considerable overlap in the characteristics of visual aura caused by migraine, epilepsy and structural cerebral lesions, certain features can help to differentiate between these conditions in order to identify patients who require further investigation. We hypothesize that the co-morbidity and overlap in clinical features of these chronic neurological disorders is due to a common underlying pathophysiology; namely a state of neuronal hyperexcitability. Whether due to genetic predisposition or acquired through brain injury, neuronal hyperexcitability increases an individuals’ susceptibility to the generation of cortical spreading depression, the electrophysiological correlate of the visual aura in migraine.
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