Case reports in neurology · 2026
Cortical Spreading Depression Mimicking Ischemic Stroke: A Case Report of Complex Hemiplegic Migraine with Reversible Cortical Magnetic Resonance Imaging Changes.
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Hammed Ali, Hammed Salah, Stein Thomas, Niemöller Ulrich, Meyer Marco, Tanislav Christian
Аннотация
INTRODUCTION: Hemiplegic migraine (HM) is a rare subtype of migraine with aura characterized by transient motor weakness and focal neurological deficits that can closely resemble acute ischemic stroke. Cortical spreading depression, the underlying electrophysiological mechanism, produces transient neuronal and vascular changes that may lead to stroke-like imaging findings, creating diagnostic challenges in emergency settings.
CASE PRESENTATION: We describe a 66-year-old man with a long-standing history of migraine with aura who presented with acute left-sided hemiparesis, dysarthria, and visual disturbances. Initial computed tomography revealed subtle sulcal effacement without evidence of hemorrhage. Brain MRI demonstrated right hemispheric diffusion-weighted hyperintensities without corresponding apparent diffusion coefficient (ADC) reduction, suggesting transient cytotoxic edema rather than infarction. Electroencephalography showed right hemispheric slowing without epileptiform discharges, and cerebrospinal fluid analysis was unremarkable. The patient experienced gradual clinical improvement over 7 days, with mild residual fine motor deficits at discharge. Preventive therapy with flunarizine was initiated.
CONCLUSION: This case underscores the importance of recognizing HM as a stroke mimic. Integration of the clinical context with MRI findings - particularly the absence of ADC restriction - can help differentiate HM from acute ischemic stroke and guide appropriate clinical management. Early and accurate diagnosis, together with individualized prophylactic treatment, may help reduce recurrence and long-term morbidity.
CASE PRESENTATION: We describe a 66-year-old man with a long-standing history of migraine with aura who presented with acute left-sided hemiparesis, dysarthria, and visual disturbances. Initial computed tomography revealed subtle sulcal effacement without evidence of hemorrhage. Brain MRI demonstrated right hemispheric diffusion-weighted hyperintensities without corresponding apparent diffusion coefficient (ADC) reduction, suggesting transient cytotoxic edema rather than infarction. Electroencephalography showed right hemispheric slowing without epileptiform discharges, and cerebrospinal fluid analysis was unremarkable. The patient experienced gradual clinical improvement over 7 days, with mild residual fine motor deficits at discharge. Preventive therapy with flunarizine was initiated.
CONCLUSION: This case underscores the importance of recognizing HM as a stroke mimic. Integration of the clinical context with MRI findings - particularly the absence of ADC restriction - can help differentiate HM from acute ischemic stroke and guide appropriate clinical management. Early and accurate diagnosis, together with individualized prophylactic treatment, may help reduce recurrence and long-term morbidity.