• Tomomi Kimiwada, Toshiaki Hayashi, Reizo Shirane, and Teiji Tominaga.
• Department of Neurosurgery, Miyagi Children's Hospital, Sendai, Japan. Electronic address: tomomi@nsg.med.tohoku.ac.jp.
• J Stroke Cerebrovasc Dis. 2013 Nov 1;22(8):1432-5.

AbstractCerebral proliferative angiopathy (CPA) is a new clinical entity demonstrating a diffuse network of densely enhanced vascular abnormalities with intermingled normal brain parenchyma and is distinguishable from classical arteriovenous malformations by specific clinical and imaging markers. However, the pathophysiological nature of this disease is unclear, and there is no consensus on the treatment. We describe cerebral perfusion abnormalities in a patient with CPA by using N-isopropyl-p-[123I] iodoamphetamine single-photon emission computed tomography (123I-IMP-SPECT) and perfusion-weighted magnetic resonance imaging. The patient, a 13-year-old boy, had reversible focal neurological deficits unrelated to cerebral hemorrhage. 123I-IMP-SPECT at resting state showed preserved uptake within the vascular lesion, yet lower uptake in the area adjacent to the lesion. In addition, acetazolamide-stressed 123I-IMP-SPECT exhibited severely impaired cerebrovascular reactivity over the affected hemisphere, suggesting that his focal neurological deficits were related to the cerebral ischemia. The perfusion abnormalities on 123I-IMP-SPECT in a CPA patient have never been previously reported. The concept of vascular malformation-related hypoperfusion is discussed.Copyright © 2013 National Stroke Association. Published by Elsevier Inc. All rights reserved.

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