NDLI: Development of Abnormal Hemispheric Vascular Networks Mimicking Cerebral Proliferative Angiopathy in a Child Originally Diagnosed with Deep-Seated Arteriovenous Fistula.

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Development of Abnormal Hemispheric Vascular Networks Mimicking Cerebral Proliferative Angiopathy in a Child Originally Diagnosed with Deep-Seated Arteriovenous Fistula.

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Development of Abnormal Hemispheric Vascular Networks Mimicking Cerebral Proliferative Angiopathy in a Child Originally Diagnosed with Deep-Seated Arteriovenous Fistula.

Content Provider	World Health Organization (WHO)-Global Index Medicus
Author	Sakata, Hiroyuki Fujimura, Miki Sato, Kenichi Niizuma, Kuniyasu Endo, Hidenori Tominaga, Teiji
Description	Country affiliation: Japan Author Affiliation: Sakata H ( Department of Neurosurgery, Tohoku University Graduate School of Medicine, Sendai, Miyagi, Japan.); Fujimura M ( Department of Neurosurgery, Tohoku University Graduate School of Medicine, Sendai, Miyagi, Japan. Electronic address: fujimur@nsg.med.tohoku.ac.jp.); Sato K ( Department of Neurosurgery, Tohoku University Graduate School of Medicine, Sendai, Miyagi, Japan.); Niizuma K ( Department of Neurosurgery, Tohoku University Graduate School of Medicine, Sendai, Miyagi, Japan.); Endo H ( Department of Neurosurgery, Tohoku University Graduate School of Medicine, Sendai, Miyagi, Japan.); Tominaga T ( Department of Neurosurgery, Tohoku University Graduate School of Medicine, Sendai, Miyagi, Japan.)
Abstract	Cerebral proliferative angiopathy (CPA), which is characterized by diffuse vascular abnormalities with intermingled normal brain parenchyma, is a rare clinical entity distinct from classical cerebral arteriovenous malformations. Its pathology at initial state and subsequent course of progression has totally been undetermined. We herein presented a case of a child who was initially diagnosed with deep-seated arteriovenous fistula (AVF), and ultimately developed symptomatic CPA-like vascular lesion over a long period of clinical follow-up. A 7-month-old boy was incidentally found to have an AVF in the right basal ganglia and conservatively followed up. Serial magnetic resonance angiograms revealed the gradual proliferation and enlargement of pial and medullary vessels surrounding the AVF. Seven years later, he had a transient ischemic attack followed by intraventricular hemorrhage. A catheter angiogram showed a diffuse large vascular malformation composed of 2 distinct structures, including AVF in the right basal ganglia and the surrounding proliferated pial and medullary arteries in the right hemisphere. Single-photon emission computed tomography with N-isopropyl[123I]-p-iodoamphetamine revealed apparent hemodynamic compromise on the right hemisphere. Targeted embolization of the pseudoaneurysm originating from the right A1 perforator was performed to prevent rebleeding without complications. The patient had no further cerebrovascular events. Perinidal hypoperfusion induced by a deep-seated AVF could be one of the underlying pathologies of progressive angiogenic activity. This is the first case showing the development of abnormal hemispheric vascular networks mimicking CPA, which offers insight into the pathogenesis of this new entity.
File Format	HTM / HTML
ISSN	10523057
Issue Number	10
Journal	Journal of Stroke and Cerebrovascular Diseases
Volume Number	25
e-ISSN	15328511
Language	English
Publisher	Elsevier
Publisher Date	2016-10-01
Publisher Place	United States
Access Restriction	One Nation One Subscription (ONOS)
Subject Keyword	Discipline Cardiology
Content Type	Text
Resource Type	Article
Subject	Rehabilitation Neurology (clinical) Surgery Cardiology and Cardiovascular Medicine

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