LAUSR

evidence of infarct or hemorrhage on MRI. Electroencephalography showed diffuse slowing throughout the right hemisphere and no epileptic discharge. Control fundoscopies were normal. We decided to operate on this patient because of the hypothesis that the right cerebral hemisphere was hemodynamically compromised as a consequence of vascular steal and therefore the possibility of a progressive ischemic course in the future. We elected to perform an indirect revascularization procedure to augment flow to the right hemisphere. A right-sided pial synangiosis and encephalomyosynangiosis were performed. The patient did not present any permanent neurological deficit during the first year of the follow-up period after the operation, and the transitory ischemic attacks became less frequent and lasting. So, in spite of his frequent headaches, inconvenience in his daily life was diminished during several months. Nevertheless, 2 years after surgery, he developed a permanent left hemiparesis with progressive gait disturbance. CPA is a rare entity occurring in 3.4% of patients with brain AVMs. It has been demonstrated to be a different disease from classic AVMs with regard to clinical presentation, angioarchitecture, and natural history [1] . Following the series of Lasjaunias et al. [1] , 4 other cases of CPA An 8-year-old previously healthy boy presented to the emergency room with acute left hemiparesis followed by intense headache which lasted 2 h. On questioning, he admitted having had intermittent headaches of moderate intensity for several months. Neurological examination was normal. Fundoscopy demonstrated bilateral papilledema. Computed tomography (CT) and magnetic resonance imaging (MRI) revealed a diffuse network of densely enhancing vascular spaces over the right cerebral hemisphere and left basal ganglia with intermingled normal brain parenchyma ( Fig. 1 ). There was no evidence of acute ischemia on diffusion-weighted sequences. Angiography showed a widespread angiopathy fed by multiple arteries and a diffuse network of vascular spaces with slow shunting, suggestive of cerebral proliferative angiopathy (CPA) ( Fig. 2 ). A lumbar puncture was performed after imaging and was noted to have an elevated cerebrospinal fluid pressure of 30 mm Hg. He underwent a lumbar-peritoneal shunt, and 1 month later the bilateral papilledema disappeared. However, his symptoms worsened over the next months with disabling headache, becoming more frequent and lasting transitory ischemic attacks. He had multiple subsequent admissions for similar complaints over the next year, each without Received: November 15, 2016 Accepted after revision: February 3, 2017 Published online: March 14, 2017