• Hidehito Kimura, Masaaki Taniguchi, Tatsuya Mori, Kohkichi Hosoda, and Eiji Kohmura.
• Department of Neurosurgery, Kobe University Graduate School of Medicine, Hyogo, Japan. Electronic address: hidekimura-nsu@umin.ac.jp.
• World Neurosurg. 2017 Jan 1; 97: 754.e17-754.e21.

BackgroundPostoperative hyperperfusion syndrome after extracranial-to-intracranial bypass causing temporary neurologic deterioration has been reported rarely as isosignal intensity on diffusion-weighted imaging (DWI) with hyperintense lesion on T2-weighted image and fluid-attenuated inversion recovery (FLAIR) imaging as an expression of vasogenic edema. We present a rare case of a patient suffering from temporary aphasia after an extracranial-to-intracranial bypass surgery, which was shown as a transient hypointense lesion on DWI with increased apparent diffusion coefficient value, evidence of postoperative hyperperfusion.Case DescriptionBy the preoperative single-photon emission computed tomography study analyzed retrospectively, preoperative cerebral blood flow (CBF) was compared between the lesions in which the hypointensity emerged and the lesions in which its signal remained unchanged in the hyperperfusion area. We found CBF after an acetazolamide challenge was much smaller and the percentage increase of CBF after an acetazolamide challenge was much less than zero in the temporal hypointense lesion on DWI.ConclusionsAn abrupt increase of CBF after bypass installation to the brain with no vascular response and complete disruption of the blood-brain barrier would cause a remarkable increase of extracellular fluid and excessive water molecule diffusion, resulting in excessive vasogenic edema. This was a plausible mechanism for the transient hypointense lesion on DWI with increased apparent diffusion coefficient value.Copyright © 2016 Elsevier Inc. All rights reserved.

23 keywords...

hide…