Σφακιανάκης Αλέξανδρος
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Κυριακή 26 Φεβρουαρίου 2017

Intraoperative visualization of subependymal arteries at the atrium supplying the descending motor pathway.

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Intraoperative visualization of subependymal arteries at the atrium supplying the descending motor pathway.

World Neurosurg. 2017 Feb 13;:

Authors: Hanihara M, Sato S, Shibahara I, Saito R, Kanamori M, Sonoda Y, Kinouchi H, Tominaga T, Kumabe T

Abstract
OBJECTIVE: We previously disclosed that damage to the subependymal arteries (SEAs) caused by coagulation of the choroid plexus at the atrium, can result in infarction within the lateral posterior choroidal artery territory, followed by hemiparesis. The present study describes the intraoperative anatomical findings of the SEAs and choroid plexus at the atrium, those were verified only by a few cadaveric studies.
METHODS: Locations of the SEA and descending motor pathway were determined with the neuronavigation system and subcortical electrical stimulation in 8 cases of periatrial brain tumor. Indocyanine green (ICG) videoangiography was performed to verify the blood flow in the choroid plexus and SEAs.
RESULTS: Intraoperative visualization of the SEAs was successfully performed in all patients. The neuronavigation system and subcortical electrical stimulation mapping demonstrated that these SEAs penetrated into the descending motor pathway. ICG depicted the blood flow of the SEAs entering the wall of the lateral ventricle and adjacent brain parenchyma. The blood flow directions between the SEAs and choroid plexus were not uniform, as the SEAs were filled ahead of the choroid plexus in 3 cases, whereas the choroid plexus was filled first in the other 2 cases.
CONCLUSIONS: Manipulations to the inner side of the choroid plexus at the transition from the atrium to the body of lateral ventricle can damage the SEAs. Not only coagulation of the SEAs themselves, but also coagulation of choroid plexus itself may reduce the blood flow in the SEAs, resulting in ischemic complications at descending motor pathway.

PMID: 28232151 [PubMed - as supplied by publisher]



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