BACKGROUND AND PURPOSE: Neuronal damage in aSAH apart from perfusion deficits has been widely discussed. We aimed to test if cerebral injury occurs in aSAH independently from visible perfusion deficit by measuring cerebral metabolites in patients with aSAH without infarction or impaired perfusion. MATERIALS AND METHODS: We performed 3T MR imaging including (1)H-MR spectroscopy, DWI, and MR perfusion in 58 patients with aSAH and 11 age-matched and sex-matched control patients with incidental aneurysm. We compared changes of NAA, Cho, Glx, Lac, and Cr between all patients with aSAH and controls, between patients with and without visible perfusion deficit or infarction and controls, and between patients with and without visible perfusion deficit or infarction by using the Wilcoxon signed-rank test. RESULTS: We found that NAA significantly (P < .005) decreased in all patients with aSAH. Cho was significantly increased in all patients compared with controls (P < .05). In patients without impaired perfusion or infarction, Glx was significantly decreased compared with both controls (P = .005) and patients with impaired perfusion or infarction (P = .006). CONCLUSIONS: The significant decrease of NAA and Glx in patients with aSAH but without impaired perfusion or infarction strongly suggests global metabolic changes independent from visible perfusion deficits that might reflect neuronal mitochondrial injury. Further, impaired perfusion in aSAH seems to induce additional metabolic changes from increasing neuronal stress that might, to some extent, mask the global metabolic changes.
BACKGROUND AND PURPOSE: Neuronal damage in aSAH apart from perfusion deficits has been widely discussed. We aimed to test if cerebral injury occurs in aSAH independently from visible perfusion deficit by measuring cerebral metabolites in patients with aSAH without infarction or impaired perfusion. MATERIALS AND METHODS: We performed 3T MR imaging including (1)H-MR spectroscopy, DWI, and MR perfusion in 58 patients with aSAH and 11 age-matched and sex-matched control patients with incidental aneurysm. We compared changes of NAA, Cho, Glx, Lac, and Cr between all patients with aSAH and controls, between patients with and without visible perfusion deficit or infarction and controls, and between patients with and without visible perfusion deficit or infarction by using the Wilcoxon signed-rank test. RESULTS: We found that NAA significantly (P < .005) decreased in all patients with aSAH. Cho was significantly increased in all patients compared with controls (P < .05). In patients without impaired perfusion or infarction, Glx was significantly decreased compared with both controls (P = .005) and patients with impaired perfusion or infarction (P = .006). CONCLUSIONS: The significant decrease of NAA and Glx in patients with aSAH but without impaired perfusion or infarction strongly suggests global metabolic changes independent from visible perfusion deficits that might reflect neuronal mitochondrial injury. Further, impaired perfusion in aSAH seems to induce additional metabolic changes from increasing neuronal stress that might, to some extent, mask the global metabolic changes.
Authors: Stella Blasel; Ulrich Pilatus; Joerg Magerkurth; Maya von Stauffenberg; Dmitri Vronski; Manuel Mueller; Lars Woeckel; Elke Hattingen Journal: Neuroradiology Date: 2012-01-03 Impact factor: 2.804
Authors: E Koźniewska; R Michalik; J Rafałowska; R Gadamski; M Walski; M Frontczak-Baniewicz; P Piotrowski; Z Czernicki Journal: J Physiol Pharmacol Date: 2006-11 Impact factor: 3.011
Authors: M Wagner; P Steinbeis; E Güresir; E Hattingen; R du Mesnil de Rochemont; S Weidauer; J Berkefeld Journal: Clin Neuroradiol Date: 2012-08-23 Impact factor: 3.649
Authors: Jens P Dreier; Sebastian Major; Andrew Manning; Johannes Woitzik; Chistoph Drenckhahn; Jens Steinbrink; Christos Tolias; Ana I Oliveira-Ferreira; Martin Fabricius; Jed A Hartings; Peter Vajkoczy; Martin Lauritzen; Ulrich Dirnagl; Georg Bohner; Anthony J Strong Journal: Brain Date: 2009-05-06 Impact factor: 13.501
Authors: K O Lövblad; S G Wetzel; T Somon; K Wilhelm; A Mehdizade; A Kelekis; M El-Koussy; S El-Tatawy; M Bishof; G Schroth; S Perrig; F Lazeyras; R Sztajzel; F Terrier; D Rüfenacht; J Delavelle Journal: Neuroradiology Date: 2004-01-29 Impact factor: 2.804
Authors: Stefan Weidauer; Heinrich Lanfermann; Andreas Raabe; Friedhelm Zanella; Volker Seifert; Jürgen Beck Journal: Stroke Date: 2007-04-19 Impact factor: 7.914
Authors: Kenneth P Hough; Jennifer L Trevor; John G Strenkowski; Yong Wang; Balu K Chacko; Sultan Tousif; Diptiman Chanda; Chad Steele; Veena B Antony; Terje Dokland; Xiaosen Ouyang; Jianhua Zhang; Steven R Duncan; Victor J Thannickal; Victor M Darley-Usmar; Jessy S Deshane Journal: Redox Biol Date: 2018-06-25 Impact factor: 10.787
Authors: Payashi S Garry; Matthew J Rowland; Martyn Ezra; Mari Herigstad; Anja Hayen; Jamie W Sleigh; Jon Westbrook; Catherine E Warnaby; Kyle T S Pattinson Journal: Crit Care Med Date: 2016-11 Impact factor: 7.598
Authors: Muhammad E Haque; Refaat E Gabr; Sarah D George; Xiurong Zhao; Seth B Boren; Xu Zhang; Shun-Ming Ting; Gunghua Sun; Khader M Hasan; Sean Savitz; Jaroslaw Aronowski Journal: Front Neurosci Date: 2019-08-21 Impact factor: 4.677
Authors: John B Williamson; Damon G Lamb; Eric C Porges; Sarah Bottari; Adam J Woods; Somnath Datta; Kailey Langer; Ronald A Cohen Journal: Front Aging Neurosci Date: 2021-02-03 Impact factor: 5.750
Authors: Ernest Jan Bobeff; Malgorzata Bukowiecka-Matusiak; Konrad Stawiski; Karol Wiśniewski; Izabela Burzynska-Pedziwiatr; Magdalena Kordzińska; Konrad Kowalski; Przemyslaw Sendys; Michał Piotrowski; Dorota Szczesna; Ludomir Stefańczyk; Lucyna Alicja Wozniak; Dariusz Jan Jaskólski Journal: J Clin Med Date: 2022-01-13 Impact factor: 4.241