Abstract W P101: Surgical Revascularization Reverses Decreased Cerebral Oxygen Metabolism in Young Patients with Moyamoya Disease

Stroke ◽  
2014 ◽  
Vol 45 (suppl_1) ◽  
Author(s):  
Satoshi Kuroda ◽  
Daina Kashiwazaki ◽  
Kiyohiro Houkin
Keyword(s):  
Cerebral Ischemia ◽  
Moyamoya Disease ◽  
Young Patients ◽  
Oxygen Metabolism ◽  
Cerebral Oxygen ◽  
Surgical Revascularization ◽  
Cerebral Oxygen Metabolism ◽  
Positron Emission ◽  
Pet Scans ◽  
Parenchymal Damage

Purpose: This prospective study was aimed to evaluate the effects of surgical revascularization on cerebral oxygen metabolism in moyamoya disease. Methods: This study included totally 41 patients who underwent STA-MCA anastomosis and indirect bypass for moyamoya disease between 2000 and 2011. There were 12 children and 29 adults. Totally 67 hemispheres underwent surgery. MR imaging and 15O-gas positron emission tomography (PET) were performed before and 3 to 4 months after surgery. Hemodynamic and metabolic parameters were precisely quantified. Results: Preoperative PET scans revealed that cerebral metabolic rate for oxygen (CMRO2) was kept normal in 15 hemispheres (22%), but decreased in other 52 (78%). The incidence did not differ between pediatric and adult patients. Pronounced cerebral ischemia was observed in all hemispheres with decreased CMRO2. After surgery, CMRO2 value significantly improved to the normal level in 20 (38%) of 52 hemispheres, but did not change in other 32 (62%). Multivariate analysis showed that the predictors for postoperative CMRO2 normalization were patient’s age (younger than 40 years) and no parenchymal damage on MRI. Conclusion: These findings strongly suggest that cerebral oxygen metabolism is often depressed in response to dense and chronic cerebral ischemia in moyamoya disease. The phenomenon may be advantageous to protect the involved hemispheres against ischemia. Surgical revascularization may readily normalize oxygen metabolism in young patients without any parenchymal damage.

scholarly journals Effects of Surgical Revascularization on Cerebral Oxygen Metabolism in Patients With Moyamoya Disease

Stroke ◽  
2014 ◽  
Vol 45 (9) ◽  
pp. 2717-2721 ◽  
Author(s):  
Satoshi Kuroda ◽  
Daina Kashiwazaki ◽  
Kenji Hirata ◽  
Tohru Shiga ◽  
Kiyohiro Houkin ◽  
...  
Keyword(s):  
Moyamoya Disease ◽  
Oxygen Metabolism ◽  
Cerebral Oxygen ◽  
Surgical Revascularization ◽  
Cerebral Oxygen Metabolism

scholarly journals Depressed Cerebral Oxygen Metabolism in Patients with Chronic Renal Failure: A Positron Emission Tomography Study.

2001 ◽  
Vol 34 (7) ◽  
pp. 1149-1155 ◽  
Author(s):  
Hideki Hirakata ◽  
Hidetoshi Kanai ◽  
Hiroshi Nakane ◽  
Ken-ichiro Fujii ◽  
Eriko Hirakata ◽  
...  
Keyword(s):  
Positron Emission Tomography ◽  
Renal Failure ◽  
Chronic Renal Failure ◽  
Oxygen Metabolism ◽  
Emission Tomography ◽  
Positron Emission Tomography Study ◽  
Cerebral Oxygen ◽  
Cerebral Oxygen Metabolism ◽  
Positron Emission

Age-related decline of cerebral oxygen metabolism in normal population detected with positron emission tomography

1992 ◽  
Vol 14 (2) ◽  
pp. 128-131 ◽  
Author(s):  
Hiroto Takada ◽  
Ken Nagata ◽  
Yutaka Hirata ◽  
Yuichi Satoh ◽  
Yasuhito Watahiki ◽  
...  
Keyword(s):  
Positron Emission Tomography ◽  
Normal Population ◽  
Oxygen Metabolism ◽  
Emission Tomography ◽  
Cerebral Oxygen ◽  
Cerebral Oxygen Metabolism ◽  
Age Related ◽  
Positron Emission

Cerebral oxygen metabolism in awake monkeys using positron emission tomography with 15O-gas

NeuroImage ◽  
1998 ◽  
Vol 7 (4) ◽  
pp. S276
Author(s):  
H. Okada ◽  
Y. Ouchi ◽  
E. Yoshikawa ◽  
T. Kakiuchi ◽  
S. Nishiyama ◽  
...  
Keyword(s):  
Positron Emission Tomography ◽  
Oxygen Metabolism ◽  
Emission Tomography ◽  
Cerebral Oxygen ◽  
Cerebral Oxygen Metabolism ◽  
Positron Emission

Hypothermic Modulation of Cerebral Ischemic Injury during Cardiopulmonary Bypass in Pigs 

1998 ◽  
Vol 88 (2) ◽  
pp. 390-402 ◽  
Author(s):  
Brendan P. Conroy ◽  
Cheng Y. Lin ◽  
Larry W. Jenkins ◽  
Douglas S. DeWitt ◽  
Mark H. Zornow ◽  
...  
Keyword(s):  
Cerebrospinal Fluid ◽  
Cardiopulmonary Bypass ◽  
Cerebral Ischemia ◽  
High Performance ◽  
Oxygen Metabolism ◽  
Global Cerebral Ischemia ◽  
Cerebral Oxygen ◽  
Cerebral Oxygen Metabolism ◽  
Sagittal Sinus ◽  
S 100

Background The aim of this study was to determine whether progressive levels of hypothermia (37, 34, 31, or 28 degrees C) during cardiopulmonary bypass (CPB) in pigs reduce the physiologic and metabolic consequences of global cerebral ischemia. Methods Sagittal sinus and cortical microdialysis catheters were inserted into anesthetized pigs. Animals were placed on CPB and randomly assigned to 37 degrees C (n = 10), 34 degrees C (n = 10), 31 degrees C (n = 11), or 28 degrees C (n = 10) management. Next 20 min of global cerebral ischemia was produced by temporarily ligating the innominate and left subclavian arteries, followed by reperfusion, rewarming, and termination of CPB. Cerebral oxygen metabolism (CMRO2) was calculated by cerebral blood flow (radioactive microspheres) and arteriovenous oxygen content gradient. Cortical excitatory amino acids (EAA) by microdialysis were measured using high-performance liquid chromatography. Electroencephalographic (EEG) signals were graded by observers blinded to the protocol. After CPB, cerebrospinal fluid was sampled to test for S-100 protein and the cerebral cortex was biopsied. Results Cerebral oxygen metabolism increased after rewarming from 28 degrees C, 31 degrees C, and 34 degrees C CPB but not in the 37 degrees animals; CMRO2 remained lower with 37 degrees C (1.8 +/- 0.2 ml x min[-1] x 100 g[-1]) than with 28 degrees C (3.1 +/- 0.1 ml x min[-1] x 100 g[-1]; P < 0.05). The EEG scores after CPB were depressed in all groups and remained significantly lower in the 37 degrees C animals. With 28 degrees C and 31 degrees C CPB, EAA concentrations did not change. In contrast, glutamate increased by sixfold during ischemia at 37 degrees C and remained significantly greater during reperfusion in the 34 degrees C and 37 degrees C groups. Cortical biopsy specimens showed no intergroup differences in energy metabolites except two to three times greater brain lactate in the 37 degrees C animals. S-100 protein in cerebrospinal fluid was greater in the 37 degrees C (6 +/- 0.9 microg/l) and 34 degrees C (3.5 +/- 0.5 microg/l) groups than the 31 degrees C (1.9 +/- 0.1 microg/l) and 28 degrees C (1.7 +/- 0.2 microg/l) animals. Conclusions Hypothermia to 28 degrees C and 31 degrees C provides significant cerebral recovery from 20 min of global ischemia during CPB in terms of EAA release, EEG and cerebral metabolic recovery, and S-100 protein release without greater advantage from cooling to 28 degrees C compared with 31 degrees C. In contrast, ischemia during 34 degrees C and particularly 37 degrees C CPB showed greater EAA release and evidence of neurologic morbidity. Cooling to 31 degrees C was necessary to improve acute recovery during global cerebral ischemia on CPB.

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