naa a22 4500 510799647 CHVBK 20180411083349.0 cr unu---uuuuu 180411e20131001xx s 000 0 eng 10.1007/s12028-013-9871-9 doi (NATIONALLICENCE)springer-10.1007/s12028-013-9871-9 Impact of Methamphetamine on Regional Metabolism and Cerebral Blood Flow After Traumatic Brain Injury [Elektronische Daten] [Kristine O'Phelan, Thomas Ernst, Dalnam Park, Andrew Stenger, Katherine Denny, Deborah Green, Cherylee Chang, Linda Chang] Background: Substance abuse is a frequent comorbid condition among patients with traumatic brain injury (TBI), but little is known about its potential additive or interactive effects on tissue injury or recovery from TBI. This study aims to evaluate changes in regional metabolism and cerebral perfusion in subjects who used methamphetamine (METH) prior to sustaining a TBI. We hypothesized that METH use would decrease pericontusional cerebral perfusion and markers of neuronal metabolism, in TBI patients compared to those without METH use. Methods: This is a single center prospective observational study. Adults with moderate and severe TBI were included. MRI scanning was performed on a 3 Tesla scanner. MP-RAGE and FLAIR sequences as well as Metabolite spectra of NAA and lactate in pericontusional and contralateral voxels identified on the MP-RAGE scans. A spiral-based FAIR sequence was used for the acquisition of cerebral blood flow (CBF) maps. Regional CBF images were analyzed using ImageJ open source software. Pericontusional and contralateral CBF, NAA, and lactate were assessed in the entire cohort and in the METH and non-METH groups. Results: Seventeen subjects completed the MR studies. Analysis of entire cohort: pericontusional NAA concentrations (5.81±2.0mM/kg) were 12% lower compared to the contralateral NAA (6.98±1.2mM/kg; p=0.03). Lactate concentrations and CBF were not significantly different between the two regions; however, regional CBF was equally reduced in the two regions. Subgroup analysis: 41% of subjects tested positive for METH. The mean age, Glasgow Coma Scale, and time to scan did not differ between groups. The two subject groups also had similar regional NAA and lactate. Pericontusional CBF was 60% lower in the METH users than the non-users, p=0.04; contralateral CBF did not differ between the groups. Conclusion: This small study demonstrates that tissue metabolism is regionally heterogeneous after TBI and pericontusional perfusion was significantly reduced in the METH subgroup. Springer Science+Business Media New York, 2013 Adult brain injury nationallicence MRI nationallicence Blood flow nationallicence Metabolism nationallicence Alcohol and drug abuse nationallicence O'Phelan Kristine Department of Neurology, Miller School of Medicine, University of Miami, 1120 NW 14th Street, 33136, Miami, FL, USA aut Ernst Thomas Neuroscience and MR Research Program, Department of Medicine, John A Burns School of Medicine, University of Hawaii at Manoa, 1356 Lusitana Street, 7th Floor, 96813, Honolulu, HI, USA aut Park Dalnam School of Medicine, Oregon Health and Science University, 3181 Southwest Sam Jackson Park Road, 97239, Portland, OR, USA aut Stenger Andrew Neuroscience and MR Research Program, Department of Medicine, John A Burns School of Medicine, University of Hawaii at Manoa, 1356 Lusitana Street, 7th Floor, 96813, Honolulu, HI, USA aut Denny Katherine Miller School of Medicine, University of Miami, 1120 NW 14th Street, 33136, Miami, FL, USA aut Green Deborah Department of Neurology, Boston Medical Center, Boston University School of Medicine, Neurology 72 E. Concord St, C-3, 02118, Boston, MA, USA aut Chang Cherylee Neuroscience and MR Research Program, Department of Medicine, John A Burns School of Medicine, University of Hawaii at Manoa, 1356 Lusitana Street, 7th Floor, 96813, Honolulu, HI, USA aut Chang Linda Neuroscience and MR Research Program, Department of Medicine, John A Burns School of Medicine, University of Hawaii at Manoa, 1356 Lusitana Street, 7th Floor, 96813, Honolulu, HI, USA aut Neurocritical Care Springer US; http://www.springer-ny.com 19/2(2013-10-01), 183-191 1541-6933 19:2<183 2013 19 12028 https://doi.org/10.1007/s12028-013-9871-9 text/html Onlinezugriff via DOI 1 research-article jats NATIONALLICENCE 856 40 https://doi.org/10.1007/s12028-013-9871-9 text/html Onlinezugriff via DOI NATIONALLICENCE 700 1- O'Phelan Kristine Department of Neurology, Miller School of Medicine, University of Miami, 1120 NW 14th Street, 33136, Miami, FL, USA aut NATIONALLICENCE 700 1- Ernst Thomas Neuroscience and MR Research Program, Department of Medicine, John A Burns School of Medicine, University of Hawaii at Manoa, 1356 Lusitana Street, 7th Floor, 96813, Honolulu, HI, USA aut NATIONALLICENCE 700 1- Park Dalnam School of Medicine, Oregon Health and Science University, 3181 Southwest Sam Jackson Park Road, 97239, Portland, OR, USA aut NATIONALLICENCE 700 1- Stenger Andrew Neuroscience and MR Research Program, Department of Medicine, John A Burns School of Medicine, University of Hawaii at Manoa, 1356 Lusitana Street, 7th Floor, 96813, Honolulu, HI, USA aut NATIONALLICENCE 700 1- Denny Katherine Miller School of Medicine, University of Miami, 1120 NW 14th Street, 33136, Miami, FL, USA aut NATIONALLICENCE 700 1- Green Deborah Department of Neurology, Boston Medical Center, Boston University School of Medicine, Neurology 72 E. Concord St, C-3, 02118, Boston, MA, USA aut NATIONALLICENCE 700 1- Chang Cherylee Neuroscience and MR Research Program, Department of Medicine, John A Burns School of Medicine, University of Hawaii at Manoa, 1356 Lusitana Street, 7th Floor, 96813, Honolulu, HI, USA aut NATIONALLICENCE 700 1- Chang Linda Neuroscience and MR Research Program, Department of Medicine, John A Burns School of Medicine, University of Hawaii at Manoa, 1356 Lusitana Street, 7th Floor, 96813, Honolulu, HI, USA aut NATIONALLICENCE 773 0- Neurocritical Care Springer US; http://www.springer-ny.com 19/2(2013-10-01), 183-191 1541-6933 19:2<183 2013 19 12028 Metadata rights reserved Springer special CC-BY-NC licence nationallicence BK010053 XK010053 XK010000 NATIONALLICENCE NATIONALLICENCE NL-springer