A Daoust1, S Dodd2, G Nair3, N Bouraoud4, S Jacobson5, S Walbridge6, D S Reich7, A Koretsky8. 1. National Institute of Neurological Disorders and Stroke, National Institutes of Health, Bethesda, MD 20892, United States. Electronic address: alexia.daoust@nih.gov. 2. National Institute of Neurological Disorders and Stroke, National Institutes of Health, Bethesda, MD 20892, United States. Electronic address: doddst@ninds.nih.gov. 3. National Institute of Neurological Disorders and Stroke, National Institutes of Health, Bethesda, MD 20892, United States. Electronic address: govind.bhagavatheeshwaran@nih.gov. 4. National Institute of Neurological Disorders and Stroke, National Institutes of Health, Bethesda, MD 20892, United States. Electronic address: bouraoudn@ninds.nih.gov. 5. National Institute of Neurological Disorders and Stroke, National Institutes of Health, Bethesda, MD 20892, United States. Electronic address: JacobsonS@ninds.nih.gov. 6. National Institute of Neurological Disorders and Stroke, National Institutes of Health, Bethesda, MD 20892, United States. Electronic address: stuartwalbridge@mail.nih.gov. 7. National Institute of Neurological Disorders and Stroke, National Institutes of Health, Bethesda, MD 20892, United States. Electronic address: reichds@ninds.nih.gov. 8. National Institute of Neurological Disorders and Stroke, National Institutes of Health, Bethesda, MD 20892, United States. Electronic address: KoretskyA@ninds.nih.gov.
Abstract
PURPOSE: To evaluate the biophysical processes that generate specific T2 values and their relationship to specific cerebrospinal fluid (CSF) content. MATERIALS AND METHODS: CSF T2s were measured ex vivo (14.1T) from isolated CSF collected from human, rat and non-human primate. CSF T2s were also measured in vivo at different field strength in human (3 and 7T) and rodent (1, 4.7, 9,4 and 11.7T) using different pulse sequences. Then, relaxivities of CSF constituents were measured, in vitro, to determine the major molecule responsible for shortening CSF T2 (2s) compared to saline T2 (3s). The impact of this major molecule on CSF T2 was then validated in rodent, in vivo, by the simultaneous measurement of the major molecule concentration and CSF T2. RESULTS: Ex vivo CSF T2 was about 2.0s at 14.1T for all species. In vivo human CSF T2 approached ex vivo values at 3T (2.0s) but was significantly shorter at 7T (0.9s). In vivo rodent CSF T2 decreased with increasing magnetic field and T2 values similar to the in vitro ones were reached at 1T (1.6s). Glucose had the largest contribution of shortening CSF T2in vitro. This result was validated in rodent in vivo, showing that an acute change in CSF glucose by infusion of glucose into the blood, can be monitored via changes in CSF T2 values. CONCLUSION: This study opens the possibility of monitoring glucose regulation of CSF at the resolution of MRI by quantitating T2.
PURPOSE: To evaluate the biophysical processes that generate specific T2 values and their relationship to specific cerebrospinal fluid (CSF) content. MATERIALS AND METHODS: CSF T2s were measured ex vivo (14.1T) from isolated CSF collected from human, rat and non-human primate. CSF T2s were also measured in vivo at different field strength in human (3 and 7T) and rodent (1, 4.7, 9,4 and 11.7T) using different pulse sequences. Then, relaxivities of CSF constituents were measured, in vitro, to determine the major molecule responsible for shortening CSF T2 (2s) compared to saline T2 (3s). The impact of this major molecule on CSF T2 was then validated in rodent, in vivo, by the simultaneous measurement of the major molecule concentration and CSF T2. RESULTS: Ex vivo CSF T2 was about 2.0s at 14.1T for all species. In vivo human CSF T2 approached ex vivo values at 3T (2.0s) but was significantly shorter at 7T (0.9s). In vivo rodent CSF T2 decreased with increasing magnetic field and T2 values similar to the in vitro ones were reached at 1T (1.6s). Glucose had the largest contribution of shortening CSF T2in vitro. This result was validated in rodent in vivo, showing that an acute change in CSF glucose by infusion of glucose into the blood, can be monitored via changes in CSF T2 values. CONCLUSION: This study opens the possibility of monitoring glucose regulation of CSF at the resolution of MRI by quantitating T2.
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