Neuroscience 2003 Abstract
| Presentation Number: | 107.17 |
|---|---|
| Abstract Title: | PET measures of cerebral blood flow, metabolism, and vascular reactivity within MRI hyperintensities in humans. |
| Authors: |
Mensh, B. D.*1
; Nobler, M. S.1
; Lisanby, S. H.1
; Koetitz, R.1
; Sackeim, H. A.1
1Biological Psychiatry, Columbia Univ, New York, NY |
| Primary Theme and Topics |
Neurological and Psychiatric Conditions - Brain Metabolism -- Blood flow |
| Secondary Theme and Topics | Neurological and Psychiatric Conditions<br />- Brain Metabolism<br />-- Blood brain barrier |
| Session: |
107. Brain Metabolism: Blood Flow I Poster |
| Presentation Time: | Saturday, November 8, 2003 1:00 PM-2:00 PM |
| Location: | Morial Convention Center - Hall F-I, Board # UU46 |
| Keywords: | leukoaraiosis, ischemia, encephalomalacia, hypoperfusion |
A common structural MRI abnormality is punctate regions of hyperintensity (HI, also called leukoaraiosis or encephalomalacia) on T2-weighted or FLAIR scans. These abnormalities occur in periventricular white, deep white, and subcortical gray matter, increase in frequency with aging and in specific neurological and psychiatric disorders. Previous research linked HIs to hypoperfusion. To further characterize their pathophysiology, we measured cerebral blood flow (CBF), metabolic rate (CMR), and vascular reactivity (CVR) within the HIs of 26 elderly participants.
Hyperintensities were segmented on FLAIR images by a seed-growing algorithm which identified the borders of lesions that had been seeded by an experienced rater. Positron emission tomograms (PET), using O15-H2O and F18-FDG (for measures of CBF and CMR, respectively), were coregistered to the FLAIRs. The CBF scan was repeated during inhalation of 5% carbon dioxide, a potent vasodilator, providing measures of CVR. Anatomical regions were defined on each participant’s T1-weighted MRI, using a semi-automated segmentation technique.
Substantial deficits in CBF and CMR were found in periventricular and deep white matter HIs compared to normal appearing white matter. Subcortical HIs, involving the putamen and globus pallidus, also had lower CBF and CMR than surrounding normal tissue. However, there was a trend towards increased vascular reactivity within deep and periventricular white matter HIs.
The findings represent the first demonstration of concomitant CBF and CMR deficits within specific regions of T2-weighted hyperintensity. This indicates that the hypoperfusion within these lesions is sufficient to compromise their metabolic requirements, contrary to the view that a compensatory process involving increased oxygen extraction is sufficient to preserve metabolism. If this ischemic process is progressive, it should result in tissue death.
Hyperintensities were segmented on FLAIR images by a seed-growing algorithm which identified the borders of lesions that had been seeded by an experienced rater. Positron emission tomograms (PET), using O15-H2O and F18-FDG (for measures of CBF and CMR, respectively), were coregistered to the FLAIRs. The CBF scan was repeated during inhalation of 5% carbon dioxide, a potent vasodilator, providing measures of CVR. Anatomical regions were defined on each participant’s T1-weighted MRI, using a semi-automated segmentation technique.
Substantial deficits in CBF and CMR were found in periventricular and deep white matter HIs compared to normal appearing white matter. Subcortical HIs, involving the putamen and globus pallidus, also had lower CBF and CMR than surrounding normal tissue. However, there was a trend towards increased vascular reactivity within deep and periventricular white matter HIs.
The findings represent the first demonstration of concomitant CBF and CMR deficits within specific regions of T2-weighted hyperintensity. This indicates that the hypoperfusion within these lesions is sufficient to compromise their metabolic requirements, contrary to the view that a compensatory process involving increased oxygen extraction is sufficient to preserve metabolism. If this ischemic process is progressive, it should result in tissue death.
Supported by MH35636,MH55646
Sample Citation:
[Authors]. [Abstract Title]. Program No. XXX.XX. 2003 Neuroscience Meeting Planner. New Orleans, LA: Society for Neuroscience, 2003. Online.
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