Acute and late changes in N-acetyl-aspartate (NAA) as a biochemical marker of the severity of neuronal damage after traumatic brain injury

Rim Al-Samsam, Beat Alessandri, Frank Corwin, Panos Fatouros, Anthony Marmarou, Ross Bullock

Research output: Contribution to journalArticle

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Abstract

Introduction: The content of the brain NAA measured by proton nuclear magnetic resonance spectroscopy (H-NMR) has been used as a marker of neuronal injury in many cerebral pathologies. The objective of this study was to examine the acute and late changes in whole brain NAA (NAAw), measured by H-NMR and the parallel changes of ECF NAA, measured by microdialysis after diffuse traumatic brain injury (TBI). Methods: The Marmarou's impact-acceleration model (weight drop injury, WDI, 500 GM 2m) was used. Three groups were studied: 1) acute changes only in the first 4 hr after WDI (n=7), 2) late changes only at 48 hr after WDI (n=7), 3) sham-operated controls (n=4). NAAw was measured by H-NMR, while ECF NAA was collected using a flexible (CMA/20,4mm) microdialysis probe inserted into the right parietal cortex. The probe was placed before the injury in the acute WDI group and at 48 hr after injury in the late WDI group. Dialysate samples were collected in 10min fractions. A Two-hour stabilization period was used to collect baseline dialysate NAA (NAAd). Baseline control spectra were collected 1 hr before the injury, then at 1-hour intervals for 4 hr in the acute group, and at 48 hr in the late group. Results: The baseline value for NAAd was 7.66±2.7μM. There were no statistically significant changes in NAAd between the sham and the acute group at baseline, 1/2 hr, 1hr, 2hr, 3hr, 4hr. The value of NAAd at 48hr was not significantly different from the sham group baseline value. Baseline NAAw as measured by H-NMR was 14.4±1.8 mM with a NAA/Cr. Ratio of 1.35±0.2. The two values were stable in all groups, with no significant changes between baseline, 1hr, 2hr, 3hr, 4hr and 48hr after WDI. Conclusion: NAA is not a sensitive marker of the severity of neuronal damage after isolated diffuse TBI. Our previous studies have however showed marked increase in NAAd with hypoxic / ischemic events; it may thus be useful clinically in identifying TBI patients with secondary injury.

Original languageEnglish
JournalCritical Care Medicine
Volume27
Issue number1 SUPPL.
StatePublished - Dec 1 1999
Externally publishedYes

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Biomarkers
Wounds and Injuries
Dialysis Solutions
Microdialysis
Parietal Lobe
Brain
Traumatic Brain Injury
N-acetylaspartate
Magnetic Resonance Spectroscopy
Pathology
Weights and Measures
Diffuse Brain Injury

ASJC Scopus subject areas

  • Critical Care and Intensive Care Medicine

Cite this

Al-Samsam, R., Alessandri, B., Corwin, F., Fatouros, P., Marmarou, A., & Bullock, R. (1999). Acute and late changes in N-acetyl-aspartate (NAA) as a biochemical marker of the severity of neuronal damage after traumatic brain injury. Critical Care Medicine, 27(1 SUPPL.).

Acute and late changes in N-acetyl-aspartate (NAA) as a biochemical marker of the severity of neuronal damage after traumatic brain injury. / Al-Samsam, Rim; Alessandri, Beat; Corwin, Frank; Fatouros, Panos; Marmarou, Anthony; Bullock, Ross.

In: Critical Care Medicine, Vol. 27, No. 1 SUPPL., 01.12.1999.

Research output: Contribution to journalArticle

Al-Samsam, R, Alessandri, B, Corwin, F, Fatouros, P, Marmarou, A & Bullock, R 1999, 'Acute and late changes in N-acetyl-aspartate (NAA) as a biochemical marker of the severity of neuronal damage after traumatic brain injury', Critical Care Medicine, vol. 27, no. 1 SUPPL..
Al-Samsam, Rim ; Alessandri, Beat ; Corwin, Frank ; Fatouros, Panos ; Marmarou, Anthony ; Bullock, Ross. / Acute and late changes in N-acetyl-aspartate (NAA) as a biochemical marker of the severity of neuronal damage after traumatic brain injury. In: Critical Care Medicine. 1999 ; Vol. 27, No. 1 SUPPL.
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abstract = "Introduction: The content of the brain NAA measured by proton nuclear magnetic resonance spectroscopy (H-NMR) has been used as a marker of neuronal injury in many cerebral pathologies. The objective of this study was to examine the acute and late changes in whole brain NAA (NAAw), measured by H-NMR and the parallel changes of ECF NAA, measured by microdialysis after diffuse traumatic brain injury (TBI). Methods: The Marmarou's impact-acceleration model (weight drop injury, WDI, 500 GM 2m) was used. Three groups were studied: 1) acute changes only in the first 4 hr after WDI (n=7), 2) late changes only at 48 hr after WDI (n=7), 3) sham-operated controls (n=4). NAAw was measured by H-NMR, while ECF NAA was collected using a flexible (CMA/20,4mm) microdialysis probe inserted into the right parietal cortex. The probe was placed before the injury in the acute WDI group and at 48 hr after injury in the late WDI group. Dialysate samples were collected in 10min fractions. A Two-hour stabilization period was used to collect baseline dialysate NAA (NAAd). Baseline control spectra were collected 1 hr before the injury, then at 1-hour intervals for 4 hr in the acute group, and at 48 hr in the late group. Results: The baseline value for NAAd was 7.66±2.7μM. There were no statistically significant changes in NAAd between the sham and the acute group at baseline, 1/2 hr, 1hr, 2hr, 3hr, 4hr. The value of NAAd at 48hr was not significantly different from the sham group baseline value. Baseline NAAw as measured by H-NMR was 14.4±1.8 mM with a NAA/Cr. Ratio of 1.35±0.2. The two values were stable in all groups, with no significant changes between baseline, 1hr, 2hr, 3hr, 4hr and 48hr after WDI. Conclusion: NAA is not a sensitive marker of the severity of neuronal damage after isolated diffuse TBI. Our previous studies have however showed marked increase in NAAd with hypoxic / ischemic events; it may thus be useful clinically in identifying TBI patients with secondary injury.",
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AU - Corwin, Frank

AU - Fatouros, Panos

AU - Marmarou, Anthony

AU - Bullock, Ross

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N2 - Introduction: The content of the brain NAA measured by proton nuclear magnetic resonance spectroscopy (H-NMR) has been used as a marker of neuronal injury in many cerebral pathologies. The objective of this study was to examine the acute and late changes in whole brain NAA (NAAw), measured by H-NMR and the parallel changes of ECF NAA, measured by microdialysis after diffuse traumatic brain injury (TBI). Methods: The Marmarou's impact-acceleration model (weight drop injury, WDI, 500 GM 2m) was used. Three groups were studied: 1) acute changes only in the first 4 hr after WDI (n=7), 2) late changes only at 48 hr after WDI (n=7), 3) sham-operated controls (n=4). NAAw was measured by H-NMR, while ECF NAA was collected using a flexible (CMA/20,4mm) microdialysis probe inserted into the right parietal cortex. The probe was placed before the injury in the acute WDI group and at 48 hr after injury in the late WDI group. Dialysate samples were collected in 10min fractions. A Two-hour stabilization period was used to collect baseline dialysate NAA (NAAd). Baseline control spectra were collected 1 hr before the injury, then at 1-hour intervals for 4 hr in the acute group, and at 48 hr in the late group. Results: The baseline value for NAAd was 7.66±2.7μM. There were no statistically significant changes in NAAd between the sham and the acute group at baseline, 1/2 hr, 1hr, 2hr, 3hr, 4hr. The value of NAAd at 48hr was not significantly different from the sham group baseline value. Baseline NAAw as measured by H-NMR was 14.4±1.8 mM with a NAA/Cr. Ratio of 1.35±0.2. The two values were stable in all groups, with no significant changes between baseline, 1hr, 2hr, 3hr, 4hr and 48hr after WDI. Conclusion: NAA is not a sensitive marker of the severity of neuronal damage after isolated diffuse TBI. Our previous studies have however showed marked increase in NAAd with hypoxic / ischemic events; it may thus be useful clinically in identifying TBI patients with secondary injury.

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