| 11 th Annual Pediatric Critical Care Colloquium |
| Session/Time | Neurology/Fri, 10:00 - 12:00 PM |
| Title | Extracelluar N-Acetyl- Aspartate as a Biochemical Marker of the Severity of Neuronal Damage Following Acute Brain Injury |
| Author | R AL-Sarnsam, B Alessandri, A Marmarou, R Bullock |
| Affiliation | Divisions of Neurosurgery and Pediatric Critical Care Medicine, Medical College of Virginia, Richmond, VA |
| Introduction | N-Acetyl-Aspartate (NAA) is a major constituent of mammalian neurons. It is characterized by a high tissue concentration and a high tissue to e=acellular gradient under normal conditions. In the developing CNS, NAA plays a key role in the myelinogenesis of nerve cells, whereas its function in the mature brain is still obscure. Tle content of NAA in the brain measured by proton nuclear magnetic resonance spectroscopy has been used as a marker of neuronal injury in several neurodegenerative diseases and in perinatal hypoxia. No transport system(s) for NAA across the cell membrane has been reported. Hence we hypothesized that changes in ECF NAA can be used as an indicator of acute neuronal damage and cell death. |
| Method | We evaluated ECF NkA concentration using niicrodialysis in the rat cortex following diffuse traumatic brain injury (TBI) alone and TBI followed by secondary insult. The Marrnarou's impact-acceleration model (Nveight drop injury, WDI) was used. Three g-roups, vere studied: 1. VIDI alone (500gm, 2 m), 2. WDI plus dili minutes of hypoxia (PaO.2- 45 mmHg) and hypotension (MABP - 45 mmHg), 3. Hypoxia-Hypotension (HH) alone. Interstitial NAA was collected using a flexible (CMA/20,4mm) micro6alysis probe inserted into the ri-ht parietal cortex through the left orbit, where it lies directly under the impact site. The probe was placed before the injury and secured in place. Then it was continuously perfused with 0.9 % NS at 2 ul/min and dialysate samples were collected in l0 min fractions. The control data and stabilization period for microdialysis was established during the first 2 hr after probe insertion and before injury. NAA analysis was done using HPLC. |
| Result | The baseline value for dialysa e NAA (NAAd) in the rats was 8.85±3.5W. NAAd was highly variable in all groups. The WDI rroup liad an early and transient increase in NAAd after trauina (2.7x baseline at 30inin for 30min then normalized). The WDI plus HH group showed a lateind persistent increase (3.5x baseline at 2 hr, persisted throughtout the study). The HH group had a smaller but persistent increase in NAAdj (1.6 x biseline at I gr, persisted throughout the study). |
| Conclusion | Secondary hypoxiz / ischemic events are required io produce a proloiiecd increase in NAAd; it may thus be useful clinically in differentiating between pure diffuse axonal injury anddiffuse axonal injury with secondary insults. |
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