Neuroscience 2003 Abstract
| Presentation Number: | 414.10 |
|---|---|
| Abstract Title: | Magnetic resonance imaging of edema after traumatic brain injury and hypoxia in rats. |
| Authors: |
Bouwhuis, M. G.*1
; van Putten, H. P.1
; Lyeth, B. G.2
; Berman, R. F.2
1Sch. of Med., Univ. Utrecht, Utrecht, The Netherlands 2CA, 13 Kwartelstraat, 3514 ES, |
| Primary Theme and Topics |
Neurological and Psychiatric Conditions - Trauma -- Brain |
| Session: |
414. Trauma: Brain II Poster |
| Presentation Time: | Monday, November 10, 2003 9:00 AM-10:00 AM |
| Location: | Morial Convention Center - Hall F-I, Board # LL3 |
| Keywords: | trauma, imaging, hippocampus, cortex |
Hypoxia and edema are frequent and serious complications of traumatic brain injury (TBI). Therefore, we examined the effects of hypoxia on edema formation after moderate lateral fluid percussion (LFP) injury using NMR diffusion weighted imaging (DWI). Adult Sprague-Dawley rats were separated into 4 groups: sham uninjured (S), hypoxia alone (H), trauma alone (T), trauma and hypoxia (TH). Rats in Groups T and TH received LFP brain injury, with Groups H and TH undergoing 30 min of severe hypoxia (FiO2 = 0.11) immediately after surgery or TBI (respectively). DWIs were obtained at 2, 4, 24 hours and 1 week postinjury and apparent diffusion coefficient (ADC) maps were constructed. Rats in Groups T and TH showed an early decrease (p<0.001) in ADC values in the ipsilateral cortex 4 hr postinjury, followed one week later by elevated ADCs (p<0.05). No significant differences were seen between T and TH groups in cortex. In contrast, the ipsilateral hippocampus for Group TH showed only increasing ADC values. This hyperintensity began at 2 hours after TBI, was significant (p<0.05) by 24 hr, and reached a maximum at 1 week. This hyperintensity was not observed in Group T. Histopathology corresponded well with the pathology observed with MRI. Midline shifts reflecting edema were only observed in TBI animals with little difference between normoxic (T) and hypoxic animals (TH). ADC changes in the cortex support an early cytotoxic edema formation followed by a later development of vasogenic edema. The pattern of ADC changes seen in the hippocampus suggests that the hippocampus might be particularly sensitive to hypoxia and the development of vasogenic edema after TBI. Overall, the addition of hypoxia to brain injury resulted in a small increase in the magnitude of edema in hippocampus and cortex.
Supported by NINDS 39090 and the UCLA Brain Injury Research Center.
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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