Document Detail

The permissive nature of blood brain barrier (BBB) opening in edema formation following traumatic brain injury.
MedLine Citation:
PMID:  11449990     Owner:  NLM     Status:  MEDLINE    
The contribution of blood brain barrier opening to traumatic brain edema is not known. This study compares the course of traumatic BBB disruption and edema formation, with the hypothesis that they are not obligately related. Sprague-Dawley rats were divided into three groups: Group A (n = 47)--Impact Acceleration (IAM); Group B (n = 104)--lateral cortical impact (CCI); Group C (n = 26)--IAM + hypoxia & hypotension (THH). BBB integrity was assessed using i.v. markers (Evan's Blue, or gadolinium-DTPA). Edema formation was evaluated with gravimetry, and T1-weighted MRI. In IAM, BBB opened immediately but closed rapidly, and remained closed for at least the next 36 hours whilst 24-hour hemispheric water content (HWC) rose by 0.9% (p < 0.01). In CCI, BBB opened in both hemispheres for up to 4 hours; four hour HWC in the uninjured hemisphere was indistinguishable from Sham, where HWC in the injured hemisphere rose by approximately 1.5% (p < 0.005). We distinguished two THH animals based on Apparent Diffusion Coefficient (ADC) recovery: in ADC-recovery animals 4 hour cortical water content (CWC) was 80.4 +/- 0.6%, cf 81.4 +/- 1.3% in ADC-non-recovery (p < 0.05). In all animals the BBB was open, however two populations of permeability were seen which likely related to flow-limited extravasation of gadolinium. In IAM edema forms despite only brief BBB opening. Although there is diffuse BBB opening with lateral contusion, edema only forms in the injured hemisphere. In THH, edema formation in the face of a widely permeable barrier is driven by ADC changes or cell swelling. Edema formation clearly does not correspond with BBB opening and an open BBB is clearly not required for edema formation. However we hypothesize that a permeable BBB permissively worsens the process, by acting as a low resistance pathway for ion and water movement. These findings are consistent with our general hypothesis that edema formation after TBI is mainly cytotoxic.
A Beaumont; A Marmarou; K Hayasaki; P Barzo; P Fatouros; F Corwin; C Marmarou; J Dunbar
Publication Detail:
Type:  Journal Article    
Journal Detail:
Title:  Acta neurochirurgica. Supplement     Volume:  76     ISSN:  0065-1419     ISO Abbreviation:  Acta Neurochir. Suppl.     Publication Date:  2000  
Date Detail:
Created Date:  2001-07-13     Completed Date:  2001-08-09     Revised Date:  2003-11-14    
Medline Journal Info:
Nlm Unique ID:  100962752     Medline TA:  Acta Neurochir Suppl     Country:  Austria    
Other Details:
Languages:  eng     Pagination:  125-9     Citation Subset:  IM    
Division of Neurosurgery, Medical College of Virginia, Richmond, VA, USA.
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MeSH Terms
Blood-Brain Barrier / physiology*
Brain Concussion / pathology,  physiopathology*
Brain Edema / pathology,  physiopathology*
Capillary Permeability / physiology*
Cerebral Cortex / blood supply,  injuries*,  pathology
Image Enhancement
Magnetic Resonance Imaging
Rats, Sprague-Dawley

From MEDLINE®/PubMed®, a database of the U.S. National Library of Medicine

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