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Blood-brain barrier permeability following traumatic brain injury.

Jungner, Mårten LU ; Siemund, Roger LU ; Venturoli, Daniele LU ; Reinstrup, Peter LU ; Scsalén, Wilhelm and Bentzer, Peter LU (2016) In Minerva Anestesiologica 82(5). p.525-533
Abstract

BACKGROUND: Brain edema and intracranial hypertension is deleterious after traumatic brain injury (TBI), but the underlying pathophysiology is complex and poorly understood. One major subject of controversy is the time course and extent of blood-brain barrier (BBB) dysfunction following trauma, and previous studies in humans have only provided semi-quantitative data. The objective of the present study was therefore to quantify changes in BBB-permeability in the early course of TBI, when brain edema is still evolving. METHODS: Sixteen non-consecutive brain trauma patients and two controls were included. Following i.v. injection of iohexol and CT perfusion scans, patients were scanned eight times from 4 to 25 minutes. Blood to brain... (More)

BACKGROUND: Brain edema and intracranial hypertension is deleterious after traumatic brain injury (TBI), but the underlying pathophysiology is complex and poorly understood. One major subject of controversy is the time course and extent of blood-brain barrier (BBB) dysfunction following trauma, and previous studies in humans have only provided semi-quantitative data. The objective of the present study was therefore to quantify changes in BBB-permeability in the early course of TBI, when brain edema is still evolving. METHODS: Sixteen non-consecutive brain trauma patients and two controls were included. Following i.v. injection of iohexol and CT perfusion scans, patients were scanned eight times from 4 to 25 minutes. Blood to brain transfer constant (Ki) for iohexol (molecular weight 821 D), reflecting permeability and available area for diffusion, was calculated offline by Patlak plot analysis of the enhancement curves of intracerebral large venous vessels and pericontusional brain parenchyma. RESULTS : In non-ischemic tissue surrounding contusions and hematomas Ki was increased 2-to 10-fold compared to normal tissue, reaching maximal values of 0.5 mL/min/100 g. In non-injured areas and in controls Ki was about 0.06 mL/min/100 g. The increase was more pronounced in the most severely injured patients, and was detectable within 24 hours after trauma and up to five days after. CONCLUSIONS: Our results suggest that traumatic brain injury is associated with early focal increases in small molecular BBB-permeability. The results indicate that in the injured brain, capillary hydrostatic and oncotic pressures may influence edema formation.

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author
; ; ; ; and
organization
publishing date
type
Contribution to journal
publication status
published
subject
keywords
Blood-brain barrier, Brain injuries, Linear models, Permeability
in
Minerva Anestesiologica
volume
82
issue
5
pages
9 pages
publisher
Edizioni Minerva Medica S.p.A.
external identifiers
  • pmid:26613239
  • scopus:84971267199
ISSN
1827-1596
language
English
LU publication?
yes
id
2a6e6cd6-16a4-4710-b61b-9a2f206e98b4 (old id 8234390)
alternative location
http://www.ncbi.nlm.nih.gov/pubmed/26613239?dopt=Abstract
date added to LUP
2016-04-04 08:53:55
date last changed
2022-04-23 18:09:59
@article{2a6e6cd6-16a4-4710-b61b-9a2f206e98b4,
  abstract     = {{<p>BACKGROUND: Brain edema and intracranial hypertension is deleterious after traumatic brain injury (TBI), but the underlying pathophysiology is complex and poorly understood. One major subject of controversy is the time course and extent of blood-brain barrier (BBB) dysfunction following trauma, and previous studies in humans have only provided semi-quantitative data. The objective of the present study was therefore to quantify changes in BBB-permeability in the early course of TBI, when brain edema is still evolving. METHODS: Sixteen non-consecutive brain trauma patients and two controls were included. Following i.v. injection of iohexol and CT perfusion scans, patients were scanned eight times from 4 to 25 minutes. Blood to brain transfer constant (Ki) for iohexol (molecular weight 821 D), reflecting permeability and available area for diffusion, was calculated offline by Patlak plot analysis of the enhancement curves of intracerebral large venous vessels and pericontusional brain parenchyma. RESULTS : In non-ischemic tissue surrounding contusions and hematomas Ki was increased 2-to 10-fold compared to normal tissue, reaching maximal values of 0.5 mL/min/100 g. In non-injured areas and in controls Ki was about 0.06 mL/min/100 g. The increase was more pronounced in the most severely injured patients, and was detectable within 24 hours after trauma and up to five days after. CONCLUSIONS: Our results suggest that traumatic brain injury is associated with early focal increases in small molecular BBB-permeability. The results indicate that in the injured brain, capillary hydrostatic and oncotic pressures may influence edema formation.</p>}},
  author       = {{Jungner, Mårten and Siemund, Roger and Venturoli, Daniele and Reinstrup, Peter and Scsalén, Wilhelm and Bentzer, Peter}},
  issn         = {{1827-1596}},
  keywords     = {{Blood-brain barrier; Brain injuries; Linear models; Permeability}},
  language     = {{eng}},
  number       = {{5}},
  pages        = {{525--533}},
  publisher    = {{Edizioni Minerva Medica S.p.A.}},
  series       = {{Minerva Anestesiologica}},
  title        = {{Blood-brain barrier permeability following traumatic brain injury.}},
  url          = {{http://www.ncbi.nlm.nih.gov/pubmed/26613239?dopt=Abstract}},
  volume       = {{82}},
  year         = {{2016}},
}