Literature DB >> 14753449

Correlation of lesion volume and brain swelling from a focal brain trauma.

J Eriskat1, M Fürst, M Stoffel, A Baethmann.   

Abstract

Brain edema and secondary growth of a traumatic brain tissue necrosis are important manifestations of secondary brain damage and of prognostic significance in severe head injury. Aim of the current study was to analyze the interdependency of the resulting brain swelling from the size of the focal traumatic lesion. Male Sprague-Dawley rats were intubated and mechanically ventilated. A trephination was made over the left parietal cortex for induction of a cold lesion. Different injury severities were achieved by varying the contact time of the cooled copper-cylinder and the exposed cortex. Animals were randomized into 12 experimental groups. Hemispheric brain swelling was measured in groups A1-A6 (n = 4-8) by gravimetry 24 hrs after lesions of six increasing severity levels. Correspondingly, in animals of groups B1-B6 (n = 5-7) the volume of necrosis was planimetrically assessed in histological serial sections of the brain obtained 24 hrs after trauma of different severity. In groups A1-A6. hemispheric brain swelling (increase in weight) was growing with increasing contact duration of the cold probe with the exposed cerebral cortex, i.e. from 7.7 +/- 0.4% (5 s) to a maximum of 9.9 +/- 0.5% (25 s). Longer contact periodes (30 s) were not further effective to increase hemispheric brain swelling. The contact times and extent of swelling were linearly correlated between 5 s and 25 s (r = 0.47; p < 0.01). The volume of necrosis in groups B1-B6 increased from 35.7 +/- 3.7 mm3 (5 s) to 106.3 +/- 10.3 mm3 (30 s). There was again a linear correlation between the duration of contact of the cold probe (i.e. injury severity) with the brain cortex and the volume of necrosis (r = 0.77; p < 0.01). Accordingly. the lesion volume could be increased in a reproducible manner from 35.7 up to 106.3 mm3 by extending the contact times of the cooling device and cerebral cortex. Hemispheric swelling, predominantly due to vasogenic brain edema, was expanding in relationship with the volume of necrosis.

Entities:  

Mesh:

Year:  2003        PMID: 14753449     DOI: 10.1007/978-3-7091-0651-8_57

Source DB:  PubMed          Journal:  Acta Neurochir Suppl        ISSN: 0065-1419


  4 in total

1.  Experimental traumatic brain injury.

Authors:  Christiane Albert-Weissenberger; Anna-Leena Sirén
Journal:  Exp Transl Stroke Med       Date:  2010-08-13

2.  Multicolor fluorescence imaging of traumatic brain injury in a cryolesion mouse model.

Authors:  Bryan A Smith; Bang-Wen Xie; Ermond R van Beek; Ivo Que; Vicky Blankevoort; Shuzhang Xiao; Erin L Cole; Mathias Hoehn; Eric L Kaijzel; Clemens W G M Löwik; Bradley D Smith
Journal:  ACS Chem Neurosci       Date:  2012-04-07       Impact factor: 4.418

3.  An experimental protocol for mimicking pathomechanisms of traumatic brain injury in mice.

Authors:  Christiane Albert-Weißenberger; Csanád Várrallyay; Furat Raslan; Christoph Kleinschnitz; Anna-Leena Sirén
Journal:  Exp Transl Stroke Med       Date:  2012-02-02

Review 4.  Modeling trauma in rats: similarities to humans and potential pitfalls to consider.

Authors:  Birte Weber; Ina Lackner; Melanie Haffner-Luntzer; Annette Palmer; Jochen Pressmar; Karin Scharffetter-Kochanek; Bernd Knöll; Hubert Schrezenemeier; Borna Relja; Miriam Kalbitz
Journal:  J Transl Med       Date:  2019-09-05       Impact factor: 5.531

  4 in total

北京卡尤迪生物科技股份有限公司 © 2022-2023.