Predominance of cellular edema in traumatic brain swelling in patients with severe head injuries

Marmarou, Anthony; Signoretti, Stefano; Fatouros, Panos P.; Portella, Gina; Aygok, Gunes A.; Bullock, M. Ross

doi:10.3171/jns.2006.104.5.720

Cited by 209 publications

(103 citation statements)

References 33 publications

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“…This could be due to brain water accumulation being more reduced after diffuse TBI than after occlusion of a terminal brain artery in rats: 0.5% to 1% in this TBI model (Cernak et al, 2004) versus 2% to 4% in models of ischemia (Barbier et al, 2005;Lin et al, 2000). Similarly, moderate brain water accumulation was reported in diffusely head-injured patients presenting brain swelling and concomitant elevated intracranial pressure (Marmarou et al, 2006).…”

Section: Discussionmentioning

confidence: 95%

Erythropoietin Protects from Post-Traumatic Edema in the Rat Brain

Verdonck

Lahrech

Francony

et al. 2007

J Cereb Blood Flow Metab

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Erythropoietin (Epo) is gaining interest in various neurological insults as a possible neuroprotective agent. We determined the effects of recombinant human Epo (rhEpo, 5000 IU per kg bw) on brain edema induced in rats by traumatic brain injury (TBI; impact-acceleration model; rhEpo administration 30 mins after injury). Magnetic resonance imaging (MRI) and a gravimetric technique were applied. In the MRI experiments, the apparent diffusion coefficient (ADC) and the tissue T 1 relaxation time were measured hourly in the neocortex and caudoputamen, during a 6 h time span after TBI. In the gravimetric experiments, brain water content (BWC) was determined in these two regions, 6 h after TBI. Apparent diffusion coefficient measurements showed that rhEpo decreased brain edema early and durably. Gravimetric measurements showed that rhEpo decreased BWC at H 6 in the neocortex as well as in the caudoputamen. No significant differences in ADC, in T 1 , or in BWC were found between rhEpo treated-TBI rats and sham-operated rats. Our findings show that posttraumatic administration of rhEpo can significantly reduce the development of brain edema in a model of diffuse TBI. Further studies should be conducted to identify the biochemical mechanisms involved in these immediate effects and to assess the use of rhEpo as a possible therapy for posttraumatic brain edema.

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Section: Discussionmentioning

confidence: 95%

Erythropoietin Protects from Post-Traumatic Edema in the Rat Brain

Verdonck

Lahrech

Francony

et al. 2007

J Cereb Blood Flow Metab

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“…Diffuse damage or a stroke may also result in diffuse swelling of the brain, but in all cases, swollen regions are associated with dead, dying or damaged cells (Kawamata et al 2007). Imaging studies have identified cytotoxic swelling as the most probable cause of this oedema (Vorisek et al 2002;Maeda et al 2003;van Pul et al 2005;Marmarou et al 2006b;Kuroiwa et al 2007).…”

Section: Discussionmentioning

confidence: 99%

Fixed negative charge and the Donnan effect: a description of the driving forces associated with brain tissue swelling and oedema

Elkin

Shaik

Morrison

2010

Phil. Trans. R. Soc. A.

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Cerebral oedema or brain tissue swelling is a significant complication following traumatic brain injury or stroke that can increase the intracranial pressure (ICP) and impair blood flow. Here, we have identified a potential driver of oedema: the negatively charged molecules fixed within cells. This fixed charge density (FCD), once exposed, could increase ICP through the Donnan effect. We have shown that metabolic processes and membrane integrity are required for concealing this FCD as slices of rat cortex swelled immediately (within 30 min) following dissection if treated with 2 deoxyglucose + cyanide (2DG+CN) or Triton X-100. Slices given ample oxygen and glucose, however, did not swell significantly. We also found that dead brain tissue swells and shrinks in response to changes in ionic strength of the bathing medium, which suggests that the Donnan effect is capable of pressurizing and swelling brain tissue. As predicted, a non-ionic osmolyte, 1,2 propanediol, elicited no volume change at 2000 × 10 −3 osmoles l −1 (Osm). Swelling data were well described by triphasic mixture theory with the calculated reference state FCD similar to that measured with a 1,9 dimethylmethylene blue assay. Taken together, these data suggest that intracellular fixed charges may contribute to the driving forces responsible for brain swelling.

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“…The degree of this type of SIS will depend on which phase of metabolic recovery the brain is in when the second concussion occurs. The severe brain swelling observed in SIS (11,14,21,44,55,64) is probably attributable to the fact that the second insult took place when the cells were still intensely engaged in restoration of their energetic integrity and were unable to withstand further mitochondrial damage, thus experiencing uncontrolled swelling and massive NAA loss (47).…”

Section: Significance Of Posttraumatic Naa Reduction and Recoverymentioning

confidence: 99%

Temporal Window of Metabolic Brain Vulnerability to Concussion

et al. 2008

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OBJECTIVE:In the present study, the occurrence of the temporal window of brain vulnerability was evaluated in concussed athletes by measuring N-acetylaspartate (NAA) using proton magnetic resonance ( 1 H-MR) spectroscopy. METHODS: Thirteen nonprofessional athletes who had a sport-related concussive head injury were examined for NAA determination by means of 1 H-MR spectroscopy at 3, 15, and 30 days postinjury. All athletes but three suspended their physical activity. Those who continued their training had a second concussive event and underwent further examination at 45 days from the initial injury. The single case of one professional boxer, who was studied before the match and 4, 7, 15, and 30 days after a knockout, is also presented. Before each magnetic resonance examination, patients were asked for symptoms of mild traumatic brain injury, including physical, cognitive, emotional, and sleep disturbances. Data for 1 H-MR spectroscopy recorded in five normal, age-matched, control volunteers, who were previously screened to exclude previous head injuries, were used for comparison. Semiquantitative analysis of NAA relative to creatine (Cr)-and choline (Cho)-containing compounds was performed from proton spectra obtained with a 3-T magnetic resonance system. RESULTS: Regarding the values of the NAA-to-Cr ratio (2.21 Ϯ 0.11) recorded in control patients, singly concussed athletes, at 3 days after the concussion, showed a decrease of 18.5% (1.80 Ϯ 0.04; P Ͻ 0.001). Only a modest 3% recovery was observed at 15 days (1.88 Ϯ 0.1; P Ͻ 0.001); at 30 days postinjury, the NAA-to-Cr ratio was 2.15 Ϯ 0.1, revealing full metabolic recovery with values not significantly different from those of control patients. These patients declared complete resolution of symptoms at the time of the 3-day study. The three patients who had a second concussive injury before the 15-day study showed an identical decrease of the NAA-to-Cr ratio at 3 days (1.78 Ϯ 0.08); however, at 15 days after the second injury, a further diminution of the NAA-to-Cr ratio occurred (1.72 Ϯ 0.07; P Ͻ 0.05 with respect to singly concussed athletes). At 30 days, the NAAto-Cr ratio was 1.82 Ϯ 0.1, and at 45 days postinjury, the NAA-to-Cr ratio showed complete recovery (2.07 Ϯ 0.1; not significant with respect to control patients). This group of patients declared a complete resolution of symptoms at the time of the 30-day study. CONCLUSION: Results of this pilot study carried out in a cohort of singly and doubly concussed athletes, examined by 1 H-MR spectroscopy for their NAA cerebral content at different time points after concussive events, demonstrate that also in humans, concussion opens a temporal window of brain metabolic imbalance, the closure of which does not coincide with resolution of clinical symptoms. The recovery of brain metabolism is not linearly related to time. A second concussive event prolonged the time of NAA normalization by 15 days. Although needing confirmation in a larger group of patients, these results show that NAA measurement by 1 H-MR spe...

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Predominance of cellular edema in traumatic brain swelling in patients with severe head injuries

Abstract: The brain swelling observed in patients with TBI appears to be predominantly cellular, as signaled by low ADC values in brain tissue with high levels of water content.

Cited by 209 publications

References 33 publications

Erythropoietin Protects from Post-Traumatic Edema in the Rat Brain

Erythropoietin Protects from Post-Traumatic Edema in the Rat Brain

Fixed negative charge and the Donnan effect: a description of the driving forces associated with brain tissue swelling and oedema

Temporal Window of Metabolic Brain Vulnerability to Concussion

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