Background

Brain swelling is one of the most dangerous complications of primary traumatic brain injury (TBI), which leads to rise of intracranial pressure (ICP). We propose that DWI can be a useful tool for evaluating the risk of malignant intracranial hypertension development and can be used to determine the need of decompressive craniectomy in patients with severe TBI.

Objectives

To determine the potential of DWI in assessing the risk of developing malignant intracranial hypertension in children with severe TBI.

Methods

We retrospectively evaluated clinical and MRI data of 36 pediatric patients with severe TBI. The severity of clinical condition of each patient was evaluated with the use of the Glasgow Coma Scale (GCS). Parenchymal ICP gauge placement was performed in all patients for adequate ICP monitoring. Patients were categorized into three groups: (1) high ICP managed conservatively; (2) malignant ICP managed with DC; (3) normal ICP. Four pairs of symmetrical ROIs were manually drawn on ADC maps. All ROIs excluded areas that appeared abnormal on T2WI.

Results

Average ADC values in the deep white matter of frontal lobes were significantly increased in children with severe TBI with following DC (851.5+/-54.3x10^-3 mm²/sec) compared to those with severe TBI and conservatively controlled ICP (756.4+/-40.5x10^-3 mm²/sec; p<0.05).

Conclusion

Assessment of DWI values in severe pediatric TBI is a potential tool for evaluating the risk of malignant ICP development. Early identification of children at high risk for this complication may assist in earlier aggressive clinical management of pediatric TBI patients.

Background

The vast majority of mild traumatic brain injury (mTBI) cases do not lead to abnormalities of brain structures. The correlation between early structural neuroimaging findings and long-term clinical outcomes is weak.

Objectives

The main aim of this work was to estimate changes in in vivo cerebral GABA and Glutamate concentrations after acute mTBI using 1H MRS.

Methods

Two groups of participants were included in the study: patients (n=11, mean age–16±2 years) with acute mTBI (mean time between trauma and MRI examination 40±20 hours); 8 healthy children (mean age-16±1 years) without history of any TBIs. MR acquisition: 1H MR spectra were acquired on scanner 3 T MRI scaner using PRESS (NAA, Creatine, Choline signals) and MEGA PRESS (GABA and Glutamate signals) pulse sequences. All voxels in size of 25×25×30 mm were located in the frontal lobe

Results

The main effect on the [GABA] was found (Z=2.03, p<0.05), with the patients having higher [GABA] as compared to the control group (36%). Absolute concentrations of NAA+NAAG, tCho, tCr and glutamate were unchanged.

Conclusion

This study for the first time revealed increased cerebral [GABA] as well as disorders in the [GABA]/[GLX] balance in the pediatric acute mTBI. The most likely cause of [GABA] increase is growth of free pool of GABA (non-related to GABA receptors). Postconcussion changes of neurotransmitter revealed in the present study could be promising for understanding of functional consequences of MRI negative TBI.

Background

Previous 1H-MRS studies reported significant decrease of major neuronal marker (N-acetylaspartate (NAA)) concentration after severe TBI, The possible reasons of NAA reduction is not still completely known. Disruption of the NAA synthesis from aspartate Asp may result to its decrease.

Objectives

The main idea of this study is investigation of dynamic changes in NAA, Asp and glutamate (Glu) concentrations using proton magnetic resonance spectroscopy.

Methods

We studied 2 patients groups: Eight children (mean age-14±2 years) with acute sTBI (23±4 hours after trauma) and seven patients with chronic sTBI (3 months after trauma). were Control group consisted of 11 healthy children (mean age-15±1 years) without history of any TBI. ^AspMEGA PRESS were acquired from voxels located in the frontal lobe (fig.1).

Results

NAA and Asp concentrations are reduced in the both patient groups (acute sTBI - on 65% and 61%, chronic sTBI – on 65% and 61%). Glu is significantly reduced only in acute sTBI, however, a significant decrease in the Asp/Glu ratio was found in patients with chronic sTBI.

Conclusion

Since stoichiometric Asp-Glu ratio is maintained by the exchange of glutamate with mitochondrial aspartate, significant reduction of [Asp]/[Glu] may indicates a disruption in the normal functioning of the malate-aspartate shuttle in chronic sTBI. Reduced Glu and Asp concentrations in acute sTBI are associated with excitotoxicity.

This work was supported by RFBR grant 17-04-01149.

Background

Hyperbaric oxygenation (HBO) has proved itself as an effective way of treatment in different cases, for example in hypoxia. However, the exact in vivo biochemical mechanisms of HBO are to be revealed.

Objectives

We used ³¹P and ¹H magnetic resonance spectroscopy (MRS), as well as resting state functional magnetic resonance imaging (rs-fMRI) in order to find the effects of one HBO session on human brain in vivo.

Methods

MRI scanner 3.0T and hyperbaric chamber Sechrist 3200 were used in the study. Seventeen subjects participated in ³¹P MRS part, and 12 subjects - in ¹H and rs-fMRI part. The data were collected in MRI scanner during ~20 minutes before HBO session and right after it. Spectroscopy data were processed in jMRUI (in case of ³¹P) and LCModel (¹H). The concentrations of creatine phosphate (PCr), ATP and NAD (indirectrly) in whole brain, and of N-acetylaspartate (NAA) in voxels, (see fig.1) after HBO were normalized on the corresponding values after HBO, these values were compared with the value=1 (Mann-Whitney). Rs-fMRI data were processed in CONN (Matlab), the effect of HBO on MPFC-PCC connectivity was found.

Results

After HBO session decreased: PCr (by 3%), NAA in MPFC and PCC (by 4%), NAD increased (by 6%), ATP remained unchanged. The MPFC-PCC connectivity increased (fig.2)

Conclusion

Decrease in PCr and NAA manifestates energy metabolism activation. Together with the increase in NAD and functional connectivity this is the confirmation of HBO effectiveness even at low pressures, that may help to overcome the effect of such diseases as acute ischemia or TBI.