NEUROTRANSMISSION DISTURBANCES AFTER MILD PEDIATRIC TBI
- Natalia Semenova, United States of America
- Petr Menshchikov, Russian Federation
- Andrei Manzhurtsev, Russian Federation
- Maxim Ublinskiy, Russian Federation
- Tolibdzhon Akhadov, United States of America
- Natalia Semenova, United States of America
Abstract
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.