Yan Li1, Trevor Flynn1, Dawn Gano1, Hannah Glass1, Donna M Ferriero1, Anthony James Barkovich1, and Duan Xu1
1University of California, San Francisco, CA, United States
Synopsis
This study evaluated neurobiochemical profiles
in 11 neonates using GABA-edited MR spectroscopy.
Introduction
Proton (H-1) MR spectroscopy
is a powerful method for non-invasively investigating brain metabolism. The
newborn brain is relatively immature and has much less neuronal activity
compared with the adult brain. The changes in metabolic profile that occur as the
brain matures can be quantified by MRS. The purpose of this study was to
evaluate neurobiochemical profiles in the neonates using GABA-edited MR
spectroscopy (1). Methods
Patient population consists of
5 term neonates with hypoxic ischemic encephalopathy (HIE) at the median age of
4 days [range, 4-5 days], 3 neonates with congenital heart defects (CHD) at the
median age of 20 days [5-35 days], and 3 preterm infants (Preterm) at the
median corrected gestational age of 36w5d [30w0d – 38w6d]. The MR data were
acquired from 3 T scanner (GE Healthcare Technologies, Waukesha, WI) using 8
channel phased array head coil. The 2D H-1 GABA-edited MRSI data were obtained
using PRESS volume selection, VSS outer volume suppression and CHESS water
suppression with a TE/TR = 68/1500 ms, matrix = 8x8, spatial resolution = 1x1x1
cm3, NEX=2, and total acquisition = 6.5 minutes. The editing pulse
was applied symmetrically to the resonance of water. The non-edited spectra were
processed and quantified using methods described previously. The difference
spectra, the subtraction of edited from non-edited spectra, after phase and
frequency corrections will be quantified by using LCModel (2), which will utilize a basis-set generated by
individual metabolite phantoms. Regions
of interest (ROIs) include basal ganglia (caudate, putamen and globus
pallidum), thalamus and insula (Figure 1). Results
An example of 2D GABA-edited
MRSI is illustrated in Figure 1. Table 1 summarize the relative
metabolite ratios for each ROI quantified from non-edited spectra. Among 3
patient population, the preterm has the lowest Cho/NAA and highest value of
mI/Cr in the BG and thalamus. The median ratios of GABA/NAA within the deep
brain were 0.50±0.07 in the HIE and 0.72±0.19 in the CHD, respectively. Discussion
The changes in metabolic
profile that occur as the brain matures can be quantified by MRS. NAA is
initially lower relative to other metabolites and its rate of increase has been
shown to correlate with the maturation process (3). Lower NAA/Cho has been observed in different regions of the brain for
preterm compared to term infants using 3D MRSI (4). This is consistent with our finding from non-edited spectra. During
the period from preterm to term, mI/Cho has been shown to decrease (5), which could explain the difference on mI/Cr among groups. Glu
(excitatory) and GABA (inhibitory) are the main neurotransmitters in the mature
brain. However, GABA acts as an important excitatory mediator on brain
development (6, 7). Recently, it is also reported that neonates had significantly lower
in vivo brain GABA+ levels than children in both the BG and cerebellum (8). Relatively high GABA/NAA was found in the regions of deep brain
structures in our study, which can be due to lower concentration of NAA in our
patient population and clinical status. Currently we are collecting the
clinical measurements and will correlate them with neurochemical profiles.
Considering relatively low SNR of GABA, we will also combine the voxels within
the ROIs first and then quantify the averaged spectra. Conclusion
We have found different brain
metabolism within the deep brain structures in the term neonates with HIE, CHD
and the preterm. Acknowledgements
This research was supported by NIH R21HD092660 and P01NS082330.References
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