Neurometabolite Concentrations in Gray and White Matter in Mild Traumatic Brain Injury: A 1H–Magnetic Resonance Spectroscopy Study

The Mind Research Network, Albuquerque, New Mexico 7131, USA.
Journal of neurotrauma (Impact Factor: 3.71). 05/2009; 26(10):1635-43. DOI: 10.1089/neu.2009-0896
Source: PubMed


Single-voxel proton magnetic resonance imaging ((1)H-MRS) and proton MR spectroscopic imaging ((1)H-MRSI) were used to compare brain metabolite levels in semi-acute mild traumatic brain injury (mTBI) patients (n = 10) and matched healthy controls (n = 9). The (1)H-MRS voxel was positioned in the splenium, a region known to be susceptible to axonal injury in TBI, and a single (1)H-MRSI slice was positioned above the lateral ventricles. To increase sensitivity to the glutamate (Glu) and the combined glutamate-glutamine (Glx) signal, an inter-pulse echo time shown to emphasize the major Glu signals was used along with an analysis method that reduces partial volume errors by using water as a concentration standard. Our preliminary findings indicate significantly lower levels of gray matter Glx and higher levels of white matter creatine-phosphocreatine (Cr) in mTBI subjects relative to healthy controls. Furthermore, Cr levels were predictive of executive function and emotional distress in the combined groups. These results suggest that perturbations in Cr, a critical component of the brain's energy metabolism, and Glu, the brain's major neurotransmitter, may occur following mTBI. Moreover, the different pattern of results for gray and white matter suggests tissue-specific metabolic responses to mTBI.

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Available from: Robert Elgie, Oct 07, 2015
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    • "Instead, the tissue water-referenced concentrations reported from LCModel (Provencher, 1993) were utilized, after correcting for partial volume and relaxation effects. This procedure was similar to Gasparovic et al. (2009), with the exception that metabolic FIGURE 1 Anatomical MR images illustrating 1H MRS voxel placement and representative 1H MRS spectrum with labeled neural metabolites from the dorsolateral prefrontal cortex (DLPFC, 1st row/left) and primary motor cortex (M1, 2nd row/right). relaxation factors, derived from the equation R H2O_met = (e "
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    Developmental Neuropsychology 02/2015; 40(1):12-7. DOI:10.1080/87565641.2014.984810 · 2.24 Impact Factor
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    • "Medial parieto-occipital MEGA-sLASER voxel: (J) sagittal view, (K) axial view, and (L) coronal view. (Cr + PCr) and total choline (Cho + PC + GPC + PE) were estimated using the water signal as an internal reference and calculated as follows (Gasparovic et al., 2009 "
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    ABSTRACT: Schizophrenia is characterized by loss of brain volume, which may represent an ongoing pathophysiological process. This loss of brain volume may be explained by reduced neuropil rather than neuronal loss, suggesting abnormal synaptic plasticity and cortical microcircuitry. A possible mechanism is hypofunction of the NMDA-type of glutamate receptor, which reduces the excitation of inhibitory GABAergic interneurons, resulting in a disinhibition of glutamatergic pyramidal neurons. Disinhibition of pyramidal cells may result in excessive stimulation by glutamate, which in turn could cause neuronal damage or death through excitotoxicity. In this study, GABA/creatine ratios, and glutamate, NAA, creatine and choline concentrations in the prefrontal and parieto-occipital cortices were measured in 17 patients with schizophrenia and 23 healthy controls using proton magnetic resonance spectroscopy at an ultra-high magnetic field strength of 7 T. Significantly lower GABA/Cr ratios were found in patients with schizophrenia in the prefrontal cortex as compared to healthy controls, with GABA/Cr ratios inversely correlated with cognitive functioning in the patients. No significant change in the GABA/Cr ratio was found between patients and controls in the parieto-occipital cortex, nor were levels of glutamate, NAA, creatine, and choline differed in patients and controls in the prefrontal and parieto-occipital cortices. Our findings support a mechanism involving altered GABA levels distinguished from glutamate levels in the medial prefrontal cortex in schizophrenia, particularly in high functioning patients. A (compensatory) role for GABA through altered inhibitory neurotransmission in the prefrontal cortex may be ongoing in (higher functioning) patients with schizophrenia.
    Schizophrenia Research 04/2014; 6. DOI:10.1016/S0920-9964(14)70179-3 · 3.92 Impact Factor
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    • "There have been variable observations of Creatine concentration in acute mTBI, with higher concentrations generally seen in white matter [6] [7], and no difference [8] in gray matter or mixed areas. This is despite the more consistent detection of lower levels of N-Acetyl Aspartate (NAA [9]) and higher levels of Choline [7], and some initial evidence of reduction in glutamine and glutamate in gray matter [3] [7].. There is a paucity of studies on creatine after head injury, and its concentration is conventionally thought to be stable in healthy individuals. "
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    ABSTRACT: This pilot study explores the metabolic changes associated with persistent postconcussion syndrome (PCS) after mild traumatic brain injury (mTBI; >12 months after injury) using magnetic resonance spectroscopy. We hypothesized that those mTBI participants with PCS will have larger metabolic differences than those without. Data were collected from mTBI participants with PCS, mTBI participants without PCS and non-head-injured participants (all groups: n=8). Magnetic resonance spectroscopy metabolite profiles within the dorsolateral prefrontal cortex showed a reduced creatine/choline ratio in mTBI patients compared with control participants. This data provides initial evidence for residual metabolic changes in chronic mTBI patients, but there was no conclusive relationship between these metabolic changes and PCS symptom report. Creatine is involved in maintaining energy levels in cells with high or fluctuating energy demand, suggesting that there may be some residual energy impairment in chronic mTBI.
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