Cerebral Metabolite Concentrations Research Articles

53 Change in Cerebral Metabolite Concentrations Following Bariatric Surgery

Objective:Obesity is associated with adverse effects on brain health, including increased risk for neurodegenerative diseases. Changes in cerebral metabolism may underlie or precede structural and functional brain changes. While bariatric surgery is known to be effective in inducing weight loss and improving obesity-related medical comorbidities, few studies have examined whether it may be able to improve brain metabolism. In the present study, we examined change in cerebral metabolite concentrations in participants with obesity who underwent bariatric surgery.Participants and Methods:35 patients with obesity (BMI > 35 kg/m2) were recruited from a bariatric surgery candidate nutrition class. They completed single voxel 1H-proton magnetic resonance spectroscopy at baseline (pre-surgery) and within one year post-surgery. Spectra were obtained from a large medial frontal brain region. Tissue-corrected absolute concentrations for metabolites including choline-containing compounds (Cho), myo-inositol (mI), N-acetylaspartate (NAA), creatine (Cr), and glutamate and glutamine (Glx) were determined using Osprey. Paired t-tests were used to examine within-subject change in metabolite concentrations, and correlations were used to relate these changes to other health-related outcomes, including weight loss and glycemic control.Results:Bariatric surgery was associated with a reduction in cerebral Cho (f[34j = -3.79, p < 0.001, d = -0.64) and mI (f[34] = -2.81, p < 0.01, d = -0.47) concentrations. There were no significant changes in NAA, Glx, or Cr concentrations. Reductions in Cho were associated with greater weight loss (r = 0.40, p < 0.05), and reductions in mI were associated with greater reductions in HbA1c (r = 0.44, p < 0.05).Conclusions:Participants who underwent bariatric surgery exhibited reductions in cerebral Cho and mI concentrations, which were associated with improvements in weight loss and glycemic control. Given that elevated levels of Cho and mI have been implicated in neuroinflammation, reduction in these metabolites after bariatric surgery may reflect amelioration of obesity-related neuroinflammatory processes. As such, our results provide evidence that bariatric surgery may improve brain health and metabolism in individuals with obesity.

Change in medial frontal cerebral metabolite concentrations following bariatric surgery.

Obesity is associated with adverse effects on brain health, including an increased risk of neurodegenerative diseases. Changes in cerebral metabolism may underlie or precede structural and functional brain changes. While bariatric surgery is known to be effective in inducing weight loss and improving obesity-related medical comorbidities, few studies have examined whether it may be able to improve brain metabolism. In the present study, we examined changes in cerebral metabolite concentrations in participants with obesity who underwent bariatric surgery. Thirty-five patients with obesity (body mass index ≥ 35 kg/m2 ) were recruited from a bariatric surgery candidate nutrition class. They completed single voxel proton magnetic resonance spectroscopy at baseline (presurgery) and within 1 year postsurgery. Spectra were obtained from a large medial frontal brain region using a PRESS sequence on a 3-T Siemens Verio scanner. The acquisition parameters were TR = 3000 ms and TE = 37 ms. Tissue-corrected metabolite concentrations were determined using Osprey. Paired t-tests were used to examine within-subject change in metabolite concentrations, and correlations were used to relate these changes to other health-related outcomes, including weight loss and glycated hemoglobin (HbA1c ), a measure of blood sugar levels. Bariatric surgery was associated with a reduction in cerebral choline-containing compounds (Cho; t [34] = - 3.79, p < 0.001, d = -0.64) and myo-inositol (mI; t [34] = - 2.81, p < 0.01, d = -0.47) concentrations. There were no significant changes in N-acetyl-aspartate, creatine, or glutamate and glutamine concentrations. Reductions in Cho were associated with greater weight loss (r = 0.40, p < 0.05), and reductions in mI were associated with greater reductions in HbA1c (r = 0.44, p < 0.05). In conclusion, participants who underwent bariatric surgery exhibited reductions in cerebral Cho and mI concentrations, which were associated with improvements in weight loss and glycemic control. Given that elevated levels of Cho and mI have been implicated in neuroinflammation, reduction in these metabolites after bariatric surgery may reflect amelioration of obesity-related neuroinflammatory processes. As such, our results provide evidence that bariatric surgery may improve brain health and metabolism in individuals with obesity.

Metabolic abnormality in acute stroke-like lesion and its relationship with focal cerebral blood flow in patients with MELAS: Evidence from proton MR spectroscopy and arterial spin labeling

Our purpose is to detect the metabolic alterations in acute stroke-like lesions (SLLs) and further investigate the correlations between metabolic concentrations and focal cerebral blood flow in patients with mitochondrial myopathy, encephalopathy, lactic acidosis and stroke-like episodes (MELAS) using proton MR spectroscopy (1H-MRS) and arterial spin labeling (ASL). A total of 23 patients with MELAS at acute stage of stroke-like episodes (SLEs) and 20 normal controls (NC) were recruited in this study, respectively. All subjects underwent conventional MRI and1H-MRS. In addition, ASL was performed in each patient. The measurements of creatine (Cr), choline (Cho), N-acetyl aspartate (NAA), lactate (Lac), glutamine/glutamate (Glx) levels and the ratios of Cho/Cr, NAA/Cr, Lac/Cr and Glx/Cr in acute SLLs for MELAS patients and left parietal and occipital lobes for NC were measured using LC-model software. Furthermore, in MELAS group, the associations between relative cerebral blood flow (rCBF) and metabolite concentrations in acute SLLs were also assessed. In MELAS group, acute SLLs were identified with metabolic abnormalities and increased rCBF. Specifically, compared with controls, MELAS patients exhibited significantly higher Lac, Cho levels and Lac/Cr, Cho/Cr ratios, and lower NAA, Glx levels and NAA/Cr and Glx/Cr ratios. Moreover, for MELAS patients, Lac concentration in acute SLLs was positively correlated with focal rCBF. This study exhibited the neural injury with increasing lactate and cerebral blood flow in the acute SLEs. It might shed light on the underlying biochemical mechanism of mitochondrial cytopathy and angiopathy in MELAS.

Cortical N-acetylaspartate concentrations are impacted in chronic stroke but do not relate to motor impairment: A magnetic resonance spectroscopy study.

Magnetic resonance spectroscopy (MRS) measures cerebral metabolite concentrations, which can inform our understanding of the neurobiological processes associated with stroke recovery. Here, we investigated whether metabolite concentrations in primary motor and somatosensory cortices (sensorimotor cortex) are impacted by stroke and relate to upper‐extremity motor impairment in 45 individuals with chronic stroke. Cerebral metabolite estimates were adjusted for cerebrospinal fluid and brain tissue composition in the MRS voxel. Upper‐extremity motor impairment was indexed with the Fugl‐Meyer (FM) scale. N‐acetylaspartate (NAA) concentration was reduced bilaterally in stroke participants with right hemisphere lesions (n = 23), relative to right‐handed healthy older adults (n = 15; p = .006). Within the entire stroke sample (n = 45) NAA and glutamate/glutamine (GLX) were lower in the ipsilesional sensorimotor cortex, relative to the contralesional cortex (NAA: p < .001; GLX: p = .003). Lower ipsilesional NAA was related to greater extent of corticospinal tract (CST) injury, quantified by a weighted CST lesion load (p = .006). Cortical NAA and GLX concentrations did not relate to the severity of chronic upper‐extremity impairment (p > .05), including after a sensitivity analysis imputing missing metabolite data for individuals with large cortical lesions (n = 5). Our results suggest that NAA, a marker of neuronal integrity, is sensitive to stroke‐related cortical damage and may provide mechanistic insights into cellular processes of cortical adaptation to stroke. However, cortical MRS metabolites may have limited clinical utility as prospective biomarkers of upper‐extremity outcomes in chronic stroke.

Cerebral Metabolite Concentrations Are Associated With Cortical and Subcortical Volumes and Cognition in Older Adults.

BackgroundCerebral metabolites are associated with different physiological processes in brain aging. Cortical and limbic structures play important roles in cognitive aging; however, the relationship between these structures and age remains unclear with respect to physiological underpinnings. Regional differences in metabolite levels may be related to different structural and cognitive changes in aging.MethodsMagnetic resonance imaging and spectroscopy were obtained from 117 cognitively healthy older adults. Limbic and other key structural volumes were measured. Concentrations of N-acetylaspartate (NAA) and choline-containing compounds (Cho) were measured in frontal and parietal regions. Neuropsychological testing was performed including measures of crystallized and fluid intelligence and memory.ResultsNAA in the frontal voxel was associated with limbic and cortical volumes, whereas Cho in parietal cortex was negatively associated with hippocampal and other regional volumes. Hippocampal volume was associated with forgetting, independent of age. Further, parietal Cho and hippocampal volume contributed independent variance to age corrected discrepancy between fluid and crystallized abilities.ConclusionThese findings suggest that physiological changes with age in the frontal and parietal cortices may be linked to structural changes in other connected brain regions. These changes are differentially associated with cognitive performance, suggesting potentially divergent mechanisms.

Fetal neurodevelopmental recovery in donors after laser surgery for twin‐twin transfusion syndrome

Fetal magnetic resonance imaging (MRI) and spectroscopy (MRS) provide a unique opportunity to non-invasively measure markers of neurodevelopment in survivors of twin-twin transfusion syndrome (TTTS). To characterize fetal brain maturation after laser surgery for TTTS by measuring brain volumes and cerebral metabolite concentrations using fetal MRI + MRS. Prospective study of dual surviving fetuses treated with laser surgery for TTTS. At 4-5 postoperative weeks, fetal MRI was used together with novel image analysis to automatically extract major brain tissue volumes. Fetal MRS was used to measure major metabolite concentrations in the fetal brain. Twenty-one twin pairs were studied. The average (±SD) gestational age at MRI was 25.89 (±2.37) weeks. Total brain volume (TBV) was lower in the donors, although cerebral volumes were not different between twin pairs. Recipients showed lower proportions of cortical and cerebellar volumes, normalized to TBV and cerebral volumes. MRS data showed that biochemical differences between twin brains were related to discrepancy in their brain volumes. Although donors have a smaller TBV compared to recipients, proportionality of brain tissue volumes are preserved in donors. MRS maturational markers of fetal brain development show that recovery in donors persists 4 weeks after surgery.

The Inter/Intra-brain Metabolite Concentration Change as Applying the Rehabilitate Treatment in Intra-cerebral Hemorrhage Rat Models: Pilot Study

If intra-cerebral hemorrhage (ICH) rehabilitation animal model studies had included processes related to imaging diagnosis, not only interim evaluation of treatment effects but also the objectification of treatment effects would have been possible. The purpose of this study was to examine the rehabilitation treatment effect on biomarkers identified on magnetic resonance imaging/spectroscopy in an animal intra-cerebral hemorrhage model. Two groups of rats were used in this study: (1) the rehabilitation treatment group, 12 6-week-old Sprague–Dawley rats with experimental hemorrhage that received rehabilitation; and (2) the control group of 12 rats with experimental hemorrhage that received no intervention. Training rehabilitation was implemented 15 min daily for 2 weeks with 55–85% of the VO2 max. We conducted MRI/MRS scans before and after ICH rat modeling to evaluate brain metabolite concentration changes. The signal intensity of T2WI was measured at the site of ICH and in a similarly sized area on the opposite side. Integration of the areas under the peaks was conducted to measure cerebral metabolite concentrations. Differences in the mean T2WI-SI ratios measured 2 weeks after ICH induction were not statistically significant (p = 0.514) between the control group and the experimental group. However, the brain tCho/tCr metabolite ratio in the control group was significantly lower than in the experimental group 2 weeks after ICH induction (0.243 ± 0.044 vs. 0.326 ± 0.061, p = 0.007). The tCho/tCr ratio might be used as a biomarker to evaluate the effect of rehabilitation treatment for ICH.

Early proton magnetic resonance spectroscopy during and after therapeutic hypothermia in perinatal hypoxic-ischemic encephalopathy.

Hypoxic-ischemic encephalopathy (HIE) remains a significant cause of mortality and neurodevelopmental impairment despite treatment with therapeutic hypothermia. Magnetic resonance H1-spectroscopy measures concentrations of cerebral metabolites to detect derangements in aerobic metabolism. We assessed MR spectroscopy in neonates with HIE within 18-24h of initiating therapeutic hypothermia and at 5-6 days post therapeutic hypothermia. Eleven neonates with HIE underwent MR spectroscopy of the basal ganglia and white matter. We compared metabolite concentrations during therapeutic hypothermia and post-therapeutic hypothermia and between moderate and severe HIE. During therapeutic hypothermia, neonates with severe HIE had decreased basal ganglia N-acetylaspartate (NAA; 0.62±0.08 vs. 0.72±0.05; P=0.02), NAA + N-acetylaspartylglutamate (NAAG; 0.66±0.11 vs. 0.77±0.06; P=0.05), glycerophosphorylcholine + phosphatidylcholine (GPC+PCh; 0.28±0.05 vs. 0.38±0.06; P=0.02) and decreased white matter GPC+PCh (0.35±0.13 vs. 0.48±0.04; P=0.02) compared to neonates with moderate HIE. For all subjects, basal ganglia NAA decreased (-0.08±0.07; P=0.01), whereas white matter GPC+PCh increased (0.03±0.04; P=0.04) from therapeutic hypothermia MRI to post-therapeutic-hypothermia MRI. All metabolite values are expressed in mmol/L. Decreased NAA and GPC+PCh were associated with greater HIE severity and could distinguish neonates who might benefit most from targeted additional neuroprotective therapies.

Chapter 10 - Neuropsychology of aging

All people want to age "successfully," maintaining functional capacity and quality of life as they reach advanced age. Achieving this goal depends on preserving optimal cognitive and brain functioning. Yet, significant individual differences exist in this regard. Some older adults continue to retain most cognitive abilities throughout their lifetime. Others experience declines in cognitive and functional capacity that range from mild decrements in certain cognitive functions over time to severe dementia among those with neurodegenerative diseases. Even among relatively healthy "successful agers," certain cognitive functions are reduced from earlier levels. This is particularly true for cognitive functions that are dependent on cognitive processing speed and efficiency. Working memory and executive and attentional functions tend to be most vulnerable. Learning and memory functions are also usually reduced, although in the absence of neurodegenerative disease learning and retrieval efficiency rather than memory storage are affected. Other functions, such as visual perception, language, semantics, and knowledge, are often well preserved. Structural, functional, and physiologic/metabolic brain changes correspond with age-associated cognitive decline. Physiologic and metabolic mechanisms, such as oxidative stress and neuroinflammation, may contribute to these changes, along with the contribution of comorbidities that secondarily affect the brain of older adults. Cognitive frailty often corresponds with physical frailty, both affected by multiple exogenous and endogenous factors. Neuropsychologic assessment provides a way of measuring the cognitive and functional status of older adults, which is useful for monitoring changes that may be occurring. Neuroimaging is also useful for characterizing age-associated structural, functional, physiologic, and metabolic brain changes, including alterations in cerebral blood flow and metabolite concentrations. Some interventions that may enhance cognitive function, such as cognitive training, neuromodulation, and pharmacologic approaches, exist or are being developed. Yet, preventing, slowing, and reversing the adverse effects of cognitive aging remains a challenge.

Effects of isoflurane, sevoflurane, propofol and alfaxalone on brain metabolism in dogs assessed by proton magnetic resonance spectroscopy (1H MRS)

BackgroundThe purpose of this study was to determine the effects of isoflurane, sevoflurane, propofol and alfaxalone on the canine brain metabolite bioprofile, measured with single voxel short echo time proton magnetic resonance spectroscopy at 3 Tesla. Ten adult healthy Beagle dogs were assigned to receive isoflurane, sevoflurane, propofol and alfaxalone at 3 different dose rates each in a randomized cross-over study design. Doses for isoflurane, sevoflurane, propofol and alfaxalone were FE’Iso 1.7 vol%, 2.1 vol%, 2.8 vol%, FE’Sevo 2.8 vol%, 3.5 vol% and 4.7 vol%, 30, 45 and 60 mg kg− 1 h− 1 and 10, 15 and 20 mg kg− 1 h− 1 respectively. A single voxel Point Resolved Spectroscopy Sequence was performed on a 3 T MRI scanner in three brain regions (basal ganglia, parietal and occipital lobes). Spectral data were analyzed with LCModel. Concentration of total N-acetylaspartate (tNAA), choline, creatine, inositol and glutamine and glutamate complex (Glx) relative to water content was obtained. Plasma concentration of lactate, glucose, triglycerides, propofol and alfaxalone were determined. Statistics were performed using repeated measures ANOVA or Wilcoxon Sign Rank test with alpha = 5%.ResultsPlasma glucose increased with isoflurane, sevoflurane and alfaxalone but decreased with propofol. Plasma lactate increased with all anesthetics (isoflurane > sevoflurane > propofol > alfaxalone). Cerebral lactate could not be detected. Only minor changes in cerebral metabolite concentrations of tNAA, choline, inositol, creatine and Glx occurred with anesthetic dose changes.ConclusionThe metabolomic profile detected with proton magnetic resonance spectroscopy at 3 Tesla of canine brain showed only minor differences between doses and anesthetics related to tNAA, choline, creatine, inositol and Glx.

7.0 T high-resolution 1H-MR spectroscopy of metabolic changes induced by chronic codeine phosphate in rat hippocampus.

Codeine phosphate is used widely to treat cough and pain. It is actually a sedative, but is known to cause codeine dependence. The exact mechanisms of codeine dependence are not fully understood, but are generally believed to be related to drug-induced neuroadaptation. Metabolites changes can provide information for pathological processes and mechanisms before the shape change. It is very useful for the diagnosis and treatment of drug addiction. We used H NMR spectroscopy in vivo to measure the concentrations of cerebral metabolites in the hippocampus of rats subjected to repeated codeine treatment. After 2 months of codeine treatment, the concentration of N-acetylaspartate was significantly decreased in hippocampi, as was that of glutamate, choline, and taurine. Our study highlights the potential use of metabolic profiling to enhance our understanding of metabolite alteration associated with codeine dependence.

Ex vivo (1)H nuclear magnetic resonance spectroscopy reveals systematic alterations in cerebral metabolites as the key pathogenetic mechanism of bilirubin encephalopathy.

BackgroundBilirubin encephalopathy (BE) is a severe neurologic sequelae induced by hyperbilirubinemia in newborns. However, the pathogenetic mechanisms underlying the clinical syndromes of BE remain ambiguous. Ex vivo1H nuclear magnetic resonance (NMR) spectroscopy was used to measure changes in the concentrations of cerebral metabolites in various brain areas of newborn 9-day-old rats subjected to bilirubin to explore the related mechanisms of BE.ResultsWhen measured 0.5 hr after injection of bilirubin, levels of the amino acid neurotransmitters glutamate (Glu), glutamine (Gln), and γ-aminobutyric acid (GABA) in hippocampus and occipital cortex significantly decreased, by contrast, levels of aspartate (Asp) considerably increased. In the cerebellum, Glu and Gln levels significantly decreased, while GABA, and Asp levels showed no significant differences. In BE 24 hr rats, all of the metabolic changes observed returned to normal in the hippocampus and occipital cortex; however, levels of Glu, Gln, GABA, and glycine significantly increased in the cerebellum.ConclusionsThese metabolic changes for the neurotransmitters are mostly likely the result of a shift in the steady-state equilibrium of the Gln-Glu-GABA metabolic cycle between astrocytes and neurons, in a region-specific manner. Changes in energy metabolism and the tricarboxylic acid cycle may also be involved in the pathogenesis of BE.

Modulation of neural activation following treatment of hepatic encephalopathy

To measure changes in psychometric state, neural activation, brain volume (BV), and cerebral metabolite concentrations during treatment of minimal hepatic encephalopathy. As proof of principle, 22 patients with well-compensated, biopsy-proven cirrhosis of differing etiology and previous minimal hepatic encephalopathy were treated with oral l-ornithine l-aspartate for 4 weeks. Baseline and 4-week clinical review, blood chemistry, and psychometric evaluation (Psychometric Hepatic Encephalopathy Score and Cognitive Drug Research Score) were performed. Whole-brain volumetric and functional MRI was conducted using a highly simplistic visuomotor task, together with proton magnetic resonance spectroscopy of the basal ganglia. Treatment-related changes in regional BV and neural activation change (blood oxygenation level dependent) were assessed. Although there was no change in clinical, biochemical state, basal ganglia magnetic resonance spectroscopy, or in regional BV, there were significant improvements in Cognitive Drug Research Score (+1.2, p = 0.003) and Psychometric Hepatic Encephalopathy Score (+1.5, p = 0.003) with treatment. This cognitive amelioration was accompanied by changes in blood oxygenation level-dependent activation in the posterior cingulate and ventral medial prefrontal cortex, 2 regions that form part of the brain's structural and metabolic core. In addition, there was evidence of greater visual cortex activation. These structurally interconnected regions all showed increased function after successful encephalopathy treatment. Because no regional change in BV was observed, this implies that mechanisms unrelated to astrocyte volume regulation were involved in the significant improvement in cognitive performance.

Quantitative Assessment of Metabolic Changes in the Developing Brain of C57BL/6 Mice by In Vivo Proton Magnetic Resonance Spectroscopy

Localized proton MRS was used to quantify cerebral metabolite concentrations in the thalamus of mice to assess the variation of major metabolites during brain development. Three sets of C57BL/6 mice were followed in a longitudinal study from a very early phase at post-natal day four (p4) until today 57 (p57). Experiments were conducted in accordance with Canadian animal care guidelines on a 7-Tesla small animal MR system. Specimens were examined under inhalation anesthesia using single-voxel MRS. A cubic volume with edge lengths of 1.9 mm was placed in the thalamus region of animals and point-resolved spectroscopy (PRESS) spectra were acquired with the following parameters (TR/TE/NEX=2500 ms/20 ms/600; Bandwidth=4000 Hz). Absolute metabolite quantification using LCModel was obtained by assigning water signal intensity measured by MRS to water concentrations determined by histobiochemical analysis and interpolation. Optimized anesthesia, immobilization, and careful monitoring led to a survival rate of 100% throughout the study. The brain water content was 84.8, 78.8, and 77.6% at p12, p31, and p66. Variation of metabolites revealed similar patterns for the total of creatine and phosphocreatine (tCr), glutamate and glutamine (Glx), and the total of N-acetyl aspartic compounds (tNAA), with steady increases from p4 to reaching a plateau after p21. The total of Cholinecontaining compounds (tCho) and myo-inositol (Ins) had high concentrations at early exam points, decreased to minima between p14 and p19, and increased to adult levels thereafter. Taurine (Tau) had highest levels at p4, decreased persistently but fast in the early development and slow in the later stages of brain development. Our results indicate that biological variance must be considered if results from studies on mouse models of pathologies are compared with results from healthy controls during development. This aspect seems to be especially important between p10 and p21. Due to the high temporal resolution used at early time points in our study and the inclusion of multiple groups of animals at time points, our data contribute important aspects to the existing literature about mouse brain development.

Relationship between fractional anisotropy of cerebral white matter and metabolite concentrations measured using 1H magnetic resonance spectroscopy in healthy adults

Fractional anisotropy (FA) of water diffusion in cerebral white matter (WM), derived from diffusion tensor imaging (DTI), is a sensitive index of microscopic WM integrity. Physiological and metabolic factors that explain intersubject variability in FA values were evaluated in two cohorts of healthy adults of different age spans (N=65, range: 28-50years; and N=25, age=66.6±6.2, range: 57-80years). Single voxel magnetic resonance spectroscopy (MRS) was used to measure N-acetylaspartate (NAA), total choline-containing compounds, and total creatine, bilaterally in an associative WM tract: anterior corona radiata (ACR). FA values were calculated for the underlying, proximal and two distal WM regions. Two-stage regression analysis was used to calculate the proportion of variability in FA values explained by spectroscopy measurements, at the first stage, and subject's age, at the second stage. WM NAA concentration explained 23% and 66% of intersubject variability (p<0.001) in the FA of the underlying WM in the younger and older cohorts, respectively. WM NAA concentration also explained a significant proportion of variability in FA of the genu of corpus callosum (CC), a proximal WM tract where some of the fibers contained within the spectroscopic voxel decussate. NAA concentrations also explained a significant proportion of variability in the FA values in the splenium of CC, a distal WM tract that also carries associative fibers, in both cohorts. These results suggest that MRS measurements explained a significant proportion of variability in FA values in both proximal and distal WM tracts that carry similar fiber-types.

Indirect Effects of Elevated Body Mass Index on Memory Performance Through Altered Cerebral Metabolite Concentrations

Elevated body mass index (BMI) at midlife is associated with increased risk of cognitive decline in later life. The goal of the current study was to assess mechanisms of early brain vulnerability by examining if higher BMI at midlife affects current cognitive performance through alterations in cerebral neurochemistry. Fifty-five participants, aged 40 to 60 years, underwent neuropsychological testing, health screen, and proton magnetic resonance spectroscopy examining N-acetylaspartate, creatine (Cr), myo-inositol (mI), choline, and glutamate concentrations in occipitoparietal gray matter. Concentrations of N-acetylaspartate, choline, mI, and glutamate were calculated as a ratio over Cr and examined in relation to BMI using multivariate regression analyses. Structural equation modeling was used to determine if BMI had an indirect effect on cognition through cerebral metabolite levels. Higher BMI was associated with elevations in mI/Cr (F(5,45) = 3.843, p = .006, β = 0.444, p = .002), independent of age, sex, fasting glucose levels, and systolic blood pressure. Moreover, a χ(2) difference test of the direct and indirect structural equation models revealed that BMI had an indirect effect on global cognitive performance (Δχ(2) = 19.939, df = 2, p < .001). Subsequent follow-up analyses revealed that this effect was specific to memory (Δχ(2) = 22.027, df = 2, p < .001). Higher BMI was associated with elevations in mI/Cr concentrations in the occipitoparietal gray matter and indirectly related to poorer memory performance through mI/Cr levels, potentially implicating plasma hypertonicity and neuroinflammation as mechanisms underlying obesity-related brain vulnerability.

Metabolic imaging of mild traumatic brain injury

Traumatic brain injury results in a metabolic cascade of changes that occur at the molecular level, invisible to conventional imaging methods such as computed tomography or magnetic resonance imaging. Non-invasive metabolic imaging tools such as single photon emission computed tomography (SPECT), positron emission tomography (PET), and magnetic resonance spectroscopy (MRS) are the ideal methods for providing insight to these changes by measuring regional cerebral blood flow, glucose metabolism, and brain metabolite concentrations, respectively, after mild traumatic brain injury (mTBI). The purpose of this review is to provide an overview of the different methodologies and provide an up-to-date summary of recent findings with SPECT, PET, and MRS technologies, specifically after mTBI, as defined by standardized criteria. Given that the different physiological and pathological responses are heterogeneous, efforts will be made to separate studies at different time points after injury (acute, subacute, and chronic stages) as well as to the different types of mTBI such sports-related head injury where repetitive head injuries are much more common and may present a unique signature.

Magnetic resonance imaging and spectroscopy: how useful is it for prediction and prognosis?

MRI/MRS can produce information on over 40 physico-chemical parameters regarded as biomarkers of structural, functional or metabolic significance. Though of undisputed worth in the detection of macroscopic lesions or of metabolic derangements, MRI’s use in prognosis and prediction has not been so extensively studied. Serial studies can be performed to show early pre-clinical changes in biomarkers caused by disease progression or therapy, such as the adverse effect on heart function of certain cancer therapies. It can utilise various haemodynamic measures to predict the evolution of stroke and so help justify certain interventions. Changes in cerebral metabolite concentrations or the volumes of brain sub-structures can be used as objective measures of drug response in psychiatric conditions. However care must be exercised as MR can sometimes be considered ‘too sensitive’ as it often detects real abnormalities even in asymptomatic volunteers, the actual predictive significance of which have yet to be fully assessed.

Wertigkeit der MR-Spektroskopie bei infektiösen und entzündlichen Hirnerkrankungen

Proton magnetic resonance spectroscopy (MRS) is a non-invasive method for measuring cerebral metabolite concentrations in various pathologic conditions. This review discusses the MRS findings in the most common infectious and inflammatory brain diseases.

Differential Diagnosis of Brain Diseases Using In Vivo Proton Magnetic Resonance Spectroscopy at 3 Tesla: A Preliminary Study

The purpose of this study was to evaluate the usefulness of in vivo 3T <TEX>$^1H$</TEX> MRS with short TE for prescreening various brain diseases. Together with ten normal volunteers, 12 brain tumor patients(2 lymphomas, 5 malignant gliomas) and 5(benign meningiomas) and 10 brain ischemic disease patients(6 acute and 4 subacute infarctions) participated. Lymphomas showed increased intensities of Cho and Lac. Likewise, gliomas showed increased Cho and Lac, but with decreased NAA and <TEX>${\beta}\;{\gamma}$</TEX>-Glx; in higher grade of gliomas, Lac, Cho, mI and Lip predominantly increased with decrease of NAA. Benign meningiomas showed increased Cho, Lac and <TEX>${\beta}\;{\gamma}$</TEX>-Glx; with decreased of NAA. The alanine peak at 1.47 ppm is a neuronal marker for meningiomas. Infarctions showed increased Lac and Lip and decreased NAA, <TEX>${\alpha}$</TEX>-Glx and <TEX>${\beta}\;{\gamma}$</TEX>-Glx where Lac increased with decreased of <TEX>${\alpha}$</TEX>-Glx in acute, and Cho, Lac and Lip increased with decrease of NAA in subacute. Elevated Lac and decreased NAA levels were more aggravated in subacute. Clinical application of the <TEX>$^1H$</TEX> MRS with short TE at 3T is able to povide valuable spectral information for prescreening various brain diseases by monitoring the changes of disease-specific cerebral metabolite concentrations in vivo, and consequently, it can be applicable to assessment of differential diagnosis and malignancy as well.