Discrimination of white matter lesions and multiple sclerosis plaques by short echo quantitative 1H-magnetic resonance spectroscopy.
ABSTRACT Multiple sclerosis (MS) plaques and age related white matter lesions (WML) are of similar morphological appearance on T2 weighted MRI. Therefore their differentiation is sometimes crucial. Proton magnetic resonance spectroscopy ((1)H-MRS) adds metabolic information to conventional imaging and may help to distinguish inflammatory MS plaques from vascular related WML. This study was performed to evaluate the metabolite pattern in MS plaques and WML. 15 MS patients, 14 elderly individuals with WML and 16 controls were investigated by conventional MRI and short echo quantitative (1)H-MRS (TE: 30ms, TR: 3000ms). The mean metabolite concentrations in normal control white matter (NCWM), MS plaques and WML were: t-NAA: 8.96 mmol/l (SD: 0.93) vs 6.79 mmol/l (SD: 1.99) vs 7.18 mmol/l (SD: 1.41); Cho:1.66 mmol/l (SD: 0.4) vs 1.49 mmol/l (SD: 0.45) vs 1.46 mmol/l (SD: 0.34); PCr:5.64 mmol/l (SD: 0.83) vs 4.9mmol/l (SD: 1.3) vs 4.95 mmol/l (SD: 0.86); myo-Ins: 4.57 mmol/l (SD:1.05) vs 6.34 mmol/l (SD: 2.03) vs 4.5 mmol/l (SD: 0.96). t-NAA reduction in MS plaques and WML was significant compared with controls (p <or= 0.001). MS plaques showed significantly elevated myo- Ins concentrations compared with controls (p = 0.002) and to WML (p = 0.003). In summary MS plaques and WML show a decrease in their t-NAA concentrations compared with controls. Elevated concentrations of myo-Ins in MS plaques but not in WML makes this metabolite of special interest for their differentiation.
- SourceAvailable from: Robert F Spetzler[show abstract] [hide abstract]
ABSTRACT: Patchy subcortical foci of increased signal intensity are frequently identified on magnetic resonance imaging (MRI) in the elderly. The incidence and clinical correlates of these lesions remain unknown. In this report, 240 consecutive MRI scans performed over a 6-month period were reviewed (excluding patients with recent brain trauma or known demyelinating disease). Subcortical incidental lesions (ILs) were identified, which could not be accounted for by the patient's current clinical diagnosis, neurological status, or CT scan. The ILs were graded according to size, multiplicity, and location. The incidence and severity of ILs increased with advancing age (p less than 0.0005). Among patients over 50 years of age, the incidence and severity of ILs were correlated with a previous history of history of ischemic cerebrovascular disease (p less than 0.05) and with hypertension (p less than 0.05). Multivariable regression analysis identified age, prior brain ischemia, and hypertension as the major predictors of ILs in the elderly. Diabetes, coronary artery diseases, and sex did not play a significant role. With the exception of cerebrovascular disease, there was no association between ILs and any particular clinical entity, including dementia. It is concluded that subcortical parenchymal lesions are frequent incidental findings on MRI in the elderly, and may represent an index of chronic cerebrovascular diseases in such patients.Stroke 17(6):1084-9. · 6.16 Impact Factor
- [show abstract] [hide abstract]
ABSTRACT: The levels of several low-molecular-weight metabolites were measured in 1H nuclear magnetic resonance (NMR) spectra of extracts of Syrian hamster brain infected with Creutzfeldt-Jakob disease (CJD). Metabolite levels were determined in cerebral cortex in CJD-infected and age-matched controls at defined times (40, 65, 85, 105, and 135 days) during the 130- to 135-day incubation period to terminal disease. At 135 days, CJD-infected hamsters showed a significant decrease in N-acetylaspartate of 32% (p < 0.05) and an increase in myo-inositol of 67% (p < 0.001) from age-matched controls. At earlier times (40 to 110 days) levels of N-acetylaspartate and myo-inositol were not significantly different from controls. No significant changes were detected in the cortical levels of glutamate, aspartate, or GABA between 40 and 135 days. The late changes in N-acetylaspartate and myo-inositol in CJD-infected hamsters are similar to those observed in magnetic resonance spectroscopy studies of human CJD. Because they also correspond to the changes found in other dementias, including Alzheimer's disease and HIV dementia, these changes indicate converging pathogenetic pathways involved in many neurodegenerative diseases.Magnetic Resonance Imaging 11/1998; 16(8):963-8. · 2.06 Impact Factor
- [show abstract] [hide abstract]
ABSTRACT: N-Acetyl-aspartate is found in high concentrations in all areas of the brain, but is undetectable in non-neuronal tissue. In order to characterize the cellular localization of N-acetyl-aspartate in brain, highly specific monoclonal antibodies against N-acetyl-aspartate were produced by fusing spleen lymphocytes obtained from mice immunized with N-acetyl-aspartate conjugated to thyroglobulin by carbodiimide with P3/x63-Ag8.653 mouse myeloma cells. Clones were selected which secrete IgG2a(k) antibodies highly specific for conjugated N-acetyl-aspartate. Only 3-6% cross-reactivity with conjugated N-acetyl-aspartate-glutamate was observed at high antibody concentrations, whereas no cross-reactivity (less than 1%) was observed with conjugated N-acetyl-glutamate or aspartate. Preincubation of the antibodies with 0.5 mg/ml conjugated N-acetyl-aspartate blocked immunoreactivity more than 90%, while preincubation with conjugated N-acetyl-aspartate-glutamate and free N-acetyl-aspartate had no effect. Immunocytochemical staining has shown that N-acetyl-aspartate-like immunoreactivity is localized in neurons, which are widely distributed throughout the brain. The immunoreactive neurons exhibited intense staining of the perikarya, proximal dendrites and axons. No consistent pattern of distribution of immunoreactivity was observed with regard to primary neurotransmitter characteristics of stained neurons although neurons with long projections or extensive arbors, such as pyramidal cells in cortex, locus coeruleus, motor neurons and Purkinje cells, stained much more intensively than local circuit neurons.Neuroscience 02/1991; 45(1):37-45. · 3.12 Impact Factor