In vivo neurometabolic profiling in orthostatic tremor
Julián Benito-León1, Elan D Louis, Virginia Mato-Abad
1Department of Neurology, University Hospital "12 de Octubre" Centro de Investigación Biomédica en Red sobre Enfermedades Neurodegenerativas (CIBERNED) Department of Medicine, Complutense University, Madrid, Spain Department of Neurology, Yale School of Medicine Department of Chronic Disease Epidemiology, Yale School of Public Health Center for Neuroepidemiology and Clinical Neurological Research, Yale School of Medicine and Yale School of Public Health, New Haven, CT Neuroimaging Laboratory, Center for Biomedical Technology, Rey Juan Carlos University, Madrid, Spain School of Health Sciences, Purdue University, West Lafayette Department of Radiology and Imaging Sciences, Indiana University School of Medicine, Indianapolis, IN Department of Radiology, International Ruber Hospital Faculty of Biosanitary Sciences, Francisco de Vitoria University, Pozuelo de Alarcón, Madrid, Spain Research Laboratory of Electronics, Massachusetts Institute of Technology, Cambridge, MA HM CINAC, HM Hospitales, Madrid, Spain.
Abstract:
The pathogenesis of orthostatic tremor (OT) remains unclear, although some evidence points to dysfunction in the brainstem or cerebellum. We used single voxel proton magnetic resonance spectroscopy (1H-MRS) (3 T) to investigate whether neurochemical changes underlie abnormal cerebellar or cortical function in OT. Fourteen OT patients and 14 healthy controls underwent 1H-MRS studies with voxels placed in midparietal gray matter and cerebellum (vermis and central white matter). Spectral analysis was analyzed using the software package LCModel (version 6.3). The absolute metabolite concentrations and ratios of total N-acetylaspartate + N-acetylaspartyl glutamate (NAA), choline-containing compounds, myoinositol, and glutamate + glutamine to creatine were calculated. In midparietal gray matter spectra, we found a significant decrease in the absolute concentration of NAA in OT patients versus healthy controls (7.76 ± 0.25 vs 8.11 ± 0.45, P = 0.017). A similar decrease in NAA was seen in the cerebellar vermis (7.33 ± 0.61 vs 8.55 ± 1.54, P = 0.014) and cerebellar white matter (8.54 ± 0.79 vs 9.95 ± 1.57, P = 0.010). No differences in the other metabolites or their ratios were observed. Reductions in both cerebral cortical and cerebellar NAA suggest that there is neuronal damage or loss in OT, raising the intriguing question as to whether OT is a neurodegenerative disease. Along with clinical history and electrophysio0logical examination, 1H-MRS could serve as a useful diagnostic aid for OT.
