In vivo neurometabolic profiling in orthostatic tremor. [artículo]
Por: Benito León, Julián [Neurología]
| Molina Arjona, José Antonio [Neurología]
| Matarazzo, Michele [Neurología]
| Romero Muñoz, Juan Pablo [Instituto de Investigación i+12]
| Sánchez Ferro, Álvaro [Neurología]
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Colaborador(es): Servicio de Neurología-Neurofisiología
| Instituto de Investigación imas12
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Tipo de material: 
Tipo de ítem | Ubicación actual | Signatura | Estado | Fecha de vencimiento |
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PC17918 (Navegar estantería) | Disponible |
Formato Vancouver:
Benito León J, Louis ED, Mato Abad V, Dydak U, Álvarez Linera J, Hernández Tamames JA et al. In vivo neurometabolic profiling in orthostatic tremor. Medicine (Baltimore). 2016 Sep;95(37):e4848.
PMID: 27631243
PMC5402586
Contiene 45 referencias
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.
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