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Multiple sclerosis in children: Cerebral metabolic alterations monitored by localized proton magnetic resonance spectroscopy in vivo
Author(s) -
Bruhn H.,
Frahm J.,
Merboldt K. D.,
DiplMath W. Hänicke,
Hanefeld F.,
Christen H. J.,
Kruse B.,
Bauer H. J.
Publication year - 1992
Publication title -
annals of neurology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 4.764
H-Index - 296
eISSN - 1531-8249
pISSN - 0364-5134
DOI - 10.1002/ana.410320205
Subject(s) - proton magnetic resonance , nuclear magnetic resonance , multiple sclerosis , magnetic resonance imaging , in vivo , nuclear magnetic resonance spectroscopy , medicine , functional magnetic resonance spectroscopy of the brain , pathology , biology , radiology , physics , psychiatry , microbiology and biotechnology
In vivo proton magnetic resonance spectroscopy of 8 children (7–16 years) with established multiple sclerosis revealed distinct alterations in regional cerebral metabolism associated with different aspects of the disease: (1) Localized proton spectra (2 to 4‐ml volumes of interest) from multiple sclerosis plaques were generally characterized by a decrease in N ‐acetylaspartate and creatines, and an increase in cholines and myo ‐inositol relative to age‐matched control subjects, (2) neither chronic nor enhancing plaques (by gadolinium‐diethylenetriamine pentaacetic acid) during an acute exacerbation showed elevated levels of lactate or lipids, (3) spectra from adjacent white matter that did not appear suspicious in magnetic resonance images were similar to those of normal control subjects, and (4) cortical gray matter related to neighboring multiple sclerosis lesions showed a notable reduction of N ‐acetylaspartate. The present results show that functional impairment in multiple sclerosis is linked to gross metabolic disturbances of neuronal cell chemistry. We suggest that focal demyelination is accompanied by increased membrane precursors of proliferative turnover and is associated with secondary neuronal shrinkage or loss, perhaps extending into related cortical gray matter.