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Proton Magnetic Resonance Spectroscopy ( 1 H MRS) in Patients with Sporadic Cerebellar Degeneration
Author(s) -
Terakawa Haruhiko,
Abe Kazuo,
Watanabe Yoshiyuki,
Nakamura Masaichi,
Fujita Norihiko,
Hirabuki Norio,
Yanagihara Takehiko
Publication year - 1999
Publication title -
journal of neuroimaging
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 0.822
H-Index - 64
eISSN - 1552-6569
pISSN - 1051-2284
DOI - 10.1111/jon19999272
Subject(s) - putamen , cerebellum , medicine , cerebellar hemisphere , cerebellar cortex , cerebellar vermis , atrophy , phosphocreatine , creatine , choline , pathology , nuclear magnetic resonance , physics , energy metabolism
The authors studied 23 patients with cerebellar degeneration including multiple systemic atrophy (MSA) and cerebellar cortical atrophy (CCA) by proton magnetic resonance spectroscopy C HMRS). 1 H‐MRS allowed noninvasive measurement of the signal intensities derived from N‐acetylaspartate (NAA), creatine+phosphocreatine (CRE), and choline‐containing compounds (CHO). There was significant reduction of the NAA/CRE level in the frontal cortex, putamen, cerebellar hemisphere and cerebellar vermis of patients with MSA, and in the frontal cortex, cerebellar hemisphere and cerebellar vermis of patients with CCA as compared with those of normal controls. There was significant reduction of the NAA/CRE level also in the putamen of patients with MSA as compared with that of patients with CCA. These results indicated the presence of a degenerative process and/or functional impairment in the frontal cortex and putamen of patients with MSA and in the frontal cortex of patients with CCA, in addition to a degenerative process in the cerebellum. There was a significant correlation between the NAA/CRE level and the severity of clinical signs. 1 H‐MRS is valuable in providing information regarding the pathophysiology and the progress of cerebellar degenerative diseases. Key words: proton magnetic resonance spectroscopy, cerebellar cortical atrophy, multiple system atrophy, N‐acetylaspartate.