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Serial proton spectroscopy, magnetization transfer ratio and T 2 relaxation in pseudotumoral demyelinating lesions
Author(s) -
Cucurella M. Gràcia,
Rovira Alex,
Grivé Elisenda,
Tintoré Mar,
Montalban Xavier,
Alonso Julio
Publication year - 2002
Publication title -
nmr in biomedicine
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.278
H-Index - 114
eISSN - 1099-1492
pISSN - 0952-3480
DOI - 10.1002/nbm.772
Subject(s) - magnetization transfer , relaxometry , lesion , pathology , nuclear magnetic resonance , creatine , medicine , cyst , nuclear medicine , extracellular fluid , pathological , extracellular , magnetic resonance imaging , chemistry , radiology , physics , spin echo , biochemistry
In some rare cases, demyelinating plaques appear on contrast‐enhanced T 1 ‐weighted images as pseudotumoral, cyst‐like lesions (hypointense, ring enhancing). Serial proton MR spectroscopy, T 2 relaxometry and magnetization transfer ratios (MTR) were performed on three pseudotumoral demyelinating lesions to obtain information about their pathological basis. Baseline and 1‐month MTR and T 2 values were similar to those of cerebrospinal fluid, while spectra showed lactate, lipids and choline. Three‐month and 1 year exams showed recovery of MTR, T 2 and N‐acetylaspartate, approaching the contralateral values, while creatine and choline were normal or surpassed contralateral values. Lipids and lactate gradually disappeared. These results suggest that pseudotumoral, cyst‐like, ring‐enhancing lesions may be characterized by an accumulation of oedema in the extracellular space with an almost complete absence of cells. Reduction of the oedema allows restoration of the tissue to its original location, indicating that cellular destruction was less important than was expected after the first exam. Thus, the evolution of this kind of lesion should be kept in mind when considering lesion volume from T 1 ‐weighted images as a marker of disability or irreversible cellular destruction in MS. Copyright © 2002 John Wiley & Sons, Ltd.