1993年12月
AMYOTROPHIC-LATERAL-SCLEROSIS - T2 SHORTENING IN MOTOR CORTEX AT MR-IMAGING
RADIOLOGY
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- 巻
- 189
- 号
- 3
- 開始ページ
- 843
- 終了ページ
- 846
- 記述言語
- 英語
- 掲載種別
- 出版者・発行元
- RADIOLOGICAL SOC NORTH AMER
PURPOSE: To determine whether decreased signal intensity of the motor cortex (T2 shortening) at magnetic resonance (MR) imaging is a useful finding for supporting the diagnosis of amyotrophic lateral sclerosis (ALS).
MATERIALS AND METHODS: High-field-strength (1.5-T) MR images of 15 patients (seven men and eight women, aged 28-80 years) and 49 neurologically normal age-matched control patients were examined for T2 shortening in the motor cortex. In addition, brains of patients with ALS were examined at autopsy.
RESULTS: The MR images of 14 of the 15 patients showed T2 shortening in precentral cortices, while the images of all but one of the control patients showed no such finding. In three of eight brains at autopsy, sections from the precentral cortex showed sparsely distributed, intensely stained astrocytes and macrophages.
CONCLUSION: Abnormal iron deposition associated with the degenerative process could be the source of T2 shortening, which is a useful MR imaging finding in the diagnosis of ALS.
MATERIALS AND METHODS: High-field-strength (1.5-T) MR images of 15 patients (seven men and eight women, aged 28-80 years) and 49 neurologically normal age-matched control patients were examined for T2 shortening in the motor cortex. In addition, brains of patients with ALS were examined at autopsy.
RESULTS: The MR images of 14 of the 15 patients showed T2 shortening in precentral cortices, while the images of all but one of the control patients showed no such finding. In three of eight brains at autopsy, sections from the precentral cortex showed sparsely distributed, intensely stained astrocytes and macrophages.
CONCLUSION: Abnormal iron deposition associated with the degenerative process could be the source of T2 shortening, which is a useful MR imaging finding in the diagnosis of ALS.
- リンク情報
- ID情報
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- ISSN : 0033-8419
- Web of Science ID : WOS:A1993MH58600038