Global N-acetylaspartate declines even in benign multiple sclerosis.

Global N-acetylaspartate declines even in benign multiple sclerosis.
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DOI:
10.3174/ajnr.a2254
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发表时间:
2011-01
期刊:
AJNR. American journal of neuroradiology
影响因子:
--
通讯作者:
Filippi M
Filippi M
中科院分区:
其他
文献类型:
--
作者:
Rigotti DJ;Gonen O;Grossman RI;Babb JS;Falini A;Benedetti B;Filippi M

文献摘要

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为了测试临床表现为良性病程的约20%的多发性硬化症(MS)患者是否也患有轻微的神经功能障碍,其MR标志物N-乙酰-天冬氨酸(NAA)的全球浓度反映了这一点。43例良性复发缓解(RR)MS患者(女30例,男13例),年龄44.7±7.3岁(平均±标准差),平均年龄21.0±4.4(范围15~35)年,扩展残疾状态量表(EDSS)评分1.9(范围0~3)。QNAA除以脑体积(来自MRI分割),归一化为全脑NAA(WBNAA)浓度。所有参与者都给予IRB批准的书面知情同意,研究符合HIPAA标准。患者的损伤负荷为12.2±7.7 cm~3。他们的WBNAA8.3±1.8mMWBNAA比对照组低35%(p<0.001)。个体平均损失率(与对照组相比的绝对损失率除以病程)聚集在0.22±0.09毫米/年(假设单调下降为1.7%/年)。这一比率可以从已报道的病程短得多的RR MS患者中推断出来。WBNAA与病变负荷或EDSS无关。正常的WBNAA不是良性MS的特征,也不是其病程的早期预测指标。因此,这些患者可能受益于成功的代偿和口才区域的保留。由于一旦他们的大脑可塑性耗尽,他们最终可能会遭受快速下降,他们可能会受益于为更多受影响的患者提供的治疗选择。
To test whether the ~20% of multiple sclerosis (MS) patients exhibiting a clinically benign disease course also suffer minimal neural dysfunction as reflected by the global concentration of their MR marker - N-acetyl-aspartate (NAA). Global brain NAA amounts, QNAA, were obtained with non-localizing whole-head proton MR spectroscopy in 43 benign relapsing-remitting (RR) MS patients (30 female, 13 male) 44.7±7.3 years old (mean ± standard deviation) of 21.0±4.4 (range: 15 – 35) years of disease duration from first symptom and Expanded Disability Status Scale (EDSS) score of 1.9 (range: 0–3). QNAA was by divided by the brain volume (from MRI segmentation) to normalize into whole-brain NAA (WBNAA) concentration. All participants gave IRB approved written informed consent and the study was HIPAA compliant. The patients' lesion load was 12.2±7.7 cm3. Their 8.3±1.8 mM WBNAA was 35% lower than controls (p<0.001). Individual average loss rates (absolute loss compared with control divided by disease duration) clustered around 0.22±0.09 mM/year (1.7%/year assuming monotonic decline). This rate could be extrapolated from that already reported for RR MS patients of much shorter disease duration. WBNAA did not correlate with lesion load or EDSS. Normal WBNAA is not characteristic of benign MS, and is not an early predictor of its course. These patients, therefore, probably benefit from successful compensation and sparing of eloquent regions. Since they may ultimately suffer a rapid decline once their brain plasticity is exhausted, they may benefit from treatment options offered to more affected patients.