Basal ganglia, thalamus and neocortical atrophy predicting slowed cognitive processing in multiple sclerosis
Basal ganglia, thalamus and neocortical atrophy predicting slowed cognitive processing in multiple sclerosis
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DOI：
10.1007/s00415-011-6147-1
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发表时间：
2012-01-01
影响因子：
6
通讯作者：
Benedict, Ralph H. B.
中科院分区：
文献类型：
--
作者：
Batista, Sonia;Zivadinov, Robert;Benedict, Ralph H. B.
信息处理速度（IPS）减慢是多发性硬化症（MS）的主要认知缺陷。基底神经节、丘脑和新皮质被认为对有效的信息处理具有关键作用，但这些结构对MS相关IPS损伤的具体相对贡献知之甚少。为了确定是否基底神经节和丘脑萎缩独立地有助于视觉和听觉IPS损害MS，控制后的影响，新皮质体积，我们招募了86名连续MS患者和25名正常对照进行3T脑MRI和神经心理学测试。使用Sienax和FIRST软件，计算新皮质和深部灰质（DGM）体积。神经心理学测试有助于听觉和视觉IPS的措施，分别使用起搏听觉串行添加测试（PASAT）和符号数字模态测试（SDMT）。MS患者表现出显着较慢的IPS相对于对照组，并显示减少新皮层，尾状核，壳核，苍白球，丘脑和丘脑核体积。SDMT和PASAT与所有DGM区域显著相关。通过控制新皮层体积的影响，这些影响得到缓解，但所有DGM体积仍与SDMT、壳核（r = 0.409，p < 0.001）和丘脑（r = 0.362，p < 0.001）具有最强的作用，而对于PASAT，壳核的相关性是显著的（r = 0.313，p < 0.01），但丘脑的相关性不是显著的。我们证实了丘脑萎缩在MS相关IPS减慢中的重要作用，并发现壳核萎缩也是导致这种疾病的重要因素。这些DGM结构在控制了新皮层萎缩的影响后具有独立的、重要的作用。
Information-processing speed (IPS) slowing is a primary cognitive deficit in multiple sclerosis (MS). Basal ganglia, thalamus and neocortex are thought to have a key role for efficient information-processing, yet the specific relative contribution of these structures for MS-related IPS impairment is poorly understood. To determine if basal ganglia and thalamus atrophy independently contribute to visual and auditory IPS impairment in MS, after controlling for the influence of neocortical volume, we enrolled 86 consecutive MS patients and 25 normal controls undergoing 3T brain MRI and neuropsychological testing. Using Sienax and FIRST software, neocortical and deep gray matter (DGM) volumes were calculated. Neuropsychological testing contributed measures of auditory and visual IPS using the Paced Auditory Serial Addition Test (PASAT) and the Symbol Digit Modalities Test (SDMT), respectively. MS patients exhibited significantly slower IPS relative to controls and showed reduction in neocortex, caudate, putamen, globus pallidus, thalamus and nucleus accumbens volume. SDMT and PASAT were significantly correlated with all DGM regions. These effects were mitigated by controlling for the effects of neocortical volume, but all DGM volumes remained significantly correlated with SDMT, putamen (r = 0.409, p < 0.001) and thalamus (r = 0.362, p < 0.001) having the strongest effects, whereas for PASAT, the correlation was significant for putamen (r = 0.313, p < 0.01) but not for thalamus. We confirm the significant role of thalamus atrophy in MS-related IPS slowing and find that putamen atrophy is also a significant contributor to this disorder. These DGM structures have independent, significant roles, after controlling for the influence of neocortex atrophy.