Cortical and subcortical white matter damage without Wernicke's encephalopathy after recovery from thiamine deficiency in the rat.
Cortical and subcortical white matter damage without Wernicke's encephalopathy after recovery from thiamine deficiency in the rat.
复制标题
大鼠从硫胺素缺乏症恢复后，皮质和皮质下白质损伤，但没有韦尼克脑病。
DOI：
10.1111/j.1530-0277.1997.tb03788.x
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发表时间：
1997
期刊：
影响因子：
--
通讯作者：
Zhang,SX
中科院分区：
文献类型：
--
作者：
Langlais,PJ;Zhang,SX
乙醇和硫胺素缺乏在慢性酒精中毒者皮质萎缩和脑白色物质丢失中的相对病因作用尚不确定。本研究检查了Sprague-道利大鼠在无乙醇条件下从硫胺素缺乏的早期症状阶段恢复到晚期症状阶段后1周皮质和皮质下束内退化轴突的分布。暴露于吡啶硫胺诱导的硫胺素缺乏症早期症状阶段（给药12-13天）的大鼠大脑在胼胝体、前连合、外囊和内囊、视和嗅觉束以及fomix和乳头丘脑束中含有变性轴突。在额叶和顶叶皮层的III-IV层中，变性轴突的密集模式是明显的。在额叶、顶叶、扣带回、颞叶、压后、枕叶和颗粒岛皮质的IV-VI层中存在强度较低且分布更均匀的退化轴突。乳头体核的神经元计数和乳头体的面积测量与对照组相比无变化，丘脑相对未受损。在硫胺素缺乏症后期和更晚期症状阶段逆转的动物中，给药14-15天，在其他皮质区域和海马中发现变性轴突，并且在乳头体和内侧丘脑中存在广泛的神经元丢失和神经胶质增生。这些结果表明，单一发作的硫胺素缺乏症可以选择性地损害皮质白色物质束，而不损害丘脑和乳头体，并可能是一个关键因素，负责病理和行为变化的酗酒者观察到Wernicke脑病。
The relative etiologic roles of ethanol and thiamine deficiency in the cortical atrophy and loss of cerebral white matter in chronic alcoholics are uncertain. The present study examined the distribution of degenerating axons within cortical and subcortical tracts 1 week after recovery from early to late symptomatic stages of thiamine deficiency in the absence of ethanol in Sprague‐Dawley rats. The brains of rats exposed to an early symptomatic stage of pyrithiamine‐induced thiamine deficiency, 12–13 days of treatment, contained degenerating axons in corpus callosum, anterior commissure, external and internal capsules, optic and olfactory tracts, and fomix and mammillothalamic tracts. A dense pattern of degenerating axons was evident in layers Ill‐IV of frontal and parietal cortex. Less intense and more evenly distributed degenerating axons were present in layers IV‐VI of frontal, parietal, cingulate, temporal, retrosplenial, occipital, and granular insular cortex. Neuronal counts in mamrnillary body nuclei and areal measurements of the mammillary body were unchanged from controls and the thalamus was relatively undamaged. In animals reversed at later and more advanced symptomatic stages of thiamine deficiency, 14–15 days of treatment, degenerating axons were found in other cortical regions and hippocampus and there was extensive neuronal loss and gliosis within mammillary body and medial thalamus. These results demonstrate that a single episode of thiamine deficiency can selectively damage cortical white matter tracts while sparing the thalamus and mammillary body and may be a critical factor responsible for the pathological and behavioral changes observed in alcoholics without Wernicke's encephalopathy.