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1、1,血糖相关脑损害,湘雅医院 李国良,2,低血糖相关的神经系统损害,低血糖相关的神经系统损害 低血糖的神经系统损害在有关著作和论文中被作为“神经低血糖”、“低血糖脑病”“低血糖偏瘫”，“低血糖昏迷”，“低血糖危象”，“缺糖性脑病”等等。 有人认为为了便于对本病综合征 的研究，称做“低血糖的神经系统损害”较为合适,3,低血糖脑病的诊断标准一,多汗、面白、肤冷、手颤腿软，全身无力。是低血糖刺激肾上腺素分泌增多所致 意识障碍，嗜睡甚至昏迷，可用葡萄糖缓解 癫痫发作，甚至出现癫痫持续状态 可有精神障碍，如举止失常，定向力、识别力、记忆力减退，伴恐惧慌乱，躁狂，木僵 局灶性神经系统损害体征,4,症状发生
2、与血糖下降的程度、速度、持续时间及患者的机体反应性有关。 当血糖下降快时，体内释放大量肾上腺素，临床表现为饥饿、出汗、心动过速、肌体震颤、无力等交感神经兴奋症状。 当血糖下降缓慢、历时长，而致交感神经兴奋症状不明显，则临床出现头痛、头晕、昏迷、抽搐、偏瘫、尿失禁等中枢神经损害征象。 低血糖反应可导致局灶神经损害，包括脑干征、偏瘫、四肢瘫、截瘫和发作性舞蹈-徐动症等 因其发病突然，并有意识障碍或肢体瘫痪，且老年人多发，故易误诊为脑血管病。,5,低血糖脑病的诊断标准二,脑电图呈弥漫性慢波，有癫痫发作者可出现痫性放电 脑脊液检查压力增高，糖含量降低,6,低血糖脑病的诊断标准,Whipple三联征 空
3、腹时具有低血糖症状和体征 血糖浓度在2.78mmol/L(50mg/dl) 静脉注射葡萄糖后症状立即缓解,7,低血糖的不典型表现,意识障碍合并抽搐，易误诊为癫痫 精神症状，烦躁不安，易激惹，情绪激动，语无伦次，有骂人、打人，幻视有时可误诊为脑病及酒精中毒 神志清楚，出现肢体，言语障碍，容易误诊为脑血管病 昏迷，瞳孔不等大，对光反射迟钝，易误诊为脑疝,8,引起本病的原因,最常见的是降糖药物使用不当所致。 对胰岛素过度敏感。 胰岛素过多：胰岛素瘤，异位胰岛素分泌瘤。 反应性低血糖症：早期糖尿病，功能性低血糖，营养性低血糖 肝脏疾病 中毒：药物中毒，酒精中毒，大量食荔枝 糖原累积病 胃大部分切除术后
4、 肾上腺皮质或垂体前叶疾病,9,低血糖性脑病可能发病机制,低血糖引起交感神经兴奋而导致脑血管痉挛 原有脑动脉硬化的动脉狭窄所引起神经功能损伤 低血糖引起神经系统的选择受损,10,低血糖脑病影像诊断,以往我国报道低血糖昏迷病例较多，除部分老年患者因合并脑梗死等颅脑CT或MRI有相应改变外，绝大多数报道称患者的神经影像学无特殊异常 因此不能单纯依靠CT或MRI来诊断，应主要依靠临床表现及血糖检查来确诊,11,颅脑MRI对诊断具有重要价值,头重颅CT扫描对HE的诊断价值不大；MRI对严低血糖患者的诊治有重要意义，尤其DWI序列 由于葡萄糖减少导致大脑能量缺失和离子泵衰竭，水分子向细胞内运动和细胞外水
5、容积显著减少，导致细胞毒性水肿，水分子弥散障碍。 可见双侧尾状核和豆状核对称性或略长T1,长T2,Flair高信号，DWI高信号 低血糖性脑病早期DWI检查，其定位及定性敏感性比CT、常规MRI高，主要表现DWI呈高信号，表面弥散系数（ADC）值降低。,12,低血糖脑损害具有一定的区域选择性，细胞愈进化，对缺糖愈敏感 尾状核、豆状核、大脑皮质、海马和黑质是低血糖的敏感区域，最易受损 也有研究提示敏感区域还包括胼胝体和皮质下白质。 几乎不累及丘脑，小脑及脑干 目前认为，天门冬氨酸的区域性表达和N-甲基-D-天（门）冬氨酸（NMDA）受体的分布与HE病变的高度选择性关系密切,13,有研究发现，严重
6、低血糖患者病损一旦侵犯到皮质和基底节区，病变多不易恢复 临床症状和DWI异常可在短时间内逆转者，病变多在胼胝体压部，皮质下白质和内囊后肢 提示DWI序列在一定程度上有助于判断预后，胼胝体压部受损者预后相对较好,14,低血糖性脑病与缺血性脑血管病神经影像学两个显著差别:,一是缺血性脑血管病可见到小的出血点灶，而低血糖性脑病时没有 二是缺血性脑血管病可见到对称性丘脑损害，而低血糖性脑病没有,15,大脑皮质双侧损害,Fig 1. Case 1, a 65-year-old man in a diabetic coma with seizures. A, Fast spin-echo millisec
7、onds/110 fluid attenuated inversion recovery (9000 milliseconds effective/2200 milliseconds TR/TE/TI) MR image shows bilateral hyperintensity of the cortex over the temporal and occipital lobes. B and C, Diffusion-weighted (10000/105, b value 1000 seconds/mm2) MR images showing corresponding hyperin
8、tensity in the cortex. D and E, ADC maps at the same levels as B and C show decreased ADC in these lesions (618 103 mm2/s) compared with normal white matter (819 103 mm2/s).,16,大脑皮质偏侧损害,Images in 26-year-old man (patient 6) found unconscious, with a Glasgow Coma Scale score of 7, and not moving left
9、 side. (a) DW MR image shows confluent hyperintense lesions in the right inferior frontal,insular, and posterior temporal lobe cortices. (b) MR angiogram shows increased vascularity of the right middle cerebral artery branches (arrow) compared with the normal left side, suggesting augmented collater
10、al flow. (c) Relative cerebral blood volume map shows no noticeable decrease in the abnormal right cerebral hemisphere; blood volume was in fact increased by 20%25%, a finding that is also suggestive of maximal vasodilatation (see text). (d) Graph of single-oxel MR spectroscopic data in affected rig
11、ht cerebral cortex shows decreased N-acetylaspartate (NAA) level, preserved choline (Cho) and creatine (Cr) levels, and no evidence of abnormal lactate level (arrow1.3 ppm).,17,大脑皮质损害，丘脑未累及,Diffusion-weighted magnetic resonance (MR) imaging (A) and T2-weighted MR imaging (B) showed a diffuse cortica
12、l high signal. The brainstem,cerebellum, and thalamus were spared as were the dorsofrontal cortex and occipital poles. The signal change in the hippocampus was relatively small on diffusion-weighted MR imaging. On T2-weighted MR imaging, a focal high-signal lesion was seen in the thalamus bilaterall
13、y (more prominent on the left side) and in the centrum semiovale. Diffuse white matter lesions were seen on the T2-weighted MR image,18,新生儿低血糖MR表现,病例1MR I 生后34 h出现低血糖表现, 58 h入院, 血糖为1. 7mm ol/L。A D 为生后3 d所见。A, B分别为矢状面T1W I和横断面T2W I, 可见顶枕叶T1W I低信号, 而T2W I改变不明显; C为DW I, 可见顶枕叶皮层高信号, 提示明显的细胞毒性水肿; D F为生后1
14、3 d T1W I( D) , T2W I( E )和DW I( F)图像, 枕部可见明显的T1W I低信号, T2W I高信号, 而DW I顶枕部转为低信号, 提示皮层发生水肿坏死。,19,皮质、基底节、脑室旁白质损害,Fig. 1 ad (Patient 5) A 57-year-old diabetic man was found in a coma 6 h after he was last seen. Glucose level was 16 mg/dL at presentation. Fluid-attenuated inversion recovery image (a) on
15、 the day of admission shows slightly increased signal intensity in the cerebral cortex and basal ganglia. Diffusion-weighted images (b, c) clearly show bilaterally symmetrical hyperintense lesions in the cerebral cortex, basal ganglia, and periventricular white matter (arrows). ADC map (d) obtained
16、at the same level as c shows corresponding reduced ADC,20,内囊、放射冠损害,Figure 1. Diffusion-weighted MRI on admission showing the hyperintensity lesions within the bilateral internal capsule, corona radiata, and frontoparietal cortex. Note that bilateral hippocampi do not disclose any hyperintensity lesions.,Figure 2. Diffusion-weighted MRI 10 days after glucose infusion showing regression of the hyperintensity lesions.,21,半卵圆中心非对称损害,Fig. 5 a, b (Patient 17) A 91-year-old diabetic man
