目的探讨急性脑梗死（acute cerebral infarction,ACI）患者应用参芎葡萄糖注射液治疗前后外周血白介素-33（IL-33）和动静脉血糖差（Da-jvGlu）的变化及临床意义。方法检测126例不同梗死体积急性脑梗死患者及10名健康体检者（正常对照组）的外周血IL-33水平和动静脉葡萄糖差,比较各组结果。结果治疗前各组血清IL-33与正常对照组比较,大体积脑梗死组IL-33水平显著增高（P ＜0.05）;小体积和中等体积脑梗死组无显著差异。静脉给予参芎葡萄糖注射液+常规治疗7 d后各组血清IL-33与治疗前比较,大体积脑梗死组IL-33水平无显著变化（P＞ 0.05）;小体积和中等体积脑梗死组两组IL-33水平均有显著增高（P ＜0.05）。各组ACI患者治疗前后Da-jvGlu变化比较,治疗前各组与正常对照组比较,大体积脑梗死组Da-jvGlu显著增高（P ＜0.05）;小体积和中等体积脑梗死组无显著差异（P＞ 0.05）。结论参芎葡萄糖注射液可通过调整IL-33水平抑制促炎作用,促进脑细胞损伤的修复和再生,同时并未干扰体内葡萄糖代谢水平。

脑室管膜炎是一种严重的颅内感染,发病率为0.2%~4%[1].该病以脑室内脑脊液化脓性改变为特征,伴脑积水,多由化脓性脑膜炎不规则治疗或延误治疗所致[2],可导致严重的神经功能损害,甚至死亡[3].

神经梅毒是病原体苍白螺旋体感染神经系统后出现大脑、脑膜或脊髓损害的一组临床综合征[1]. 神经梅毒可发生于梅毒的各个时期[2] ,临床表现复杂,易误诊、漏诊. 现将我科2017年收治的1例以脊髓炎为首发症状的神经梅毒病例进行回顾性分析.

This study describes the case of a 41-year-old woman admitted for anterograde memory loss, right facial grimacing and right arm posturing that had begun 1 month previously. Cranial magnetic resonance-diffusion weighted imaging and -fluid-attenuated inversion recovery imaging revealed a hyperintense signal in the left hippocampus and right basal ganglia, but no contrast enhancement. An electroencephalogram revealed rhythmic sharp and slow waves and rhythmic θ build-ups in the left temporal area. Single-photon emission computed tomography showed increased regional blood flow perfusion in the left cerebral frontal lobe and the right basal ganglia. The cerebrospinal fluid was normal, with the exception of the presence of leucine-rich glioma-inactivated 1 (LGI1) antibodies, and LGI1 antibodies were also found in the blood serum. The presence of the antibodies, the faciobrachial dystonic seizures (FBDSs) and the memory loss indicated limbic encephalitis. After 3 months of immunotherapy, the patient was free from epileptic seizures and had undergone a partial memory restoration. FBDSs alone justify the immediate initiation of immunotherapy, even prior to laboratory confirmation of the disease, as early treatment limits the duration of the illness.

A few cases of cerebral cavernous malformation (CCM) have been reported in Chinese families with different mutations during the past decade. Herein, we report a case of CCM in a proband in a Chinese family, for whom the mutation type of the CCM remains to be identified. The proband of the family presented a range of clinical symptoms and features that included paralysis, aphasia, multiple lesions in the brain, and cutaneous capillary–venous malformations. PCR was performed to amplify all of the coding exons of the three CCM genes (CCM1, CCM2, and CCM3) in the proband and revealed a heterozygous T deletion in exon 15 (c.1542delT) of CCM1 gene. Targeted mutation analysis in family members demonstrated that this mutation segregated with the disease in the family. This is the first report of a heterozygous CCM1 deletion mutation. Our findings provide a new CCM gene mutation profile in a Chinese family which will be of significance in genetic counseling for CCM.