抗 NMDAR 脑炎患者癫痫发作与 MRI 的相关性。
- 作者列表："Ni G","Lin W","Cai X","Qin J","Feng L","Zhu S","Zhou L","Chen Z
OBJECTIVES:Seizures are a prominent feature of anti-N-methyl-D-aspartate receptor (anti-NMDAR) encephalitis. Nearly half of brain magnetic resonance image (MRI) results are abnormal. The aim of our study was to evaluate the associations between seizures and brain MRI results in patients with anti-NMDAR encephalitis. METHODS:Patients with anti-NMDAR encephalitis were enrolled between January 2015 and December 2018. The patients included were divided into normal and abnormal MRI groups. Seizure outcomes and modified Rankin scale scores at the 1-year follow-up were assessed. Seizure characteristics and outcomes were compared between groups. RESULTS:Of 35 patients with anti-NMDAR encephalitis, 28 patients (80%) had reported seizures in the acute phase. Patients with abnormal MRI findings more frequently had focal seizures than patients with normal MRI findings (72.7% vs 17.6%, P<0.01). The incidence of patients treated with 2 or more antiepileptic drugs was higher in the normal MRI group than in the abnormal MRI group (100% vs 45.4%, P<0.01). The onset-immunotherapy time was shorter in the abnormal MRI group than in the normal MRI group (P<0.05). There were no statistically significant differences in seizure outcomes between the normal and abnormal MRI groups (P>0.05). CONCLUSIONS:Focal seizures were most common in patients with abnormal MRI lesions. In the acute stage of the disease, the abnormal MRI group was more likely than the normal MRI group to achieve seizure control. Abnormal MRI findings did not affect the overall good prognosis of patients with anti-NMDAR encephalitis with seizures.
目的: 癫痫发作是抗 N-甲基-D-天冬氨酸受体 (NMDAR) 脑炎的一个显著特征。近一半的脑磁共振图像 (MRI) 结果异常。我们研究的目的是评估抗 NMDAR 脑炎患者癫痫发作与脑部 MRI 结果之间的相关性。 方法: 纳入 2015 年 1 月至 2018 年 12 月间的抗 NMDAR 脑炎患者。将纳入患者分为 MRI 正常组和异常组。评估 1 年随访时的癫痫发作结局和改良 Rankin 量表评分。比较组间癫痫发作特征和结局。 结果: 35 例抗 NMDAR 脑炎患者中，28 例 (80%) 在急性期报告癫痫发作。MRI 表现异常的患者比 MRI 表现正常的患者更容易出现局灶性癫痫发作 (72.7% vs 17.6%，P<0.01)。MRI 正常组使用 2 种及以上抗癫痫药物的发生率高于 MRI 异常组 (100% vs 45.4%，P<0.01)。MRI 异常组发病-免疫治疗时间短于 MRI 正常组 (P<0.05)。MRI 正常组与异常组的发作结局差异无统计学意义 (P>0.05)。 结论: 局灶性癫痫发作在 MRI 异常病变患者中最常见。在疾病的急性期，异常 MRI 组比正常 MRI 组更容易达到癫痫控制。异常的 MRI 表现不影响伴有癫痫发作的抗 NMDAR 脑炎患者的总体良好预后。
METHODS::Multiple sclerosis (MS) is a chronic neurodegenerative disorder with clinical symptoms of neuroinflammation and demyelination in the central nervous system. Recently, herbal medicines are clinically effective against MS as the current disease-modifying drugs have limited effectiveness. Hence, the present study evaluated the therapeutic potential of Ocimum basilicum essential oil (OB) in ethidium bromide (EB)-induced cognitive deficits in the male rats. Further, the effect of OB (50, 100 and 200 μL/kg) was evaluated on EB-induced neuroinflammation, astrogliosis and mitochondrial dysfunction in the pre-frontal cortex (PFC) of the animals. The EB was injected through bilateral intracerebroventricular route into hippocampus to induce MS-like manifestations in the rats. OB (100 and 200 μL/kg) and Ursolic acid (UA) significantly reduced the EB-induced cognitive deficits in Morris water maze and Y-maze test paradigms. OB (100 and 200 μL/kg) and UA significantly attenuated the EB-induced neuroinflammation in terms of increase in the levels of pro-inflammatory cytokines (TNF-alpha and IL-6) in the rat PFC. Further, OB (100 and 200 μL/kg) and UA significantly attenuated the EB-induced astrogliosis in terms of increase in the levels of GFAP (Glial fibrillary acidic protein) and Iba-1 (Ionized calcium binding adaptor molecule-1) in the rat PFC. In addition, OB (100 and 200 μL/kg) and UA significantly attenuated the EB-induced decrease in the mitochondrial function, integrity, respiratory control rate and ADP/O in the PFC of the rodents. Moreover, OB (100 and 200 μL/kg) and UA significantly reduced the EB-induced mitochondria-dependent apoptosis in the PFC of the rat. Hence, it can be presumed that OB could be a potential alternative drug candidate in the pharmacotherapy of MS.
METHODS::Sleep fragmentation is an increase in sleep-wake transitions without an overall decrease in total sleep time. Sleep fragmentation is well documented during acute and chronic hospitalization and can result in delirium and memory problems in children. Sleep fragmentation is also often noted in neurodevelopmental disorders. However, it is unclear how sleep fragmentation independent of disease affects brain development and function. We hypothesized that acute sleep fragmentation during the neonatal period in otherwise healthy animals would result in neuroinflammation and would be associated with abnormalities in cognitive development. The orbital shaker method was used to fragment sleep for 72 h in postnatal day 3 New Zealand white rabbit kits (fragmentation group). To control for maternal separation, the sham group was separated from the dam and maintained in the same conditions without undergoing sleep fragmentation. A naïve control group remained with the dam. Kits underwent behavioral testing with novel object recognition and spontaneous alternation T-maze tests at 2-3 weeks post-fragmentation and were sacrificed 3-50 days after fragmentation. Sleep fragmentation resulted in acute and chronic changes in microglial morphology in the hippocampus and cortex, and regional differences in mRNA expression of pro- and anti-inflammatory cytokines at 3, 7 and 50 days post-fragmentation. Impaired novel object recognition and a longer latency in T-maze task completion were noted in the fragmented kits. This was in spite of normalization of sleep architecture noted at 2 months of age in these kits. The results indicate that transient neonatal sleep fragmentation results in short-term and long-term immune alterations in the brain, along with diminished performance in cognitive tasks long-term.
METHODS:BACKGROUND:Deep brain stimulation (DBS) of the anterior nucleus of the thalamus (ANT) is a recently approved therapy for patients with drug-resistant epilepsy. To date, there is a poor understanding of the mechanism of action and lack of in vivo biomarkers. We propose a method for investigating the in vivo stimulation effects using blood-oxygen-level dependent (BOLD) MRI and present the brain activation pattern associated with ANT DBS. METHODS:Two patients undergoing ANT DBS for epilepsy underwent BOLD MRI using a block design after the DBS was programmed to alternate ON/OFF in 30 second blocks. The scanner was triggered utilizing surface electrophysiological recording to detect the DBS cycle. Nine total runs were obtained and were analyzed using a general linear model. RESULTS:Active ANT stimulation produced activation within several areas of the brain, including the thalamus, bilateral anterior cingulate and posterior cingulate cortex, precuneus, medial prefrontal cortex, amygdala, ventral tegmental area, hippocampus, striatum, and right angular gyrus. CONCLUSIONS:Utilizing block-design BOLD MRI, we were able to show widespread activation resulting from ANT DBS. Overlap with multiple areas of both the default mode and limbic networks was shown suggesting that these nodes may modulate the effect of seizure control with ANT DBS.