Increased expression of Notch1 in temporal lobe epilepsy: animal models and clinical evidence

Temporal lobe epilepsy is associated with astrogliosis. Notchl signaling can induce astrogliosis in glioma. However, it remains unknown whether Notchl signaling is involved in the pathogenesis of epilepsy. This study investigated the presence of Notchl, hairy and enhancer of split-l, and glial fibrillary acidic protein in the temporal neocortex and hippocampus of lithium-pilocar- pine-treated rats. The presence of Notchl and hairy and enhancer of split-1 was also explored in brain tissues of patients with intractable temporal lobe epilepsy. Quantitative electroencephalo- gram analysis and behavioral observations were used as auxiliary measures. Results revealed that the presence of Notchl, hairy and enhancer of split-l, and glial fibriUary acidic protein were en- hanced in status epilepticus and vehicle-treated spontaneous recurrent seizures rats, but remain unchanged in the following groups： control, absence of either status epilepticus or spontaneous recurrent seizures, and zileuton-treated spontaneous recurrent seizures. Compared with patient control cases, the presences of Notch1 and hairy and enhancer of split- 1 were upregulated in the temporal neocortex of patients with intractable temporal lobe epilepsy. Therefore, these results suggest that Notchl signaling may play an important role in the onset of temporal lobe epilepsy via astrogliosis. Furthermore, zileuton may be a potential therapeutic strategy for temporal lobe epilepsy by blocking Notchl signaling.

The brain activation pattern of the medial temporal lobe during chewing gum: a functional MRI study

The human brain is known to be influenced by environmental stimuli（Feeney et al.,1982;Kaplan,1988）.Therefore,research on the brain activation pattern by external stimuli has been an important topic in neuroscience（Kaplan,1988）.Chewing gum has been known to have a positive effect on cognition,including alertness,attention,cognitive processing speed,

Anomalous expression of chloride transporters in the sclerosed hippocampus of mesial temporal lobe epilepsy patients

The Na＋-K＋-CI- cotransporter 1 and K＋-CI- cotransporter 2 regulate the levels of intracellular chloride in hippocampal cells. Impaired chloride transport by these proteins is thought to be involved in the pathophysiological mechanisms of mesial temporal lobe epilepsy. Imbalance in the relative expression of these two proteins can lead to a collapse of CI- homeostasis, resulting in a loss of gamma-aminobutyric acid-ergic inhibition and even epileptiform discharges. In this study, we investigated the expression of Na＋-K＋-CI- cotransporter 1 and K＋-CI- cotransporter 2 in the sclerosed hippocampus of patients with mesial temporal lobe epilepsy, using western blot analysis and immunohistochemistry. Compared with the histologically normal hippocampus, the sclerosed hippocampus showed increased Na＋-K＋-Cl- cotransporter 1 expression and decreased K＋-CI- cotransporter 2 expression, especially in CA2 and the dentate gyrus. The change was more prominent for the Na＋-K＋-CI- cotransporter 1 than for the K＋-CI- cotransporter 2. These experimental findings indicate that the balance between intracellular and extracellular chloride may be disturbed in hippocampal sclerosis, contributing to the hyperexcitability underlying epileptic seizures. Changes in Na＋-K＋-CI-cotransporter 1 expression seems to be the main contributor. Our study may shed new light on possible therapies for patients with mesial temporal lobe epilepsy with hippocampal sclerosis.

Extracellular signal regulated kinases 1/2 signal pathway and responses of astrocytes after diffuse brain injury

BACKGROUND： The treatment of diffuse brain injury during an acute period is focused on relieving degrees of secondary brain injury. Generation and development of pathological changes of secondary brain injury depend on signal conduction, so down-regulating over response of astrocyte through interfering a key link of signal conduction pathway may bring a new thinking for the treatment of diffuse brain injury. OBJECTIVE： To observe the effect of over activity of extracellular signal regulated kinases 1/2 （ERK1/2） signal pathway on the response of astrocyte during an acute period of diffuse brain injury. DESIGN： Completely randomized grouping and controlled animal study. SETTINGS： Department of Neurosurgery, the Third Affiliated Hospital, Nanchang University; Department of Neurosurgery, Union Hospital Affiliated to Tongji Medical College, Huazhong University of Science and Technology. MATERIALS： A total of 158 healthy male SD rats, of 11 weeks old, weighing 320-370 g, were provided by Experimental Animal Faulty, Tongji Medical College, Huazhong University of Science and Technology. Rabbit-anti-phosphorylated ERK1/2 （pERK1/2） polyclonal antibody was provided by R＆D Company; rabbit-anti-glial fibrillary acidic protein （GFAP） polyclonal antibody, SP immunohistochemical kit and horseradish peroxidase （HRP）-labeled goat-anti-rabbit IgG by Santa Cruz Company; specific inhibitor U0126 of ERK1/2 signal pathway by Alexis Company. METHODS： The experiment was carried out in the Laboratory of Neurosurgery, Union Hospital Affiliated to Tongji Medical College, Huazhong University of Science and Technology from September 2004 to March 2006. ① Detection of pERK1/2 expression： A total of 110 rats were randomly divided into sham operation group （n =5）, model group （n =35）, high-dosage U0126 group （n =35） and low-dosage U0126 group （n =35）. Rats in the sham operation group were only treated with incision of epicranium and fixation of backup plate, but not hit. Rats in the model group were used to establish diffuse brain injury models based on Marmarou free falling body without drug intervention. Rats in the high- and low-dosage U0126 groups were injected into caudal vein with 0.1 and 0.05 mg/kg U0126, respectively, and then, rats were hit to establish injured models. Every 5 rats were collected from model, high- and low-dosage U0126 groups at 5, 30 minutes, 3, 12, 24, 72 hours and 7 days after diffuse brain injury to detect pERK1/2 expression in cortex of parietal lobe based on Western blot technique. ② Distribution of pERK1/2 and positive GFAP cells in brain tissue： Another 48 rats were randomly divided into sham operation group （n =3）, model group （n =15）, high-dosage U0126 group （n =15） and low-dosage U0126 group （n =15）. The intervention and administration were dealt as the same as those mentioned above. Every 3 rats were collected from model, high- and low-dosage U0126 groups at 30 minutes, 3, 12, 24 and 72 hours after model establishment to observe the distribution of pERK1/2 and postive GFAP cells in brain tissue which was cut from coronal section at Bregma -4.8 mm layer with immunohistochemical staining. MAIN OUTCOME MEASURES： pERK1/2 expression in cortex of parietal lobe and distribution of pERK1/2 and positive GFAP cells in brain tissues. RESULTS： ① pERK1/2 expression： After diffuse brain injury, pERK1/2 expression in cortex of parietal lobe was rapidly increased in the model group, reached at peak at 5 minutes and then decreased gradually. But the expression was still in a high level until the 72nd hour and fallen to the basic level on the 7th day. pERK1/2 level was lower in high- and low-dosage U0126 groups than that in model group at various time points （P 〈 0.01）; meanwhile, pERK1/2 level was lower in high-dosage U0126 group than that in low-dosage U0126 group. The results showed that there was a certain dosage dependence on pERK1/2 expression. ② Distribution of pERK1/2 and positive GFAP cells in brain tissue： Positive expression of pERK1/2 lasted inbrain tissue from 30 minutes to 72 hours after diffuse brain injury （P 〈 0.05）. In addition, from 30 minutes to 3 hours, brown-yellow stained cells were mainly distributed in plasma, but rarely in nucleus. A lot of positive cells had tree-like apophysis, which was similar to neurons. With the time passing by, more and more nuclei manifested positive stains; moreover, nuclei mainly manifested positive staining until 24 hours after diffuse brain injury. Immune-positive pERK1/2 cells were widely distributed in brain tissue, especially mainly in binding site between deep cortex and cerebral white matter, and then in hippocampus. In addition, ependymal cell and vascular endothelial cells of choroids plexus also manifested strongly positive staining. As compared with model group, positive cells were decreased gradually in high- and low-dosage U0126 groups. However, number of positive cells was less in high-dosage U0126 group than that in low-dosage U0126 group. CONCLUSION： Diffuse brain injury strongly induces the activity of ERK1/2 signal pathway and response of astrocyte; in addition, U0126 can inhibit response of glial cells during an acute period, and the effect manifests dosage dependence.

GAP-43 Expression and Pathological Changes of Temporal Infarction in R.ats and Effects of Batroxobin

To study the changes of the expression of growth-associated protein-43 (GAP-43) and pathology in temporal infarction of rats photochemically induced and the effects of batroxobin. METHODS: Immunohistochemical technique and hematoxylin-eosin stain was used to show the changes of the expression of GAP-43 and pathology. RESULTS: In infarction group, GAP-43 expression was markedly increased on the infarction and surrounding tissues at 24 h cerebral infarction. The expression reached peak level at 72 h after cerebral infarction and was decreased at 7 d after cerebral infarction. However, in batroxobin-treated group, GAP-43 expression was increased and the pathological changes were much slight as compared with infarction group. CONCLUSION: The expression of GAP-43 increases in infarction of temporal neocortex and batroxobin promotes the expression of GAP-43 and ameliorates the pathological changes in infarction of temporal neocortex.

Effects of Batroxobin on Spatial Learning and Memory Disorder of Rats with Temporal Ischemia and the Expression of HSP32 and HSP70

The effect of Batroxobin on spatial memory disorder of left temporal ischemic rats and the expression of HSP32 and HSP70 were investigated with Morri`s water maze and immunohistochemistry methods. The results showed that the mean reaction time and distance of temporal ischemic rats in searching a goal were significantly longer than those of the sham-operated rats and at the same time HSP32 and HSP70 expression of left temporal ischemic region in rats was significantly increased as compared with the sham-operated rats. However, the mean reaction time and distance of the Batroxobin-treated rats were shorter and they used normal strategies more often and earlier than those of ischemic rats. The number of HSP32 and HSP70 immune reactive cells of Batroxobin-treated rats was also less than that of the ischemic group. In conclusion, Batroxobin can improve spatial memory disorder of temporal ischemic rats; and the down-regulation of the expression of HSP32 and HSP70 is probably related to the attenuation of ischemic injury.

Effect of Batroxobin on Expression of C-Jun in Left Temporal Ischemic Rats with Spatial Learning and Memory Disorder

The effect of Batroxobin on expression of c-Jun in left temporal ischemic rats with spatial memory disorder was investigated by means of Morri's water maze and immunohistochemistry methods. The results showed that the mean reaction time and distance of temporal ischemic rats for searching a goal were significantly longer than those of sham-operated rats, and at the same time c-Jun expression of left temporal ischemic region was significantly increased. However, the mean reaction time and distance of Batroxobin-treated rats were shorter and they used normal strategies more often and earlier than those of ischemic rats. The number of c-Jun immune reactive cells of Batroxobin-treated rats was also less than that of ischemic group. In conclusion, Batroxobin can improve spatial memory disorder in temporal ischemic rats, and the down-regulation of the expression of c-Jun is probably related to the neuroprotective mechanism.

Regional volume changes of the brain in migraine chronification

The pathophysiology of migraine is complex.Neuroimaging studies reveal functional and structural changes in the brains of migraine patients.We sought to explore regional volume differences in intracranial structures in patients with episodic and chronic migraine.Sixteen episodic migraine patients,16 chronic migraine patients,and 24 normal controls were recruited and underwent 3.0 T MRI scanning.The volumes of 142 brain regions were calculated by an automatic volumetric algorithm and compared with clinical variables.Results demonstrated that the volumes of specific regions in the frontal and occipital lobes,and the right putamen,were increased and the volume of the fourth ventricle was decreased in the episodic migraine patients compared with controls.The volumes of the left basal forebrain,optic chiasm,and,the fourth ventricle were decreased in the chronic migraine patients,while the occipital cortex and the right putamen were larger.Compared to episodic migraine patiants,chronic migraine patients displayed larger left thalamus and smaller frontal regions.Correlation analysis showed that headache frequency was negatively correlated with the volume of the right frontal pole,right lateral orbital gyrus,and medial frontal lobes and positively correlated with the volume of the left thalamus.The sleep disturbance score was negatively correlated with the volume of the left basal forebrain.This suggests that migraine patients have structural changes in regions associated with pain processing and modulation,affective and cognitive processing,and visual perception.The remodeling of selective intracranial structures may be involved in migraine attacks.This study was approved by the Ethics Committee of Chinese PLA General Hospital(approval No.S2018-027-02)on May 31,2018.

Hippocampus chronic deep brain stimulation induces reversible transcript changes in a macaque model of mesial temporal lobe epilepsy

Background:Deep brain stimulation(DBS)has seizure-suppressing effects but the molecular mechanisms underlying its therapeutic action remain unclear.This study aimed to systematically elucidate the mechanisms underlying DBS-induced seizure suppression at a molecular level.Methods:We established a macaque model of mesial temporal lobe epilepsy(mTLE),and continuous high-frequency hippocampus DBS(hip-DBS)was applied for 3 months.The effects of hip-DBS on hippocampus gene expression were examined using high-throughput microarray analysis followed by bioinformatics analysis.Moreover,the microarray results were validated using quantitative real-time polymerase chain reaction(qRT-PCR)and Western blot analyses.Results:The results showed that chronic hip-DBS modulated the hippocampal gene expression.We identified 4119 differentially expressed genes and assigned these genes to 16 model profiles.Series test of cluster analysis showed that profiles 5,3,and 2 were the predominant expression profiles.Moreover,profile 5 was mainly involved in focal adhesion and extracellular matrix-receptor interaction pathway.Nine dysregulated genes(Arhgap5,Colla2,Itgbl^Pik3rl,Lama4,Fnl,Col3al,Itga9,and Shc4)and three genes(Colla2,Itgbl,and Flna)in these two pathways were further validated by qRT-PCR and Western blot analyses,respectively,which showed a concordance.Conclusion:Our findings suggest that hip-DBS could markedly reverse mTLE-induced abnormal gene expression.Findings from this study establish the basis for further investigation of the underlying regulatory mechanisms of DBS for mTLE.

Endovascular Application of Low-Energy Laser in the Treatment of Dyscirculatory Angiopathy of Alzheimer’s Type

Purpose: We propose an analysis of dyscirculatory angiopathy of Alzheimer’s type (DAAT) endovascular treatment method based on transcatheter revascularization and recovery of collateral and microvascular bed of the brain by means of low-energy transluminal laser irradiation as well as its comparison with traditional Alzheimer’s disease (AD) treatment methods. Methods: The research involved 81 patients aged 34 - 79 (average age 67). 46 (46.8%) patients were treated using endovascular method—Test Group. 35 (43.2%) patients were given conventional treatment—Control Group. Patients were subdivided: Group (CDR-0): 9 (11.1%), pre-clinical stage or increased AD risk;Group (CDR-1): 24 (29.6%), mild dementia and cognitive impairment;Group (CDR-2): 31 (38.3%), moderate dementia and persistent cognitive impairment;Group (CDR-3): 17 (21.0%), severe dementia and cognitive impairment. Research plan included CT or MRI with subsequent temporal lobes volume calculation, brain scintigraphy (SG), rheoencephalography (REG), and cerebral MUGA. There were indications and contraindications for treatment in Test Group. In Group CDR-0, endovascular intervention was prophylactic, against the background of increasing memory impairment;in Groups CDR-1, CDR-2, CDR-3, it was conducted in 1 to 12 years period from AD symptoms appear-ance. Conservative treatment with Memantin and Rivastigmine was carried out in Control Group. Results: In Test Group, positive outcome accompanied by prolonged dementia decline, cognitive impairment decrease, and patients’ transition to CDR group of an earlier stage, was obtained in all cases. In Control Group, patients’ temporary stabilization in their own CDR group was achieved. Conclusions: Endovascular treatment of patients with AD different stages can not only reduce DAAT phenomena but can also cause AD regression possibly accompanied by regenerative processes in the cerebral tissue. Conservative treatment only allows stabilizing the patient’s condition for a while.

Why psychosis is frequently associated with Parkinson's disease?

Psychosis is a common non-motor symptom of Parkinson’s disease whose pathogenesis remains poorly understood. Parkinson’s disease in conjunction with psychosis has been shown to induce injury to extracorticospinal tracts as wel as within some cortical areas. In this study, Parkinson’s disease patients with psychosis who did not receive antipsychotic treatment and those without psychosis underwent diffusion tensor imaging. Results revealed that in Parkinson’s disease patients with psychosis, damage to the left frontal lobe, bilateral occipital lobe, left cingulated gyrus, and left hippocampal white-matter fibers were greater than damage to the substantia nigra or the globus pal idus. Damage to white-matter fibers in the right frontal lobe and right cingulate gyrus were also more severe than in the globus pal idus, but not the substantia nigra. Damage to frontal lobe and cingulate gyrus white-matter fibers was more apparent than that to occipital or hippocampal fiber damage. Compared with Parkinson’s disease patients without psychosis, those with psychosis had significantly lower fractional anisotropy ratios of left frontal lobe, bilateral occipital lobe, left cingu-lated gyrus, and left hippocampus to ipsilateral substantia nigra or globus pal idus, indicating more severe damage to white-matter fibers. These results suggest that psychosis associated with Par-kinson’s disease is probably associated with an imbalance in the ratio of white-matter fibers be-tween brain regions associated with psychiatric symptoms （frontal lobe, occipital lobe, cingulate gyrus, and hippocampus） and those associated with the motor symptoms of Parkinson’s disease （the substantia nigra and globus pal idus）. The relatively greater damage to white-matter fibers in psychiatric symptom-related brain regions than in extracorticospinal tracts might explain why psy-chosis often occurs in Parkinson’s disease patients.

The tomography dementia rating scale (TDR)—The rating scale of Alzheimer’s disease stages

The purpose of this research is to develop a morphologically determined scale—the Tomography Dementia Rating scale (TDR) to diagnose AD stages, based on the measurement of the severity of voluminal atrophic changes of the temporal lobes of the brain detected among patients during CT and MRI at various stages of the disease. The research included 140 patients aged 28 - 79. Test Group comprised 81 patients aged 34 - 79 suffering from various AD stages. Control Group consisted of 59 patients aged 28 - 78 who had various types of brain lesions with manifestations of dementia and cognitive impairment but who did not suffer from AD. CT and MRI data obtained has made it possible to create a scale that allows determining the severity of atrophic changes in the temporal lobes at each stage of AD development: 1) Pre-clinical AD stage—TDR-0: temporal lobes atrophy with a 4% - 8% decrease in tissue mass (corresponds to 26 - 28 MMSE points);2) Early AD Stage—mild dementia—TDR-1: temporal lobes atrophy with a 9% - 18% decrease in tissue mass (corresponds to CDR-1 and to 20 - 25 MMSE points);3) Middle AD stage—moderate dementia—TDR-2: temporal lobes atrophy with a 19% - 32% decrease in tissue mass (corresponds to CDR-2 and to 12 - 19 MMSE points);4) Late AD stage—heavy dementia—TDR-3: temporal lobes atrophy with a 33% - 62% decrease in tissue mass (corresponds to CDR-3 and to 7 - 11 MMSE points). Thereby, the developed Tomography Dementia Rating scale (TDR) complements the Clinical Dementia Rating scale (CDR) and allows a correct and objective determination of AD stages as well as an easy differentiation of existing lesions with neurodegenerative changes characteristic for other diseases accompanied by dementia and cognitive impairment.

原发性早泄中枢丘脑-额叶-躯体感觉皮层环路MRI研究进展

原发性早泄(lifelong premature ejaculation,LPE)是男性最常见的性功能障碍疾病,但中枢发病机制尚不明确。近年来,研究人员借助多模态磁共振成像(magnetic resonance imaging,MRI)技术检测和分析了LPE患者大脑结构和功能的特定变化,尤其是与奖赏系统相关的丘脑-额叶环路,以及参与射精周期的躯体感觉皮层。本文将基于丘脑-额叶-躯体感觉皮层环路对LPE患者的大脑MRI研究发现进行综述,探寻丘脑-额叶-躯体感觉皮层环路在LPE中枢神经系统中的作用机制,为开辟新的早泄评估和疗效评价方法提供科学依据。

阴性颞叶癫痫患者静息态脑功能连接网络特征融合策略的分析

静息态功能磁共振成像(rfMRI)的功能连接(FC)可为阴性颞叶癫痫提供脑功能异常指标,但冗余特征影响了精准性。为此,本研究提出结合特异性指数模型与判别相关分析(DCA)的特征融合策略以改善识别效果。将20位患者与20位健康人的rfMRI数据预处理后,以健康人为对照组,构建两类特异性指数模型以量化FC和脑网络FC;采用最小冗余最大相关(mRMR)及独立样本t检验去除冗余特征,应用DCA融合2类FC特异性指标;将融合特征分别输入到K近邻、支持向量机和逻辑回归分类器中,并以嵌套10次10折交叉验证与嵌套10次5折分层交叉验证的平均分类精度来评估算法有效性。结果表明,融合特征识别率达到了91.25%~92.50%,高于非融合方案的识别水平。所提出的特征融合策略可有效地处理冗余信息,增强特征判别能力,为精准识别阴性颞叶癫痫提供了新思路。

海马-杏仁核脑深部电刺激术治疗难治性内侧颞叶癫痫长期疗效及其对认知功能的影响

目的 探讨海马-杏仁核脑深部电刺激术(AH-DBS)治疗难治性内侧颞叶癫痫的长期疗效及其对认知功能的影响。方法 共纳入2014年1月至2018年12月解放军总医院第一医学中心收治的7例难治性内侧颞叶癫痫患者,均行AH-DBS,对比手术前后癫痫发作形式、发作频率和抗癫痫发作药物应用情况,采用韦氏成人智力量表修订版(WAIS-R)评估认知功能;术后记录刺激参数以及手术相关并发症。结果 共7例患者行双侧AH-DBS 4例,左侧AH-DBS 2例,左侧AH-DBS联合右侧颞前叶切除术1例;经枕部入路6例,经额部入路1例;仅1例患者术后出现头皮切口愈合不良,经局部植皮后痊愈。术后平均随访(73.00±8.98)个月,随访期间复杂部分性发作频率[1.00(0.00,31.00)次/月对2.00(1.50,60.00)次/月;Z=-2.207,P=0.027]、继发性全面性强直-阵挛发作频率[0.00(0.00,1.00)次/月对2.00(1.00,3.00)次/月;Z=-2.428,P=0.015]和总发作频率[1.00(0.50,31.00)次/月对5.00(2.50,64.00)次/月;Z=-2.366,P=0.018]均较术前减少,而手术前后抗癫痫发作药物种类[1.00(1.00,2.00)种对1.00(1.00,3.00)种;Z=-1.633,P=0.102]和WAIS-R评分[(85.50±7.09)分对(89.00±9.47)分;t=-1.761,P=0.078]差异无统计学意义。结论 AH-DBS作为一种新型抗癫痫治疗方法,可以减少难治性内侧颞叶癫痫发作频率,无严重不良事件,且对认知功能无明显影响。

MRI检查鼻咽癌放射性颞叶损伤的漏诊原因

目的:放射治疗是鼻咽癌的主要治疗方法,但容易发生放射性颞叶损伤(radiotherapy-induced temporal lobe injury,RTLI)。磁共振成像(magnetic resonance imaging,MRI)检查是鼻咽癌放射治疗后RTLI的主要诊断方法,但容易漏诊。本研究旨在探讨MRI检查鼻咽癌放射治疗后RTLI漏诊的原因。方法:回顾性分析2010年1月至2021年4月在中南大学湘雅医院诊断为鼻咽癌且接受放射治疗患者的临床和MRI资料。由2位放射科医生重新审阅患者放射治疗前、后所有头颈部(包括鼻咽部和颅脑)MRI资料,对首次发现颞叶晚迟发反应型放射性脑损伤的患者作出首次RTLI诊断。若首次诊断鼻咽癌RTLI患者的原始诊断未报告颞叶病变,则定义为漏诊。将首次诊断鼻咽癌RTLI患者分为漏诊组和非漏诊组。比较漏诊组与非漏诊组的一般临床资料和影像学资料,并进一步采用多因素Logistic回归分析MRI漏诊首次RTLI的独立危险因素。结果:共纳入符合要求的鼻咽癌放射治疗后首次诊断为RTLI的患者187例,原始诊断报告漏诊120例,未漏诊67例,首次诊断RTLI的准确率为35.8%,漏诊率为64.2%。漏诊组与未漏诊组在病灶大小、病灶是否仅在内侧颞叶、对侧颞叶有无病灶、有无白质高信号/囊变及出血、MRI检查部位以及有无水抑制反转恢复序列(fluid attenuated inversion recovery,FLAIR)序列方面的差异均有统计学意义(均P<0.05)。多因素Logistic回归分析显示:病灶≤25 mm、病灶无强化、病灶无囊变及出血、病灶仅在内侧颞叶和仅检查鼻咽部MRI是MRI漏诊首次RTLI的独立危险因素(均P<0.05)。结论:MRI首次诊断RTLI的漏诊主要与病灶的大小和部位、病灶的影像学特点及MRI检查部位相关。

基于Freesurfer自动分割技术评估不同类型颞叶癫痫患者大脑皮层厚度的改变

目的探讨Freesurfer自动分割技术评估成人颞叶癫痫(TLE)大脑皮层厚度的变化。资料与方法回顾性收集2021年1月—2023年9月宁夏医科大学总医院经临床表现和脑电图共同确诊的84例TLE,包括MRI阴性TLE 32例、左侧海马硬化30例、右侧海马硬化22例,招募50例健康志愿者作为对照组,均行轴位T1WI三维磁化强度预备梯度回波序列扫描。使用Freesurfer软件对T1WI图像行大脑皮层分割,比较不同类型TLE患者各皮层厚度的差异。结果MRI阴性TLE组与对照组比较有14个区域皮层厚度均减小,主要集中在双侧额叶和右侧顶叶,差异有统计学意义(P均<0.05);左侧海马硬化组与对照组比较有34个区域皮层厚度均减小,主要集中在双侧额叶、颞叶及顶叶,差异有统计学意义(P均<0.05);右侧海马硬化组与对照组比较有27个区域皮层厚度均减小,主要集中在双侧额叶、顶叶及右侧颞叶,差异有统计学意义(P均<0.05)。结论自动分割技术可评价不同类型TLE患者大脑不同皮层区域厚度的变化,有助于临床进一步了解TLE的发展,为完善治疗方法或术前评估提供参考。

基于自动脑分割技术对海马硬化型颞叶内侧癫痫颞叶白质体积的分析及其应用价值

目的:利用自动脑分割技术(FreeSurfer)分析海马硬化型颞叶内侧癫痫(MTLE-HS)患者颞叶亚区白质体积的变化,探讨该技术在MTLE-HS中的临床应用价值。方法:搜集2021年1月至2023年9月经术后病理或MRI诊断为MTLE-HS的患者53例,其中左侧MTLE-HS(LMTLE-HS)30例,右侧MTLE-HS(RMTLE-HS)23例;同期招募性别、年龄相匹配的健康对照者43例。所有受试者均在3.0T磁共振上行T 1加权三维磁化强度预备梯度回波序列(3D-T 1WI-MPRAGE)扫描。使用FreeSurfer软件对T 1-MARAGE图像进行全脑分割,搜集颞叶亚区(颞上回后部、颞极、颞横回、颞上回、颞中回、颞下回、梭状回、海马旁回)的白质体积数据,采用配对t检验比较对照组左、右两侧颞叶各亚区白质体积的差异,采用独立样本t检验分别比较对照组与LMTLE-HS组、RMTLE-HS组患侧、对侧之间颞叶各亚区白质体积的差异。结果:对照组左、右两侧颞横回、颞上回、颞中回、颞下回、梭状回的白质体积差异有统计学意义(P<0.05)。对照组左、右两侧分别与LMTLE-HS组、RMTLE-HS组患侧、对侧进行比较,结果显示对照组左侧与LMTLE-HS组患侧颞极、颞横回、颞上回、颞中回、颞下回、梭状回、海马旁回的白质体积差异有统计学意义(P<0.05),对照组右侧与LMTLE-HS组对侧颞上回后部、颞上回、颞中回、颞下回、梭状回、海马旁回及RMTLE-HS组患侧颞上回后部、颞中回、颞下回、梭状回、海马旁回的白质体积差异有统计学意义(P<0.05),其余亚区体积差异无统计学意义(P>0.05)。结论:基于自动脑分割技术的MTLE-HS颞区白质体积定量分析对颞叶癫痫术前评估及手术方式的选择具有一定意义。

鼻咽癌调强放射治疗后颞叶损伤预测与预防研究现状

现代放射治疗技术的进步和综合治疗策略的优化,使得鼻咽癌(NPC)的治疗效果取得长足进步。随着长期存活患者的增加,如何降低放射治疗相关晚期并发症变得越来越重要。放射性颞叶损伤作为NPC放射治疗后相对少见,但严重影响患者生活质量的并发症之一,目前治疗手段有限,因此尚以预防为主。本文主要针对调强放射治疗年代颞叶损伤的变化、剂量学预测研究以及预防策略进行简要综述。

应用脑深部电极准确定位颞叶癫痫致痫灶

目的探讨脑深部电极准确定位颞叶癫痫致痫灶的临床价值。方法28例疑似颞叶癫痫病人,均实施脑深部电极植入术,均以颞叶内侧为靶点,对重点怀疑致痫灶侧,分别经额叶、颞叶外侧及顶枕叶最多植入3枚电极,对侧依情况植入1~2枚,疑似双颞叶癫痫者最多植入6枚。结果27例病人明确了致痫灶的具体部位并实施相应手术治疗,其中颞叶内侧型癫痫19例,颞叶外侧型癫痫5例,颞叶外器质性病变导致癫痫发作3例。CT/MRI显示器质性病变9例,其中1例为非致痫性病变。术后癫痫发作总消失率为62.96%(17/27),其中立体定向海马杏仁复合体毁损术5例,海马横切术3例,前颞叶切除术5例,单纯器质性病变切除术4例。结论准确应用脑深部电极,可达到颞叶癫痫致痫灶的准确定位效果并减少手术创伤,保护脑组织功能,对于颞叶外器质性病变导致的癫痫发作也有定位价值。