目的:探讨细节护理在神经外科重症患者机械通气中的应用效果.方法:回顾性分析2019年11月至2020年11月该院收治的74例神经外科重症患者的临床资料.依据护理方法不同将患者分为研究组和对照组各37例.对照组应用常规护理,研究组在对照组基础上应用细节护理.比较两组不良事件发生率,护理前后血气指标[动脉血氧分压(PaO2)、二氧化碳分压(PaCO2)及碱剩余]水平、生命质量综合评定问卷(GQOLI-74)评分,以及机械通气时间、住院时间.结果:研究组不良事件发生率低于对照组,机械通气时间和住院时间均短于对照组,差异有统计学意义(P<0.05);护理后,研究组PaO2、碱剩余水平及躯体功能、心理功能、社会功能、物质生活状态等GQOLI-74评分均高于对照组,PaCO2水平低于对照组,差异有统计学意义(P<0.05).结论:细节护理应用于机械通气治疗的神经外科重症患者中,可有效预防肺部感染,降低不良事件发生率,缩短机械通气时间和住院时间,改善血气指标水平,提高生命质量.

目的:探讨综合护理在儿童后颅窝术治疗小脑肿瘤中的应用价值.方法:选取行颅窝手术的患儿 73 例为研究对象,分为对照组(n=37)与观察组(n=36),对照组患儿术后予以常规护理,观察组患儿在对照组基础上联合综合护理,比较两组护理效果.结果:两组患儿神经功能、吞咽功能、平衡功能与语言功能比较,观察组均优于对照组(P＜0.05).结论:在儿童后颅窝手术后实施综合护理效果理想.

目的:观察循证护理在高血压脑出血合并吞咽障碍患者中的应用效果.方法:选取2019年9月至2020年9月该院收治的82例高血压脑出血合并吞咽障碍患者进行前瞻性研究,按照随机数字表法分为对照组和研究组各41例.对照组给予常规护理,研究组在对照组基础上给予循证护理,比较两组护理前后吞咽功能[标准吞咽功能评价量表(SSA)]评分、洼田饮水试验分级、生命质量[吞咽障碍特异性生活量表(SWAL-QOL)]评分和负性情绪[抑郁自评量表(SDS)、焦虑自评量表(SAS)]评分.结果:护理1、2周后,研究组SSA评分低于对照组,差异有统计学意义(P<0.05);护理2周后,研究组洼田饮水试验分级优于对照组,SAS、SDS评分均低于对照组,差异有统计学意义(P<0.05);护理28 d、3个月后,研究组SWAL-QOL评分高于对照组,差异有统计学意义(P<0.05).结论:在常规护理基础上给予循证护理可降低高血压脑出血合并吞咽障碍患者SSA评分和负性情绪评分,提高生命质量评分,改善洼田饮水试验分级,效果优于单纯常规护理.

目的 直肠指力刺激在脑室腹腔分流术后腹胀患者中的疗效观察.方法 选择2019年1月—2020年4月本院收治的脑室腹腔分流术后腹胀患者80例作为研究对象,随机数表法分为对照组和观察组两组,每组各40例.对照组采用腹部环形按摩,观察组在对照组基础上联合直肠指力刺激治疗,两组治疗后均完成4周随访,比较两组肠鸣音、腹围、首次排便间隔时间、首次排便耗时、应激反应及便秘发生率.结果 观察组干预后肠鸣音、首次排便间隔、首次排便耗时间、腹围水平均短(少)于对照组,差异具有统计学意义(P<0.05);两组干预后3周、4周便秘发生率比较,差异无统计意义(P>0.05);观察组干预后1周、2周便秘发生率低于对照组,差异具有统计学意义(P<0.05).结论 脑室腹腔分流术后腹胀患者给予直肠指力刺激干预能促进胃肠蠕动,降低患者应激反应及便秘发生率,值得推广应用.

目的:分析神经外科术后消化不良合并高钠血症治疗中鼻肠管联合鼻胃管的应用价值.方法:随机将150例神经外科术后消化不良合并高钠血症患者分为两组,以接受鼻胃管治疗者为对照组,以接受鼻肠管联合鼻胃管治疗者为联合组,每组75例.对比两组消化不良及高钠血症治疗效果,并分析两组营养状态及炎性指标变化情况.结果:①联合组治疗总有效率明显高于对照组,具统计学差异(P<0.05).②入组时两组血清Na、Hb、Alb及PAB比较,差异未见统计学意义,而在2周治疗完成后,联合组Na低于对照组、Hb、Alb及PAB高于对照组,差异存在统计学意义(P<0.05).③入组时两组血清TNF-α、hs-CPR比较,差异未见统计学意义,而在2周治疗完成后,联合组TNF-α及hs-CPR低于对照组,差异存在统计学意义(P<0.05).结论:鼻肠管联合鼻胃管不仅可有效地改善神经外科术后消化不良合并高钠血症,同时可在一定程度上改善患者的营养状态及炎性指标水平.

目的 通过对罕见疾病一Menkes病患者的病例报道,并复习相关文献,加深临床医生对该疾病的认识.方法 回顾性分析2018年9月-2019年8月广东三九脑科医院癫痫中心收治的3例确诊为Menkes病的患者病例资料,通过高通量测序筛选与Sanger测序验证癫痫致病基因,对3例先证者及两例父母进行突变基因验证,并进一步分析患者临床表现、脑电图、影像学、基因和预后特点.结果 3例先证者均在婴儿期起病,均出现头发稀疏、卷曲,癫痫发作形式多样,3例先证者脑电图间歇期均有癫痫样放电,均记录到临床癫痫发作.头部核磁共振成像可见白质长T1、长T2异常信号,脑动脉迂曲,先证者3出现硬膜下积液.3例先证者服用抗癫痫药物后疗效欠佳,先证者一及先证者二使用组氨酸铜后病情未见明显进展,但不能缓解已有的神经功能损伤.结论 Menkes病多于婴儿期起病,临床表现可能轻重不一,部分临床表现可不典型,目前是不可治愈的疾病,但在新生儿期开始使用组氨酸铜治疗能提高生存率及减轻神经系统的损伤,应尽早诊断,治疗的适应证不应以患者的基因型为指导.

目的 探讨PCDH19基因相关癫痫患者的临床特征及治疗效果.方法 回顾性分析2014年9月至2019年1月在广东三九脑科医院就诊的11例PCDH19基因相关癫痫患者的资料,包括临床特征、检查结果、治疗及随访结果等.结果 11例患者均为女性,癫痫起病年龄6～24 m不等,9例(82％)患者在1岁以内起病.所有患者均有丛集性发作,91％(10/11)患者具有热敏感,只有1例患者有癫痫持续状态.发作形式主要是局灶性发作及全面强直阵挛发作.7例患者存在发育落后.9例患者基因突变位于1号外显子,2例位于3号外显子,5例错义突变,4例移码突变,2例无义突变,7例患者的基因突变为新发突变.非丛集性发作期的70％(7/10)脑电图提示正常,丛集性发作期脑电图均有异常,但有13％(3/23)未见癫痫样放电,同一个患者癫痫样放电部位不恒定.所有患者至少使用两种抗癫痫药物,其中5例患者加用左乙拉西坦后至少10 m无发作,最长1例患者有37 m无发作,其次有效的药物是丙戊酸、托吡酯、氯硝西泮及苯巴比妥,最多见有效的治疗组合是丙戊酸添加左乙拉西坦治疗.结论 PCDH19基因相关癫痫具有起病年龄小、热敏感及丛集性发作的特点,非丛集性发作期脑电图往往正常,多需要多药联合治疗,添加左乙拉西坦对该病有明显的效果.

To characterize human leukocyte antigen (HLA) loci as risk factors in aromatic antiepileptic drug-induced maculopapular exanthema (AED-MPE). A case-control study was performed to investigate HLA loci involved in AED-MPE in a southern Han Chinese population. Between January 2007 and June 2019, 267 patients with carbamazepine (CBZ), oxcarbazepine (OXC), or lamotrigine (LTG) associated MPE and 387 matched drug-tolerant controls from six centers were enrolled. HLA-A/B/C/DRB1 genotypes were determined using sequence-based typing. Potential risk alleles were validated by meta-analysis using data from different populations and in silico analysis of protein-drug interactions. HLA-DRB1*04:06 was significantly associated with OXC-MPE ( p = 0.002, p c = 0.04). HLA-B*38:02 was associated with CBZ-MPE ( p = 0.03). When pooled, HLA-A*24:02, HLA-A*30:01, and HLA-B*35:01 additionally revealed significant association with AED-MPE. Logistic regression analysis showed a multiplicative interaction between HLA-A*24:02 and HLA-B*38:02 in CBZ-MPE. Meta-analysis of data from different populations revealed that HLA-24*:02 and HLA-A*30:01 were associated with AED-MPE ( p = 0.02 and p = 0.04, respectively). In silico analysis of protein-drug interaction demonstrated that HLA-A*24:02 and HLA-A*30:01 had higher affinities with the three aromatic AEDs than the risk-free HLA-A allele. HLA-DRB1*04:06 showed relatively specific high affinity with S-monohydroxy derivative of OXC. HLA-DRB1*04:06 is a specific risk allele for OXC-induced MPE in the Southern Han Chinese. HLA-A*24:02, possibly HLA-A*30:01, are common risk factors for AED-MPE. The multiplicative risk potential between HLA-A*24:02 and HLA-B*38:02 suggests that patients with two risk alleles are at greater risk than those with one risk allele. Inclusion of these HLA alleles in pre-treatment screening would help estimating the risk of AED-MPE.

The clinical data of a case of paroxysmal extreme pain disorder(PEPD) in Guangdong 999 Brain Hospital were retrospectively analyzed.The male patient, age of first examination was 7 months, began to have recurrent tonic accompanied by facial redness or cyanosis at 5 months after birth.The patient was diagnosed with epilepsy.The oral solution of sodium valproate and Levetiracetam were not effective.The video electroencephalogram examination displayed that, when the patient had tonic and bradycardia, the synchro electroencephalogram did not show epileptic discharge, so the patient was considered to have non-epileptic tonic.Genetic examination suggested that SCN9A gene mutation of c. 5240T >C resulted in amino acid changes: Val1747Ala.Combined with the skin changes, the patient was diagnosed as PEPD caused by SCN9A gene mutation.After the treatment with Carbamazepine, the patient′s abnormal skin changed and his-epileptic tonic disappeared, and his condition improved significantly.The early stage of PEPD can be mainly manifested as non-epileptic tonic.It is easy to be misdiagnosed as epilepsy, so the patient′s characteristic skin changes should be noticed, and genetic examination is also helpful in the diagnosis of the disease.

Background The ketogenic diet (KD) has been implemented in many different counties. However, in China, study concerning the efficacy of the KD is still at an early-stage of evaluation. Furthermore, the KD is thought to be incompatible with Chinese children because of its lack of palatability, especially for the Asian population. In addition, its substantial antiepileptic effect remains to be confirmed. Methods To evaluate the efficacy and safety of the KD treatment of refractory childhood epilepsy in China, we prospectively enrolled 147 children with refractory epilepsy for KD treatment in Guangdong 999 Brain Hospital and followed up the children for 6 months. Outcome was measured by seizure frequencies before and after the KD diet and adverse effects. We also evaluated influences of different variables (starting age, duration of epilepsy, and others) on the outcome. Results We found after 1 month, 3 months, and 6 months of KD treatment, 28.0%, 55%, and 67.9% of the subjects remained on diet with a >50% seizure reduction and seizure-free rates of 6.5%, 13.2%, and 23.3%, respectively. Gender, starting age, duration, etiology, classification, and seizure type of epilepsy showed no significant influence on efficacy. Anorexia, diarrhea, and gravel were the main side-effects of the KD treatment. Conclusions In conclusion, the KD is a safe and efficacious method for childhood refractory epilepsy treatment.

Objective:To investigate the clinical features of encephalocraniocutaneous lipomatosis (ECCL).Methods:The clinical characteristics, imaging manifestations and electroencephalogram changes of five patients with ECCL from Guangdong 999 Brain Hospital between December 2016 and February 2019 were collected and analyzed.Results:All five cases showed ocular, skin and central nervous system anomalies. Corneal anomalies were found in five cases, eyelid coloboma in three cases, calcification of the globe in two cases, and choristoma in one case. All five cases presented with naevus psiloliparis, three cases with small nodular skin tags on eyelids, and three cases with café-au-lait spots on the trunk. Dysplasia of the right cerebral hemisphere was observed in all five cases, four cases with enlargement of the right ventricle, three cases with arachnoid cysts, and one case with dysplasia of the corpus callosum. The onset of the seizures of five cases was found within one year old. Spasms were observed in five cases, partial seizure in three cases, and tonic seizure in one case. Five cases were drug-resistant epilepsy. Seizures decreased significantly after adrenocorticotropic hormone treatment in one case and seizures free after surgery in one case. One case had seizure free by corpus callosotomy, but had a relapse after four months. Three cases used ketogenic diet, including one case with epileptic seizure reduction, one case with development progress. All five cases had developmental delays. The exon gene sequencing of four cases was found normal. KRAS gene mutation was found in brain tissue of one patient.Conclusions:ECCL is a rare clinical disease that often involves the nervous system, skin and eyes. The seizures of the patients are often difficult to control and have development delays. Surgery may be necessary to control the seizures. ECCL is thought to be somatic mutations, which are hard to detect in the blood and can be found in affected tissues.

癫痫性脑病(epileptic encephalopathies)是指频繁癫痫发作和癫痫样放电造成的进行性神经功能障碍或退化,如语言、认知、感觉及运动,且这些认知行为损害随着癫痫的持续存在而不断加重,它是一组癫痫疾患的总称,已有包括SCNA1在内的多个基因可导致这一疾病,ITPA基因突变导致癫痫脑病病例国外已有相关报道,而国内鲜有相关报道,现报道1例2017年6月我院癫痫儿科收治的患儿,分析其临床发作形式、脑电图结果、头颅磁共振成像(MRI)基因检测结果等资料.

目的:本研究旨在明确中国人群中药物难治性癫痫(drug-refractory epilepsy,DRE)及本身有免疫疾病的癫痫患者谷氨酸脱羧酶(glutamic acid decarboxylase,GAD)抗体的分布,明确免疫治疗在这部分患者中的临床疗效.方法:对我院癫痫中心就诊的DRE患者235例及本身有免疫疾病的癫痫患者25例进行GAD抗体检测,严格纳入与排除标准,并予高滴度阳性患者免疫治疗观察疗效.结果:2016年3月至2018年7月共收集患者260例,其中GAD抗体高(高于正常高值10倍)及极高滴度(＞2 000 U/mL)患者确诊为阳性的患者共6例.其中5例为女性,年龄19～35岁,均表现为DRE,其中2例患者既往有甲亢并相关治疗史,合并有甲状腺相关受体抗体增高,1例无甲亢病史,但甲状腺相关受体抗体增高.5例女性患者均进行相关免疫治疗,3例有效,2例启动二线免疫治疗,1例免疫治疗未见明显疗效.6例中另1例为男性,20岁,伴有1型糖尿病,GAD抗体滴度高度升高,仅出现2次癫痫发作,目前单药控制1年无发作,未进行免疫治疗.结论:GAD抗体相关自身免疫性癫痫是以癫痫为核心症状的一种免疫性疾病,多表现为局灶性尤其边缘系统起始发作,伴有甲亢或甲状腺功能抗体增高,青年女性患者多发,尽早免疫治疗可改善预后.

Antiepileptic drugs frequently cause cutaneous adverse reactions (cADRs). Numerous studies have reported associations between human leukocyte antigen (HLA) alleles and cADRs caused by single antiepileptic drug in Southern Han Chinese people. However, the relationship between the HLA allele and cADRs sequentially induced by two or more antiepileptic drugs (AEDs-induced cross-reactivity) is unclear. To explore the associations between HLA alleles and AEDs-induced cross-reactivity, we prospectively recruited patients with AEDs-induced cross-reactivity from 2009 to 2017 and performed high-resolution genotyping to detect the HLA-A, B, C, and DRB1 alleles in patients for comparison with normal controls. To verify the important genotype, we compared its presence in patients with cross-reactivity to enlarged normal controls, and its presence in patients with carbamazepine (CBZ)-induced maculopapular exanthema (MPE) to CBZ-tolerant controls. Further, the important allele was replicated by meta-analysis. Twenty-three patients with AED-induced cross-reactivity and 500 healthy individuals were enrolled from Southern China. All patients had a mild rash without mucosal or systemic involvement. The HLA-B*13:01 allele was present in 34.78% (8/23) of patients, 14.60% (73/500) of healthy individuals, and 14.5% (763/5,270) healthy individuals, revealing a significant association (8/23 vs. 73/500; P = 0.02; OR: 3.12; 95% CI: 1.28-7.62; 8/23 vs. 763/5,270; P = 0.014; OR: 3.15; 95% CI: 1.33-7.46). HLA-B*13:01 was presented numerically higher in CBZ-induced MPE than that in CBZ-tolerant individuals without statistical significance (33/145, 22.76%, vs. 28/179, 15.64%; P = 0.103). Meta-analysis revealed an association between HLA-B*13:01 and cADRs induced by single AEDs or/and non-AEDs in Chinese and Thai populations (P = 0.000). This study suggests that HLA-B*13:01 is potentially associated with AED-cADRs in general, possibly with stronger effect in cross-reactivity. Screening for HLA-B*13:01 prior to starting AEDs therapy may help to avoid cADRs. However, this association requires further analysis in a multi-center study with a larger sample size.

目的 探讨PIGA基因突变与早发性癫痫性脑病(Early-onset epileptic encephalopathies,EOEE)的关系.方法 回顾分析2016年3月广东三九脑科医院癫痫中心收治的1例EOEE伴PIGA基因突变患儿临床资料,并查阅万方、中国知网(CNKI)、PubMed等数据库,结合相关文献进行总结.结果 所报道患儿1岁内起病,有癫痫家族史,电生理及临床诊断为EOEE,辅助检查遗传代谢、尿有机酸、血生化等检测未见异常,头颅核磁共振示大脑发育不全.癫痫基因检测发现PIGA基因有新发错义突变,符合X连锁遗传方式,而该基因突变导致EOEE在国外相关文献中已有报道,但国内罕有相关报道.结论 X连锁PIGA基因新发突变更可能是部分EOEE的致病基因.

Objective To explore the clinical features of classic late infantile neuronal ceroid lipofuscinosis (LINCL). Method The clinical data, EEG data and MRI data of two patients diagnosed by gene in our hospital were collected to analyze the characteristics of LINCL. Results The onset age of the two patients is 3 years old . Seizure is the main symptom. They were drug refractory epilepsy. Case 1 patient presented the progressive motor and cognitive function deterioration within one year. MRI showed the cerebellar atrophy. The gene detection found TPPI complex heterozygous mutation and TPPI enzyme activity was significantly lower than normal. Case 2 patient developed the progressive myoclonic epilepsy. The patient presented the progressive motor, cognitive function deterioration and vision loss, and ultimately developed the vegetable status. MRI showed the progressive cerebral and cerebellar atrophy. The gene detection found TPPI complex heterozygous mutation. Conclusion Classic LINCL is a uniformly fatal lysosomal storage disease resulting from mutations in the CLN2 gene. The patients present the progressive cerebral and cerebellar atrophy. The prominent neurodegenerative features include vision loss, seizures, ataxia,motor and cognitive function deterioration.

线粒体为环状的DNA分子,目前已确定有13个为蛋白质编码的区域,包括细胞色素B、细胞色素氧化酶的3个亚基、ATP酶的2个亚基、NADH脱氢酶的7个亚基;NADH脱氢酶(NADH dehydrogenation,ND)功能缺失是引起线粒体呼吸链受损最常见的原因,其基因突变会导致线粒体蛋白质合成受损,影响线粒体的电子传递链复合体亚单位和线粒体能源生产.根据线粒体DNA(mitochondrial DNA,mt-DNA)分子中碱基对位置,ND可分为ND1、ND2、ND3、ND4L、ND4、ND5、ND6共7个亚基.近年来,由ND1、ND3、ND4、ND5、ND6的基因突变导致的线粒体脑肌病屡见报道[1-5].其中,ND3在mt-DNA第10 059至10 404碱基对中,能产生由115种氨基酸构成的13kDa蛋白质,其结构呈“L-型”,长臂由疏水性跨膜结构组成,短臂为亲水性跨膜结构.其基因突变能引起多种线粒体脑肌病,包括线粒体脑肌病伴高乳酸血症和卒中样发作综合征(Mitochondrial encephalomyopathy with latic acidemia and strokelike episodes,MELAS)、Leber遗传性视觉缺失、Leigh综合征、线粒体脑肌病重叠综合征,合并或不合并肌张力障碍[6-10].

Neuronal ceroid lipofuscinosis is a hereditary disease, and ceroid-lipofuscinosis neuronal protein 5 (CLN5) has been proved to be associated with neuronal ceroid lipofuscinosis. Here we report 3 patients from 2 families diagnosed with CLN5 neuronal ceroid lipofuscinosis. Whole genome sequencing of DNAs from 3 patients and their families revealed 3 novel homozygous mutations, including 1 deletion CLN5.c718 719delAT and 2 missense mutations c.1082T>C and c.623G>A. We reviewed 278 papers about neuronal ceroid lipofuscinosis resulting from CLN5 mutations and compared Chinese cases with 27 European and American cases. The overall age of onset of European and American patients occur mainly at 3 to 6 years (66%, 18/27), 100% (27/27) of patients had psychomotor regression, 99% (26/27) patients presented vision decline, and 70% (19/27) of patients suffered seizures. In China, the age of onset in 3 patients was 5 years, but for 1 patient it was at 17 months. Four Chinese patients presented psychomotor deterioration and seizures; only 1 had visual problems.

目的 以运动皮质细胞构筑的观点剖析1例腹侧运动皮层起始的癫痫发作的症状学及致痫网络,并探讨DEPDC5基因突变癫痫患者相关局灶性发育不良(Focal cortical dycplasia,FCD)的影像学特点.方法 系统评估1例DEPDC5基因突变的耐药性癫痫患者,明确致痫区,行手术治疗,并结合文献进行分析.结果 患者的核磁共振提示中央前沟降支可疑FCD,行立体定向电极植入,详细分析间隙期和发作期立体定向脑电图(SEEG)和症状学特征,明确发作起始区在左侧中央前沟降支的异常影像改变核心部分,早期扩散到同侧岛前小叶、中央盖及中央前回腹侧部,因此可理解症状学中早期出现右上肢肌张力障碍,继而舞蹈徐动样症状.手术切除致痫区,病理证实为FCDI型,术后1个月无发作.其他家系中,FCD出现较多的在运动皮质,经SEEG证实的致痫区除多数在运动皮质外,还可在岛前小叶.结论 中央前沟降支起始的癫痫发作可早期出现对侧肌张力障碍和同侧舞蹈徐动样症状;DEPDC5基因突变需警惕大脑运动皮质隐匿的FCD.

目的:本文通过明确枕叶癫痫致痫灶位置、视觉先兆和第一运动症状学,试图解释致痫灶位置和发作症状学的关系.方法:回顾性分析在三九脑科医院已行致痫灶切除手术、且术后随访至少1年未再出现发作的纯枕叶癫痫患者9例(其中4例经过立体定向脑电植入,5例直接手术治疗),使用枕叶集群分区方法明确枕叶致痫灶位置,按照病程记载的视觉先兆,回放术前评估时发作期录像,明确第一个运动症状学;回放4例患者的立体定向脑电图(SEEG)资料,明确发作起始和早期扩散区;阐述致痫灶位置和发作症状学之间的关系.结果:有视觉先兆的患者共7例,占78％,其中有两种视觉先兆的患者共3例.致痫区在枕叶背内侧、腹内侧和内侧表面(累及集群1、2、3)的患者4例,其中4例出现视觉缺失,还有1例合并出现单纯视幻觉.致痫区在枕叶背外侧和外侧面(累及集群4、5、8)的患者4例,产生复杂视幻觉.以自动运动为第一运动症状学的患者共6例,占67％,致痫区在枕叶背内侧、腹内侧和后下区(累及集群1、2、8),其中2例SEEG证实异常电活动的传播通过颞叶产生.以轴-肢带性强直为第一运动症状学的患者1例,致痫灶位于枕叶背内侧、内侧表面和背外侧(累及集群2、3、4).以复杂运动为第一运动症状学的患者1例,致痫区位于枕叶外侧面(累及集群5),SEEG证实复杂运动时异常电活动并不向相邻组织传播.以偏转发作为第一运动症状学的患者1例,致痫区位于枕叶背内侧(累及集群2),SEEG证实偏转发作并不产生于同侧的额眼区.结论:枕叶癫痫致痫灶位置与发作症状学相关;枕叶背内侧、腹内侧和内侧表面的致痫区容易产生视觉缺失;枕叶背外侧和外侧面的致痫区容易产生复杂视幻觉;枕叶背内侧、腹内侧和后下区的致痫灶容易出现自动运动;枕叶背内和背外侧均受累的致痫灶可以产生轴性强直;枕叶外侧面的致痫灶可以出现复杂运动;而枕叶背内侧的致痫灶可以出现偏转发作,后3种症状学均可能通过投射纤维产生.