儿童非惊厥性持续状态的脑电图五例

目的 总结分析儿童非惊厥性癫痫持续状态(NCSE)多种脑电图(EEG)异常放电模式。方法 2016年9月至2020年9月首都医科大学宣武医院儿科收治的5例NCSE患儿,分析患儿的发作诱因、临床表现、EEG异常及治疗反应等情况。结果 报道的5例患儿,男童2例,女童3例。发病年龄1～12岁(中位值4岁2月)。5例均有反应迟钝,不同程度的智力倒退,其中例5有性格改变。NCSE诱因分析发现5例中感染引起惊厥持续状态后出现NCSE 1例(例4),抗癫痫药物调整过程中发作1例(例2),癫痫发作控制不佳1例(例5),突然停用所有抗癫痫药物1例(例3),诱因不明1例(例1)。发作期EEG特征多样,包括反复长时间的发作期放电,局部起始伴扩散和演变,左右反复交替出现(例1);全导高波幅慢波及右侧局灶性(Rolandic区)持续放电(例2);全导弥漫性高幅2.5～3Hz左右慢波、棘慢波长程发放(例3);全导持续周期性高幅慢波、尖慢波呈发放(例4)。双侧前头部(额极、额、中央、顶为主导联)5Hz高幅持续性慢波(例5)。所有患儿发作时静脉推注地西泮,临床症状及EEG均有不同程度的改善。结论 NCSE的临床表现和...     

成人非惊厥性癫(癎)持续状态的临床及脑电图特点

目的:探讨成人非惊厥性癫癎持续状态(NCSE)的临床及脑电图特点.方法:对7例NCSE患者的临床资料进行回顾性分析.结果:本组7例NCSE患者中,复杂部分性NCSE6例,全面性NCSE1例.临床表现以不同程度意识障碍为主,伴反应迟钝、定向力障碍、自动症、精神行为异常等.脑电图检查均可见癎性发放,且癫癎波形态与临床表现有关.按癫癎持续状态治疗原则治疗后均明显好转.结论:NCSE患者临床表现复杂多样;脑电图改变明显且与临床症状可能有某些相关性,有助于诊断;及时治疗预后良好.     

昏迷患者非惊厥性癫痫持续状态的临床特点

目的 探讨昏迷患者非惊厥性癫痫持续状态(NCSE)的临床特点.方法 回顾性分析6例昏迷NCSE患者的临床资料.结果 6例患者中1例病毒性脑炎,1例大面积脑梗死,2例脑外伤,1例心肺复苏术后缺血缺氧性脑病,1例肾移植后代谢性脑病.其中,2例出现躁动,1例摇头、嘴唇咂动,2例四肢微小抽动,1例颜面抽动.所有患者的持续EEG(CEEG)监测均出现广泛或者局灶并发广泛的异常放电.结论 昏迷患者发生NCSE时多表现为躁动或面部、四肢微小抽动,CEEG监测能发现异常放电,有助于指导临床诊治.     

非惊厥性癫癎持续状态3例病例报告

非惊厥性癫持续状态(nonconvulsive statusepilepticus,NCSE)的发作形式多种多样,其临床表现主要为不同程度的意识障碍、精神异常,容易造成漏诊、误诊。本病例报告中的3例患者的具体发作表现各自3例患者最后均诊断为非惊厥性癫持续状态,考虑为复杂部分性癫持续状态,给予卡马西平治疗,例3患者因嗜唾改服丙戊酸钠。讨论NCSE指伴有EEG癫样节律的行为和思维迟缓、意识障碍,有时以木僵或昏迷为特征,症状持续最少30 min。分为失神性癫持续状态(absence status epilepticus,ASE)和复杂部分性癫持续状态(complex partial status epilepticus,C…     

表现为非惊厥性癫痫持续状态的边缘叶脑炎的临床和脑电图特征

目的探讨为非惊厥性癫痫持续状态(NCSE)的边缘叶脑炎(LE)的临床及EEG特征。方法回顾性分析9例表现有NCSE的LE患者的临床资料。结果 4例患者为急性起病,5例为亚急性起病。首发症状为复杂部分性癫痫持续状态(CPSE)7例,轻微发作癫痫持续状态(SSE)1例,简单部分性癫痫持续状态(SPSE)1例。9例患者均有精神症状、记忆障碍及自主神经功能紊乱,肺癌1例。头颅MRI显示脑实质急性炎症,主要集中于边缘系统,呈双侧对称或不对称信号异常改变,T_1WI为略低信号,T_2WI及Flair呈高信号。EEG表现为θ波背景6例,均可见δ波,其中棘慢波或尖慢波4例;α波背景2例,均可见δ波,表现为δ波背景1例。视频脑电图(VEEG)示1例SSE患者呈持续的痫性放电,在病侧蝶骨电极更显著,但无运动性癫痫发作。1例SPSE患者在皮质和颞近中央区有不同频率的局灶性棘波或棘慢综合波持续发放。7例CPSE患者呈颞区为主的各种形式癫痫性电活动广泛持续发放或反复阵发性出现,如节律性的棘波、尖波、δ或/和θ节律,可向邻近区域或对侧半球扩散,或左右交替;在无凝视反应或刻板自动症时呈现扩散至双侧半球的高波幅棘慢综合波或δ节律爆发。结论表现有NCSE的LE的临床和EEG有特征性改变,EEG和VEEG是LE是否存在NCSE的主要诊断依据。左右半球边缘叶病变出现的精神症状并不相同。各型LE对治疗反应不一,非副肿瘤性LE疗效较满意。     

非惊厥性癫痫持续状态临床及脑电图表现四例

目的由于非惊厥性癫痫持续状态(NCSE)的临床表现及脑电图的变化在儿童和成人很难被识别,容易被误诊,本研究主要是探讨NCSE的临床特点及脑电图表现。方法收集我院诊治过的4例NCSE患者的临床资料及脑电图资料,分析其特点。结果 4例患者既往均有癫痫发作。例1患者停药后出现NCSE发作,例3、例4患者由于药物控制不佳,例2患者的NCSE均发生在惊厥发作后,每次发作持续时间从0.5h至3d不等。例2、例3及例4患者反复多次出现NCSE。4例患者均表现为行为异常,例1、例2及例4患者发作时不讲话,不能和外界进行交流,例3患者发作时构音不清。随访后发现例2、例3患者记忆力下降,例1、例4患者智能基本正常。从脑电图来看,均表现为持续性棘慢波发放。例1为失神发作癫痫持续状态,例2、例3及例4为部分性发作癫痫持续状态。结论 NCSE在早期易漏诊,反复NCSE可导致患者记忆力下降,如癫痫患者出现持续半小时以上的行为异常等表现,应急行脑电图检查明确是否NCSE,使用苯二氮卓类及抗癫痫药物可终止NCSE。     

Creutzfeldt-Jakob病的临床及脑电图特点

目的 探讨Creutzfeldt-Jakob病(CJD)的临床及脑电图(EEG)特点.方法 回顾性分析14例CJD患者的临床资料.结果 14例患者临床表现均有进行性痴呆和肌阵挛,12例早期表现为抑郁、失眠、头痛、头晕、记忆力减退、行走不稳.14例患者EEG均呈阵发周期波,周期波为高波幅双相、三相或多相尖波、尖-慢综合波,其中3例发病后4～9周第2次EEG检查时出现特征性周期波,1例发病后14周第3次EEG检查时出现特征性周期波.2例行MR弥散加权成像检查示额顶叶皮质区出现异常信号.结论 CJD的临床特征为进行性痴呆和肌阵挛,发病后3～14周EEG出现阵发周期波.对于早期病例应行EEG跟踪检查.     

发作性黑矇:MRI、E:MRI、EEG和临床特征

作者报告了7例以发作性黑矇为主要临床特征的癫痫患者的MRI、发作间期脑电图(EEG)及临床特点。7例癫痫患者的发作均以一过性黑矇为突出临床表现,年龄7～20岁,平均发作年龄13.3岁。所有病人头颅MRI检查包括轴位、冠状位及矢状位的T_1及T_2加权成像。每例均进行常规的EEG检查,病例1、4和5还进行了遥控EEG监测,病例2在行EEG检查时曾出现过癫痫发作。结果6例病人MRI异常,其中5例MRI异常位于枕叶或顶枕区。3例为缺血性病变,占位性病变及结节性硬化各1例。     

2例非惊厥癫痫持续状态患者的临床特征及脑电图分析

非惊厥性癫痫持续状态（Nonconvulsive Status Epilepticus,NCSE）年发病率为5.6～18.3/10万[1],约占癫痫持续状态的一半,并非罕见,以往由于对其认识不足和诊断标准不一致[2],常被误诊或漏诊,得不到及时有效的治疗.不同类型的NCSE,临床表现和脑电图特点各不相同[3].现将首都医科大学宣武医院神经内科2012年7～10月收治的2例NCSE患者的临床特征及脑电图结果报道如下.     

Creutzfeldt-Jakob病的临床和影像学特点

目的探讨Creutzfeldt-Jakob病(CJD)的临床及影像学特征。方法回顾性分析29例CJD患者的临床资料。结果本组有12例CJD患者以快速进展性痴呆起病;典型的临床表现为进行性痴呆(100%)、共济失调(93.1%)、肌阵挛(89.6%)。EEG均异常,出现典型三相波17例、不典型三相波8例。头颅MRI表现双侧皮质高信号或基底节区T2WI对称性高信号15例,单侧皮质高信号6例,单侧基底节区高信号4例;20例行MR弥散加权成像(DWI)扫描,双侧皮质或基底节区出现高信号14例,一侧皮质或基底节区高信号各3例。14例双侧DWI高信号的患者均出现EEG典型三相波。3例行脑脊液14-3-3蛋白检查,2例阳性。结论 CJD患者多以快速进展性认知功能障碍起病,典型的临床表现为痴呆、共济失调、肌阵挛;EEG、DWI、CSF 14-3-3检测是诊断CJD的重要检查手段;DWI双侧皮质及基底节高信号可能与EEG出现三相波有关。     

Nonconvulsive status epilepticus in children: clinical and EEG characteristics

BACKGROUND: Nonconvulsive status epilepticus (NCSE) is a highly heterogeneous clinical condition that is understudied in the pediatric population. OBJECTIVE: To analyze the epidemiological, clinical, and electroencephalograpic features in pediatric patients with NCSE. METHODS: We identified 19 pediatric patients with NCSE from the epilepsy database of the Comprehensive Epilepsy Center at, Columbia University between June 2000 and December 2003. Continuous electroencephalographic (EEG) monitoring was analyzed and chart review was performed. RESULTS: The patients ranged from 1 month old to 17 years of age. Five patients developed NCSE following convulsive status epilepticus (CSE), and a further 12 patients developed NCSE after brief convulsions. Two developed NCSE as the first manifestation during a comatose state following hypoxic events. Acute hypoxic-ischemic injury was the most frequent etiology of NCSE in our population (5 of 19; 26%), followed by exacerbation of underlying neurometabolic disease (4 of 19; 21%), acute infection (3 of 19; 16%), change in antiepileptic drug regimen (3 of 19;16%), refractory epilepsy (2 of 19; 11%) and intracranial hemorrhage (2 of 19; 11%). Six patients had associated periodic lateralized epileptiform discharges (PLEDs), one had generalized periodic epileptiform discharges (GPEDs). Five (5 of 19; 26%) patients died of the underlying acute medical illness. Periodic discharges were associated with worse outcome. CONCLUSION: The majority of our patients with NCSE had preceding seizures in the acute setting prior to the diagnosis of NCSE, though most of these seizures were brief, isolated convulsions (12 patients) rather than CSE (five patients). Prolonged EEG monitoring to exclude NCSE may be warranted in pediatric patients even after brief convulsive seizures. Prompt recognition and treatment may be necessary to improve neurological outcome.     

Tiagabine-induced generalised non convulsive status epilepticus in patients with lesional focal epilepsy.

PURPOSE: To report 3 cases with focal lesional epilepsy that had non-convulsive status epilepticus (NCSE) induced by treatment with tiagabine (TGB) and review the previously published cases. Drugs that enhance GABAnergic transmission are recognised to promote absence seizures in patients with generalised epilepsy syndromes and may on occasions even induce NCSE. However, that TGB can also induce NCSE in focal lesional epilepsy is not widely recognised in clinical practice. METHOD: The clinical history, EEG and MRI findings were reviewed in 3 patients with lesional focal epilepsy who presented to our epilepsy programs over a 12 month period with TGB-induced NCSE. All previously reported cases in the English medical literature were reviewed. RESULTS: The three patients had longstanding complex partial and secondarily generalised seizures refractory to multiple different anti-epileptic drugs. In two cases, MRI demonstrated a focal malformation of cortical development in the left parieto-occipital region and in the third left mesial temporal sclerosis. Following commencement of TGB in one patient and dose escalation in two, prolonged episodes of confusion and poor responsiveness were noted. Prolonged EEG monitoring demonstrated continuous high amplitude, generalised, 2-4 Hz delta activity with intermingled spikes during the episodes of unresponsiveness, consistent with NCSE. The clinical and EEG activity normalised following the administration of IV clonazepam followed by dose reduction or withdrawal of the TGB. Eleven previously reported cases of patients with partial epilepsy and a focal underlying lesion on MRI were identified, all of whom had similar features to that seen in our cases. CONCLUSIONS: These cases illustrate that TGB may induce generalised NCSE in patients with focal lesional epilepsy, in addition to those with generalised syndromes. We hypothesise that patients may have developed an acquired alteration in the sensitivity of their thalamocortical circuitry that renders them more sensitive to the effects of drugs that enhance GABAnergic activity.     

Status epilepticus and tiagabine therapy revisited

PURPOSE: To determine whether antiepileptic treatment with tiagabine (TGB) is associated with an increased frequency of nonconvulsive status epilepticus (NCSE) in patients with refractory epilepsy. METHODS: We reviewed retrospectively the medical and EEG records of all inpatients with refractory localization-related epilepsy at the National Society for Epilepsy treated with TGB between January 1997 and December 2000. Clinical and electroencephalographic (EEG) data before, during, and after TGB therapy were evaluated in those patients who experienced a deterioration in seizure control suggestive of NCSE. Frequency of NCSE was determined in a comparable, non-TGB-treated patient population. RESULTS: Seven (7.8%) of 90 TGB-treated patients were identified who experienced episodes of electroclinically confirmed NCSE. Serial EEGs showed deterioration during TGB treatment, with resolution of abnormality on discontinuation of TGB in all seven patients. During the same observation period, 32 (2.7%) of 1,165 non-TGB-treated patients developed electroclinically defined NCSE. CONCLUSIONS: Treatment with TGB is associated with an increased frequency of NCSE in patients with refractory localization-related epilepsy.     

Nonconvulsive status epilepticus in patients with brain tumors

PurposeThe prevalence of nonconvulsive status epilepticus (NCSE) in brain tumor patients is unknown. Since NCSE has been associated with significant mortality and morbidity, early identification is essential. This study describes the clinical and EEG characteristics, treatment, and outcome in brain tumor patients with NCSE.MethodAll patients admitted to Mount Sinai Hospital from 2009 to 2012 with an ICD-9 brain tumor code were cross-referenced with the epilepsy department's database. EEGs from matching patients were reviewed for NCSE. Relevant information from the medical records of the patients with NCSE was extracted.Results1101 brain tumor patients were identified, of which 259 (24%) had an EEG and 24 (2%) had NCSE. The vast majority of seizures captured were subclinical with 13 patients (54%) having only subclinical seizures. Treatment resolved the NCSE in 22 patients (92%) with accompanying clinical improvement in 18 (75%) of those patients. Tumor recurrence or progression on MRI was associated with decreased 2-month survival (75% mortality, p = 0.035) compared to stable tumors (20% mortality). Patients with metastatic disease had median survival from tumor diagnosis of 1.2 months.ConclusionNCSE in brain tumor patients may be under diagnosed due to the frequent lack of outward manifestations and highly treatable with improvement in the majority of patients. NCSE patients with progressing brain lesions, tumor recurrence, or metastatic disease are at serious risk of mortality within 2 months. Continuous EEG monitoring in brain tumor patients with recent clinical seizures and/or a depressed level of consciousness may be critical in providing appropriate care.     

Non convulsive status epilepticus after replacement of valproate with lamotrigine

Purpose: Lamotrigine (LTG) and valproate (VPA) are widely used in the treatment of generalized epilepsies. Nevertheless seizure aggravation with LTG has been reported in juvenile myoclonic epilepsy and epilepsy with myoclonic absences. The aim of this study was to describe clinical features and EEG findings in patients with non convulsive status epilepticus (NCSE) after replacement of VPA with LTG. Method: Retrospective analysis of three identified patients in a large university hospital. Results: We describe three adult patients aged 39, 50 and 75 years, who developed non-convulsive status epilepticus (NCSE) after replacement of VPA with LTG. The episodes of NCSE presented as an acute confusional state with mild myoclonus. Ictal EEG showed generalized spike-wave or polyspike wave activity. The clinical symptoms and the EEG responded promptly to IV benzodiazepines and patients remained well controlled with dose reduction of LTG (in one patient) or discontinuation of LTG (in two patients). Conclusion: The reported episodes of NCSE in these patients with generalized epilepsy may be either due to a possible paradoxical reaction to LTG or due to a withdrawal effect of VPA. Received: 5 November 2001, Received in revised form: 8 April 2002, Accepted: 23 April 2002 Correspondence to Eugen Trinka, MD     

Non-convulsive seizures and non-convulsive status epilepticus monitoring in the intensive care unit. A real need for the Gulf Cooperation Council countries

Continuous EEG (cEEG) monitoring in the intensive care unit (ICU) is essential for detecting non-convulsive seizures/status epilepticus (NCSs, NCSE). Currently there exist a number of continuous EEG monitoring systems adapted for use in the ICU. However, these systems have been trained using EEG data collected from healthy, neurologically intact patients with epileptic seizures, a very different patient population from ICU patients. The review consists of 2 parts, clinical and technological aspects. In the first one, we summarize the electroencephalographic aspects of NCSs/NCSE and other EEG patterns encountered in the ICU. In the second part, we explain how to develop a novel cEEG monitoring system to be used in Hamad Medical Corporation ICUs, Doha, Qatar, that is able to detect pathological EEG patterns commonly occurring in the critically ill patient. Real-time monitoring of seizure discharges, and other pathological EEG patterns will allow correct diagnosis and adequate treatment in a timely fashion.     

Creutzfeldt-Jakob disease and non-convulsive status epilepticus: a clinical and electroencephalographic follow-up study.

OBJECTIVE: To describe the clinical and electroencephalographic findings from a confused elderly woman with Creutzfeldt-Jakob disease (CJD) that initially were compatible with the diagnosis of non-convulsive status epilepticus (NCSE). METHODS AND RESULTS: A 75-year-old right-handed woman was admitted to our hospital because of confusion and alteration of mental status. The two first electroencephalograms (EEGs) showed continuous diffuse spikes, rhythmic sharp waves and sharp-and-slow wave complexes which were completely abolished after the administration of 10 mg of intravenous diazepam. Over the following days, the clinical state of the patient was unmodified despite aggressive antiepileptic therapy. A third EEG revealed pseudo-periodic negative or positive-negative slow waves localised in the right frontal region. Subsequently, two consecutive EEGs showed continuous periodic generalised bi-triphasic complexes at a rate of 1 Hz, compatible with the diagnosis of CJD. Finally, the patient died, and postmortem examination was diagnostic of the sporadic form of CJD. CONCLUSIONS: Clinical and electroencephalographic features in the early stages of CJD may resemble NCSE. The administration of intravenous benzodiazepines and its clinical and electroencephalographic correlation, response to the antiepileptic therapy, and monitoring with serial EEG recordings may be helpful considerations in the differential diagnosis.