荧光屏诱发癫痫发作国例报告

目的：回顾性分析4例光敏性癫痫病人的资料，以提高对荧光屏诱发癫痫发作的认识。方法：对2000年1月至2001年12月来院求诊的4例光敏性癫痫病人的临床资料进行分析，结果：4例中2例仅由转换电视频道诱发作，1例看电视中诱发发作，另1例玩计算机游戏诱发发作。4例中2例为全身强直阵挛发作（GTCS），1例为部分性发作继发全身发作，1例为失神及部分性发作。结论：荧光屏诱发癫痫可以有多种发作类型，不仅有GTCS，还可以有部分发作及失神。     

荧光屏诱发癫痫发作四例报告

目的　回顾性分析 4例光敏性癫痫病人的资料 ,以提高对荧光屏诱发癫痫发作的认识。方法　对 2 0 0 0年 1月至 2 0 0 1年 12月来院求诊的 4例光敏性癫痫病人的临床资料进行分析。结果　4例中 2例仅由转换电视频道诱发发作 ,1例看电视中诱发发作 ,另 1例是玩计算机游戏诱发发作。 4例中 2例为全身强直阵挛发作 (GTCS) ,1例为部分性发作继发全身发作 ,1例为失神及部分性发作。结论　荧光屏诱发癫痫可以有多种发作类型 ,不仅有GTCS ,还可以有部分发作及失神     

癫(癎)与可疑癫(癎)临床发作时的动态脑电图分析

目的探讨癫痫与可疑癫痫临床发作时的动态脑电图（AEEG）的变化特征。方法本文对316例癫痫临床发作时的动态脑电图进行分析。结果临床发作时癫痫组162例中，AEEG监测结果正常为49例（30．25％），异常为113例（69．75％）；在临床诊断可疑癫痫的154例中，AEEG监测结果正常为110例（71．43％），异常44例（28．57％）。癫痫组与可疑癫痫组临床发作时癫痫样波的发放有非常显著性差异（x^2=53．56，P〈0．001）。结论AEEG因大大增加了描记时间而使EEG阳性率明显提高，临床发作与同步的AEEG痫样波的发放对癫痫的诊断非常重要。尤其对许多非痫性发作性疾病与癫痫发作的鉴别诊断更有重要意义。     

局灶性癫痫与非酮性高血糖症

早在1965年Maccario等就强调局灶性癫痫可能是非酮性高血糖症的症状之一，但这并未引起临床医生对本病的重视。本文报告2例非酮性高血糖症并发局灶性癫痫的病倒，其癫痫发作与高血糖症相关，单纯的抗癫痫药物治疗无效，某些药物甚至可能有害，只在血糖降至正常或接近正常时癫痫发作才能得以控制，非酮性高血糖症所致的局灶性癫痫发作可能是一种特殊的神经内分泌综合征。     

国际癫痫发作分类建议（2001年）在部分性发作中的应用

目的 探讨国际抗癫痫联盟关于癫痫发作分类的建议（2001年）在部分性癫痫发作中的应用价值和特点。方法收集1996年6月至2004年10月在我院癫痫中心就诊，经过录像脑电监测捕捉到发作的128例部分性癫疴患者的发作情况，应用1981、2001年两种癫痫发作分类方案，由3位受过正规癫痫和脑电图训练的神经科医生进行分类。结果128例患者共检测到298次发作。按照1981年分类标准，97次（32％）属于简单部分性发作，105次（35％）为复杂部分发作，12次（4％）部分性发作难以准确划分为简单或者复杂性，81次（27％）为继发全面性发作，3次（1％）为部分性癫痫持续状态；应用2001年分类建议，有295次发作为自限性局灶性发作，其中67次（22％）为局灶性感觉性发作，140次（47％）为局灶性运动性发作，包括81次（27％）伴随颞叶自动症的局灶运动性发作，81次（27％）为继发全面性发作，3次为局灶性癫痫持续状态发作。2001年分类方案中，发作类型体现了特征性的临床症状，与发作期的癫痫性放电的解剖部位有紧密的对应，但是，高级皮层的发作症状在一定程度上受到了忽略。结论2001年国际癫痫发作分类体现了良好的发作症状、发作类型、解剖部位之间的联系，可以试用于临床，但需要进一步的完善。     

转换障碍伴类似癫痫发作误诊1例

本文目的是为心因性假性癫痫发作（PNES）的早期诊断、鉴别及治疗提供参考。PNES是转换障碍最常见临床表现之一,常于患者情绪激动或受暗示时突然发病,表现类似癫痫发作,但并无大脑异常的癫痫样放电活动。本案例报道了一例中年女性多次出现类似癫痫发作,结合病史及辅助检查诊断为“转换障碍-心因性假性癫痫发作”,经对症治疗后病情好转。     

癫痫发作与非癫痫性发作的鉴别诊断研究进展

癫痫发作是大脑神经元过度同步化异常放电引起的阵发性神经功能障碍,发作时伴脑电图痫样放电。非癫痫性发作是多种原因引起的,与癫痫发作有类似临床表现的一组疾病,不伴与发作同步的发作期脑电图痫样放电,与癫痫发作鉴别诊断存在一定困难。视频脑电图已广泛应用于神经系统疾病的诊断与治疗,对癫痫发作与非癫痫性发作的鉴别诊断具有重要意义。本文综述症状学特征和脑电图特征对癫痫发作与非癫痫性发作的鉴别诊断意义,以及与癫痫发作相鉴别的常见非癫痫性发作,为癫痫的精准诊断与治疗提供理论依据。     

头痛型癫痫的临床表现和脑电图分析

目的：探讨头痛型癫痫的临床和脑电图表现及预后。方法：本文报告53例头痛型癫痫，病程2周-7年，全部患者发作或发作间歇期均作神经系统检查和多次脑电图及头颅CT检查。结果：发作时表现为剧烈头痛，缓解后无特殊不适。神经系统检查和头颅CT查未见异常，头痛发作和间歇期作常规或睡眠诱发的脑电图检查，均可获痫性放电。结论：头痛型癫痫是植物神经发作中常见的发作类型，其唯一发作表现是头痛，病变部位与下丘脑，颞叶、边缘系统有关。脑电图检查对诊断和鉴别诊断有重要意义。诊断时切忌将功能性或血管性头痛误诊为头痛型癫痫。     

急性脑卒中后癫痫发作─附68例报告

本文报告６８例急性脑卒中后癫痫发作，其中５１例脑出血，１７例为脑梗塞。脑出血５１例中３５．２９％为即刻发作，５６．８６％为早期发作，３．９２％为后期发作，３５．２９％为癫痫持续状态，４１．１８％为大发作，２３．５３％为局灶发作。脑梗塞１２例中即刻发作，早期发作及后期发作分别为５．８８％、６４．７１％和２９．４１％，其癫痫持续状态、大发作和局灶发作分别为２３．５３％、４７．０６％和２９．４１％。本文资料证实，１、癫痫是由于出血灶或梗塞灶波及大脑皮层，２、抗癫痫药物在紧危状态时应用是必须的，特别是病灶波及大脑皮层时应用抗癫药物预防是必须的，３、急性脑卒中后伴癫痫患者较不伴癫痫者预后差，两者有非常显著差异。     

额叶性癫痫的临床分析

额叶性癫痫的临床分析李露斯，吴盛荣额叶性癫痫是起源于额叶的癫痫综合征。其临床特点是以单纯部分性发作，复杂部分性发作，继发全部性发作以及以上症状的综合［１］。由于表现的多样性，给临床诊断及治疗常带来一定的困难。本文就我科门诊癫痫专病随访病人中确诊的额叶...     

Reflex Seizures are Frequent in Patients with Down Syndrome and Epilepsy

In a retrospective study of 30 Down syndrome (DS) patients with epilepsy, we found 6 cases (20%) with reflex seizures. One patient had benign myoclonic epilepsy of infancy with clinical photosensitivity. The other 5 cases had all startle-induced epileptic seizures and a form of symptomatic epilepsy. Three patients had a Lenox-Gastaut syndrome, one had generalized symptomatic epilepsy, and one had partial symptomatic epilepsy (PSE). Reflex epilepsy was also used as a classification category in the PSE case, as most or all seizures were stimulus-related in this patient. Seizures precipitated by stimuli were stereotyped in 4 patients, but 2 patients responded to stimuli with different types of seizures. The actual occurrence of reflex seizures in DS patients with epilepsy is probably underestimated. These cases seem to confirm previous reports showing deficiencies in cortical inhibition in the brain of DS patients.     

Family studies of individuals with eyelid myoclonia with absences

Purpose: Eyelid myoclonia with absences (EM) is an uncommon type of absence seizure associated with a variety of epilepsy syndromes. The syndrome of epilepsy with EM (EMA) has been proposed to denote the onset of frequent EM induced by eye closure and photic stimulation beginning in childhood. The clinical genetics of EMA has not been well characterized, although a family history of seizures is not infrequent. Methods: Individuals with EMA were ascertained by referral and through the investigators’ clinical practices. All available family members were assessed for seizures using a validated seizure questionnaire. Electroclinical data were obtained on each proband and all affected family members; pedigrees were constructed. Families were analyzed for phenotypic patterns. Key Findings: Eighteen individuals with EMA were recruited. A history of seizures was found in 34 relatives in 15 (83%) of 18 families. In terms of epilepsy syndromes, 9 relatives from 7 of 15 families had febrile seizures. Two relatives had EMA. Classical genetic generalized epilepsy (GGE) syndromes were seen in five relatives: two generalized tonic–clonic seizures alone, two childhood absence epilepsy (CAE), and one juvenile myoclonic epilepsy (JME). Genetic epilepsy with febrile seizures plus (GEFS+) phenotypes occurred in 16 relatives. On review of the epilepsy syndromes within each family, seven families had a pattern consistent with GEFS+, whereas three families had classical GGE. Significance: The clinical genetics of EMA is suggestive of complex inheritance with shared genetic determinants overlapping with both classical GGE and GEFS+. The epilepsy syndromes in relatives of probands with EMA differ from those found in families of probands with CAE, supporting the concept that patients with EMA have a syndrome that is distinct from CAE. This presumably reflects different genetic components contributing to their genetic architecture.     

Clinical characteristics of 92 patients with temporal lobe focal cortical dysplasia identified by pathological examination

Focal cortical dysplasia (FCD) is frequently associated with focal epilepsy, and a broad spectrum of histopathology is included in the diagnosis of FCD. In 2011, an International League Against Epilepsy (ILAE) task force proposed an international consensus for a classification system to better characterise specific clinicopathological FCD entities. The clinical characteristics of patients with FCD should be confirmed according to the new ILAE classification. We retrospectively analysed 92 patients who had undergone surgical treatment for temporal lobe epilepsy and received a pathological diagnosis of FCD. The pathological sections were re-examined and diagnosed according to the 2011 ILAE classification. The clinical data from patients with different FCD subtypes were evaluated, including a detailed history regarding spontaneous abortions, trauma, ischaemic injury, encephalitis, and febrile seizures at an early age. The age of epilepsy onset, duration of epilepsy, age at surgery, seizure frequency, history of febrile seizures, and seizure type, particularly whether the seizures were secondarily generalised tonic-clonic seizures, were recorded. Clinical differences were found in the patients with temporal lobe FCD. The associated FCD subtypes have unique clinical characteristics, including a later age of epilepsy onset and a shorter duration of epilepsy, especially in FCD Type IIIc; and a high susceptibility to febrile seizures was observed in FCD Type IIIa.     

The influence of vigilance states on paroxysmal EEG activities and clinical seizures in children.

We studied the relationships between clinical variables and those related to the states of vigilance in 18 cases of benign partial epilepsy with centro-temporal spike-waves, 22 cases of definite symptomatic partial epilepsy, and 16 cases of undetermined partial epilepsy. The time of day during which the seizures appeared and the paroxysmal activity densities during non-REM and REM sleep are not distributed differently among the 3 electro-clinical types. However, the benign epilepsy with centro-temporal spikes group had more patients with sleep-sensitive paroxysmal activities. Patients who mainly had nocturnal seizures were found to have more frequent generalized seizures and a greater sleep-sensitive paroxysmal activity. Three cases demonstrated continuous spike-waves during sleep. The patients who had little or no paroxysmal activity during sleep were the youngest. This study illustrates that sleep-sensitive seizures and paroxysmal activities are not specific to benign childhood epilepsy with centro-temporal spikes, and that seizures and paroxysmal activities are two manifestations associated with epilepsy, affected in different ways by states of vigilance.     

Alcohol and epilepsy: a case report between alcohol withdrawal seizures and neuroborreliosis

Objectives

This work consists in a study of the links between alcohol, a psychoactive substance and different related epileptic manifestations in order to clarify predominant factors both on conceptual, clinical and therapeutic levels.

Background

If alcohol is a frequent risk factor for seizures, its scientific evidence is less clear and ad hoc literature is rich in controversies and not firmly supported by systematic surveys. Alcohol has variable roles in the physiopathological determinism of seizures, the nosographical status of which needs to be clarified: alcohol withdrawal seizures, alcoholic epilepsy, and sometimes symptomatic epilepsy caused by coincidental disorders.

Methods

A synthesis of relevant literature describing the links between alcohol and epilepsy is illustrated by a clinical case: a patient admitted in our psychiatric ward for chronic alcoholism had had two seizures questioning their nosographical status. An infectious process with protean neurological manifestations, neuroborreliosis, was diagnosed.

Discussion

Three distinct clinical pictures illustrate the links between alcohol and epilepsy: the first, convulsive inebriation corresponds to a seizure during severe acute alcohol intoxication. The second deals with alcohol withdrawal seizures following a partial or complete sudden withdrawal of alcohol; these are the clinical features the most documented in the literature representing, with delirium tremens, the main complication of alcohol withdrawal. The third clinical picture, alcoholic epilepsy, is characterized by repetitive seizures in patients presenting alcohol abuse without former history of epilepsy or other potentially epileptic disorder, and without relationship to alcohol withdrawal or acute alcohol intoxication. Acute and chronic effects of alcohol on central nervous system have been depicted, while a unified classification of alcohol related seizures has been recently established by Bartolomei. This classification based on the Ballenger hypothesis of kindling (1978) could explain withdrawal and hazardous seizures as clinical expressions of the same epileptogenic process over different stages. Although theoretically criticized, such a model offers a conceptual interest while able to unify the varied understanding of convulsive crises related to alcohol, and a practical one, whilst being a basis for a therapeutic approach. Our clinical case illustrates the delay in the diagnosis established after two iterative generalized seizures, 72 hours after the beginning of a programmed weaning of a patient presenting alcohol dependency. If the withdrawal seizure hypothesis was underlined, some data led to symptomatic epilepsy. Firstly atypia, the well-supervised preventive treatment of convulsion did not avoid seizures. Secondly, the EEG showed focal anomalies strongly linked in the literature with a cerebral disorder, which was confirmed by MRI; thirdly, cognitive alterations, which are not usual in alcohol dependency, were observed clinically and confirmed by neuropsychological tests. Finally a neuroborreliosis was diagnosed, while the main neuropsychiatric complications of Lyme disease were described. In accordance with the recommendations made by some authors, it appeared legitimate to consider neuroborreliosis as a potential differential diagnosis of every atypical psychiatric disorder, the interest of such an identification laying in the existence of a specific treatment.     

The neurobiology of epilepsy

Epilepsy is a complex disease with diverse clinical characteristics that preclude a singular mechanism. One way to gain insight into potential mechanisms is to reduce the features of epilepsy to its basic components: seizures, epileptogenesis, and the state of recurrent unprovoked seizures that defines epilepsy itself. A common way to explain seizures in a normal individual is that a disruption has occurred in the normal balance of excitation and inhibition. The fact that multiple mechanisms exist is not surprising given the varied ways the normal nervous system controls this balance. In contrast, understanding seizures in the brain of an individual with epilepsy is more difficult because seizures are typically superimposed on an altered nervous system. The different environment includes diverse changes, making mechanistic predictions a challenge. Understanding the mechanisms of seizures in an individual with epilepsy is also more complex than understanding the mechanisms of seizures in a normal individual because epilepsy is not necessarily a static condition but can continue to evolve over the lifespan. Using temporal lobe epilepsy as an example, it is clear that genes, developmental mechanisms, and neuronal plasticity play major roles in creating a state of underlying hyperexcitability. However, the critical control points for the emergence of chronic seizures in temporal lobe epilepsy, as well as their persistence, frequency, and severity, are questions that remain unresolved.     

Factors influencing clinical features of absence seizures

Purpose: The clinical features of absence seizures in idiopathic generalized epilepsy have been held to be syndrome‐specific. This hypothesis is central to many aspects of epilepsy research yet has not been critically assessed. We examined whether specific factors such as epilepsy syndrome, age, and state determine the features of absence seizures. Methods: Children with newly presenting absence seizures were studied using video electroencephalography (EEG) recording. We analyzed whether a child's epilepsy syndrome, age, state of arousal, and provocation influenced specific clinical features of their absence seizures: duration, eyelid movements, eye opening, and level of awareness during the seizure. Results: Seizures (509) were evaluated in 70 children with the following syndromes: Childhood absence epilepsy (CAE), 37; CAE plus photoparoxysmal response (PPR), 10; juvenile absence epilepsy (JAE), 8; juvenile myoclonic epilepsy (JME), 6; unclassified, 9. Seizure duration was associated with epilepsy syndrome as children with JME had shorter seizures than in other syndromes, independent of age. Age independently influences level of awareness and eye opening. Arousal or provocation affected all features except level of awareness. Specific factors unique to the child independently influenced all features; the nature of these factors has not been identified. Discussion: The view that the clinical features of absence seizures have syndrome‐specific patterns is not supported by critical analysis. We show that confounding variables profoundly affect clinical features and that syndromes also show marked variation. Variation in clinical features of absence seizures results from a complex interaction of many factors that are likely to be genetically and environmentally determined.     

Ictal single photon emission computed tomography in absence seizures: apparent implication of different neuronal mechanisms

Absence seizures represent a complex group of epilepsy, characterized by lapse of consciousness with staring. Bilateral, synchronous, and symmetric bursts of 3-Hz spike-and-wave discharges are observed on the electroencephalogram, whereas interictal background activity is normal. This kind of epilepsy has to be differentiated from other generalized epilepsies such as juvenile absence epilepsy and juvenile myoclonic epilepsy. Moreover, absence seizures, together with generalized spike-and-wave discharges, may coexist with other types of epilepsy such as frontal lobe epilepsy, temporal lobe epilepsy, benign epilepsy with centrotemporal spikes, and childhood epilepsy with occipital paroxysms. We have carried out ictal single photon emission computed tomography (SPECT) in 10 patients with clinical evidence of absence seizures with the aim to better understand and to distinguish this kind of seizure as primarily or secondarily generalized to a specific area and to obtain more information on the neuronal mechanisms involved in the different types of seizures, usually not identifiable at the first appearance. During the long follow-up period (9 months to 14 years), 7 of the 10 examined patients underwent interictal SPECT when they became seizure free. Our data permitted, in two patients, the diagnosis of childhood absence seizures; in three patients, they suggested the possibility of later appearance of other seizure types, on the basis of focal hyperperfusion indicating a possible focal firing. In three of the examined patients, the diagnosis of idiopathic localization-related epilepsies mimicking childhood absence seizures could be performed. In the last two patients, the hypothesis of a coexistence of absences with partial and generalized seizures was considered. From our results, it can be presumed that ictal SPECT findings may contribute to the physiopathologic classification of the different types of epilepsies. Moreover, anticonvulsant treatment more appropriate to the different forms of seizures can be used.     

Parietal and Occipital Lobe Epilepsy: A Review

Summary: Parietal and occipital seizures have been investigated relatively little. Recent interest in seizures of frontal lobe origin has led to a definition of several well-identifiable clinical patterns of frontal lobe seizures. A similar delineation of the clinical and EEG pattern of parietal and occipital epilepsy, using modern investigations, appears appropriate, not least because the few reported series of surgical treatment in parietal and occipital epilepsy have indicated that operation may be relevant in selected cases, not only for removal of space-occupying lesions. Such a study is currently being undertaken at the National Hospital for Neurology and Neurosurgery and The Chalfont Centre for Epilepsy with the aim of developing and evaluating diagnostic criteria for these seizures. From the existing literature we can conclude that precise incidence and prevalence are largely unknown. A recent community-based study of 252 subjects with partial epileptic seizures in an epileptic population of 594, showed that parietal seizures and seizures of posterior origin each comprised 6.3% and central or sensory-motor seizures comprised 32.5% of focal seizures in the 160 cases in which seizures could be subclassified (Manford et al., 1992). This incidence seems low for occipital seizures as compared with the 1953 study by Gibbs and Gibbs, who observed occipital epileptiform activity in 8% of subjects with focal epilepsy. The most prominent clinical manifestations of parietal epilepsy are elementary sensory phenomena at the beginning of seizures and elementary visual hallucinations in occipital epilepsy. These symptoms are not associated solely with posterior hemisphere epilepsy, however, and more studies are obviously needed to define how close this relation is. Scalp EEG is frequently negative or maybe misleading; further-more, spread of epileptic discharges from the parietal and occipital lobes to frontal and temporal regions may obscure seizure origin. Because of these controversial symptoms, diagnostic criteria may be difficult to define. The wide difference in clinical and EEG manifestations between reported series of parietal and occipital epilepsy also reflects a considerable problem with patient sampling. Classification of epilepsy according to the anatomic division of the brain may be arbitrary, and it may be appropriate to define epileptic syndromes such as sensorimotor seizures or occipitotemporal seizures that cross such artificial divides.     

Viral encephalitis and epilepsy

Viral encephalitis presents with seizures not only in the acute stage but also increases the risk of late unprovoked seizures and epilepsy. Acute symptomatic and late unprovoked seizures in different viral encephalitides are reviewed here. Among the sporadic viral encephalitides, Herpes simplex encephalitis (HSE) is perhaps most frequently associated with epilepsy, which may often be severe. Seizures may be the presenting feature in 50% patients with HSE because of involvement of the highly epileptogenic frontotemporal cortex. The occurrence of seizures in HSE is associated with poor prognosis. In addition, chronic and relapsing forms of HSE have been described and these may be associated with antiepileptic drug-resistant seizures. Among the epidemic (usually due to flaviviruses) viral encephalitides, Japanese encephalitis (JE) is most common and is associated with acute symptomatic seizures, especially in children. The reported frequency of acute symptomatic seizures in JE is 7–46%. Encephalitis due to other flaviviruses such as equine, St. Louis, and West Nile viruses may also manifest with acute symptomatic seizures. In Nipah virus encephalitis, seizures are more common in relapsed and late-onset encephalitis in comparison to acute encephalitis (4% vs. 1.8%). Other viruses like measles, varicella, mumps, influenza, and entero-viruses may cause seizures depending on the area of brain involved. There is no comprehensive data regarding late unprovoked seizures in different viral encephalitides. Prospective studies are required to document the risk of late unprovoked seizures and epilepsy following viral encephalitis due to different viruses as well as to determine the clinical characteristics, course, and outcome of post-encephalitic epilepsy.