EEG features in Encephalopathy related to Status Epilepticus during slow Sleep

Encephalopathy related to Status Epilepticus during slow Sleep (ESES) is a peculiar electro‐clinical condition, with variable etiologies, characterized by an age‐dependent phenomenon of extreme activation of epileptic activity during sleep, i.e. “status epilepticus during sleep”, that is strictly associated with the appearance of cognitive and behavioral disturbances. Even though the peculiar EEG picture is fundamental for the diagnosis of ESES, clear‐cut and shared diagnostic criteria for defining the EEG boundaries of this syndrome are still lacking. The diagnosis of ESES can be further complicated by the variability of the EEG findings, that during the course of the disease can change from diffuse to more or less focal and viceversa, depending both on the spontaneous clinical evolution of this condition and/or on the effects of medications. Given the complexity and the heterogeneity of EEG parameters during the ESES course, it is important to correlate the EEG findings with the concomitant cognitive and behavioral status, possibly taking into account not only the spike‐wave index, but also other parameters, such as for instance the topography of the epileptic abnormalities, their patterns of spread, and their fluctuations over time. Moreover, the epileptiform activity not only during sleep, but also during wakefulness, the presence of focal slowing, the organization of the EEG background and a derangement of the sleep architecture may play a role in determining the clinical picture.     

Acetazolamide for electrical status epilepticus in slow‐wave sleep

Electrical status epilepticus in slow‐wave sleep (ESES) is characterized by nearly continuous spike–wave discharges during non–rapid eye movement (REM) sleep. ESES is present in Landau‐Kleffner syndrome (LKS) and continuous spike and wave in slow‐wave sleep (CSWS). Sulthiame has demonstrated reduction in spike–wave index (SWI) in ESES, but is not available in the United States. Acetazolamide (AZM) is readily available and has similar pharmacologic properties. Our aims were to assess the effect of AZM on SWI and clinical response in children with LKS and CSWS. Children with LKS or CSWS treated with AZM at our institution were identified retrospectively. Pre‐ and posttherapy electroencephalography (EEG) studies were evaluated for SWI. Parental and teacher report of clinical improvement was recorded. Six children met criteria for inclusion. Three children (50%) demonstrated complete resolution or SWI <5% after AZM. All children had improvement in clinical seizures and subjective improvement in communication skills and school performance. Five of six children had subjective improvement in hyperactivity and attention. AZM is a potentially effective therapy for children with LKS and CSWS. This study lends to the knowledge of potential therapies that can be used for these disorders, which can be challenging for families and providers.     

Functional brain connectivity in electrical status epilepticus in sleep

Aims. Electrical status epilepticus in sleep (ESES) is an age‐related, self‐limited epileptic encephalopathy. The syndrome is characterized by cognitive and behavioral abnormalities and a specific EEG pattern of continuous spikes and waves during slow‐wave sleep. While spikes and sharp waves are known to result in transient cognitive impairment during learning and memory tasks performed during the waking state, the effect of epileptiform discharges during sleep on cognition and behavior is unclear. There is increasing evidence that abnormalities of coherence, a measure of the consistency of the phase difference between two EEG signals when compared over time, is an important feature of brain oscillations and plays a role in cognition and behavior. The objective of this study was to determine whether coherence of EEG activity is altered during slow‐wave sleep in children with ESES when compared to typically developing children. Methods. We examined coherence during epochs of ESES versus epochs when ESES was not present. In addition, we compared coherence during slow‐wave sleep between typically developing children and children with ESES. Results. ESES was associated with remarkably high coherences at all bandwidths and most electrode pairs. While the high coherence was largely attributed to the spikes and spike‐and‐wave discharge, activity between spikes and spike‐and‐wave discharge also demonstrated high coherence. Conclusions. This study indicates that EEG coherence during ESES is relatively high. Whether these increases in coherence correlate with the cognitive and behavioral abnormalities seen in children with this EEG pattern remains to be determined.     

Interictal epileptiform discharges in sleep and the role of the thalamus in Encephalopathy related to Status Epilepticus during slow Sleep

EEG activation of interictal epileptiform discharges (IEDs) during NREM sleep is a well‐described phenomenon that occurs in the majority of epileptic syndromes. In drug‐resistant focal epilepsy, IED activation seems to be related to slow wave activity (SWA), especially during arousal fluctuations, namely phase A of the cyclic alternating pattern (CAP). Conversely, in childhood focal epileptic syndromes, including Encephalopathy related to Status Epilepticus during slow Sleep (ESES), IED activation seems primarily modulated by sleep‐inducing and maintaining mechanisms as reflected by the dynamics of spindle frequency activity (SFA) rather than SWA. In this article, we will review the effect of sleep on IEDs with a particular attention on the activation and modulation of IEDs in ESES. Finally, we will discuss the role of the thalamus and cortico‐thalamic circuitry in this syndrome.     

Encephalopathy related to Status Epilepticus during slow Sleep: a link with sleep homeostasis?

Encephalopathy related to Status Epilepticus during slow Sleep (ESES) is a childhood epilepsy syndrome characterized by appearance of cognitive and behavioural disturbances in conjunction with a striking activation of EEG epileptic abnormalities during sleep. The link between the extreme amount of epileptic discharges during sleep and the deterioration of cognitive functions and behavior is poorly understood. We hypothesize that the negative effects of ESES may depend on the impairment of the synaptic homeostasis processes occurring during normal sleep and that are particularly important in the developmental age. Sleep ensures synaptic homeostasis by promoting synaptic weakening/elimination after the increase of synaptic strength that occurs during wakefulness. Changes in synaptic strength are reflected in the EEG by changes of sleep slow wave activity (SWA). Recent studies in ESES have failed to show changes of sleep SWA, particularly at the site of the epileptic focus, suggesting a spike‐related impairment of the homeostatic recovery of sleep. This impaired synaptic homeostasis in the critical period of development may alter cortical wiring and thereby disrupt, often irreversibly, cognitive functions and behavior, leading to the neuropsychological compromise typical of ESES.     

Guidelines for EEG in encephalopathy related to ESES/CSWS in children

Electrical status epilepticus during slow sleep (ESES) or continuous spikes and waves during slow sleep (CSWS) is a phenomenon characterized by strong activation of epileptiform activity in the electroencephalogram (EEG) during sleep. The literature contains several small series of patients and many case reports. Large prospective studies are lacking. Definitions of the syndromes and EEG criteria and methods vary, as does their classification. The fluctuating clinical course and EEG findings complicate the diagnostic process and evaluation of effect of therapy. Studies describing quantitative aspects of the epileptiform abnormalities in EEG are overrepresented in literature, whereas qualitative aspects are relatively undervalued. Guidelines for evaluation of the EEG in these syndromes, which focus on both aspects, are presented.     

The tower of Babel: Survey on concepts and terminology in electrical status epilepticus in sleep and continuous spikes and waves during sleep in North America

Purpose: The terms “electrical status epilepticus during sleep (ESES)” and “continuous spikes and waves during sleep (CSWS)” have been used interchangeably when referring to related but different concepts. In addition, the quantification of epileptiform activity has not been standardized, and different approaches to quantification have been used. The aim of this study was to evaluate the extent to which pediatric neurologists and epileptologists use a homogeneous terminology and conceptualization in CSWS and ESES and to characterize the current understanding of these conditions. Methods: A survey addressing the use of terminology in “ESES” and “CSWS” and the understanding of related concepts was distributed online to all members of the Child Neurology Society and the American Epilepsy Society mailing lists. Surveys were self‐administered and collected using an online survey website ( http://www.surveymonkey.com ). Key Findings: Two hundred nineteen surveys were completed, 137 from the Child Neurology Society mailing list and 82 from the American Epilepsy Society mailing list. ESES and CSWS were considered synonymous by 117 respondents, not synonymous by 61, 21 respondents did not know, and 20 did not respond. Most respondents (63.1%) considered CSWS as a devastating epileptic encephalopathy with severe sequelae even if treated correctly, but 25.1% of respondents indicated that it does not leave sequelae if epilepsy was treated early and another 11.8% noted that cognitive difficulties resolved with age. Cognitive and/or language regression were considered mandatory for the diagnosis of CSWS by only 27% of the respondents. The diagnosis of CSWS was based on electroencephalography (EEG) assessment alone by 31% of respondents. Respondents used different methods for calculation of the epileptiform activity, different EEG samples for calculation, and considered differently the lateralized epileptiform activity. The cut‐off values for percentage of the sleep record occupied by spike‐waves were variable depending on the respondent. There was no agreement on whether these cutoff values were mandatory for the diagnosis of ESES and CSWS. Significance: Our data show that the professionals caring for children with ESES and CSWS in North America use the terms, concepts, and defining features heterogeneously. The lack of a common language may complicate communication among clinicians and jeopardize research in this field. We anticipate that our data will fuel the development of much needed common terminology and conceptualization of ESES and CSWS.     

Encephalopathy related to status epilepticus during slow sleep (ESES) as atypical evolution of Panayiotopoulos syndrome: an EEG and neuropsychological study

Aim: We report two patients with Panayiotopoulos syndrome (PS) who developed encephalopathy related to status epilepticus during slow sleep (ESES) at the peak of their clinical course. Methods: Clinical charts and EEG data were reviewed. Results: The patients exhibited nocturnal autonomic seizures and occipital EEG foci, the latter of which later evolved into multifocal EEG foci with synchronous frontopolar and occipital spikes (Fp‐O EEG foci), and finally into continuous spikes‐waves during sleep (CSWS; spike‐wave index >85% based on whole‐night sleep recording) at eight years and seven years of age, respectively. The occipital spikes always preceded frontopolar spikes by 30～50 mseconds based on the analysis of CSWS. Neuropsychological ability, including IQ, deteriorated during the CSWS period in both patients. The autonomic seizures and focal to bilateral tonic‐clonic seizures were initially resistant to antiepileptic drugs (AEDs), and occurred more than 10 times in both patients. However, the seizures and EEG findings gradually resolved, and AEDs were successfully terminated in both patients. Conclusion: PS can progress to ESES if the clinical course exhibits atypical evolution. The initial autonomic symptom of the seizures and interictal Fp‐O EEG foci should be carefully monitored in patients with CSWS or ESES.     

Electrical status epilepticus in sleep (ESES)/continuous spikes and waves during slow sleep (CSWS) syndrome in children: An electroclinical evaluation according to the EEG patterns

ObjectiveThe aim of this study was to describe the electroclinical spectrum in children with electrical status epilepticus in sleep (ESES)/continuous spikes and waves during slow sleep (CSWS) syndrome according to the EEG patterns.MethodsClinical data of 44 patients with ESES/CSWS syndrome who were treated and followed at least two years were analyzed. Records of EEGs of patients were reevaluated to determine two aspects of the ESES pattern: (1) the spike–wave index (SWI) on the NREM sleep EEG (Group I: typical vs. atypical ESES pattern (33/11 patients)) and (2) the area of maximum amplitude of continuous epileptic activity (Group II: anterior vs. posterior ESES pattern (33/11 patients)).ResultsSymptomatic etiology was more defined in patients with the typical ESES pattern (40%) than the group with the atypical ESES pattern (9%) by a factor of four. All patients were receiving at least two antiepileptic drug (AED) treatments. Eighteen patients (41%) received AEDs plus ACTH therapy. Complete disappearance of the ESES pattern on the EEG was observed in 18 patients (41%), more than 50% reduction was observed in five patients (11%), less than 50% reduction was observed in eight patients (18%), and no response was observed in five patients (11%). No significant difference was found when comparing the groups in terms of reduction of seizures and the SWI. Seizure outcome at the two-year follow-up was similar between the group with ESES treated with AEDs plus ACTH and the group with ESES treated with AEDs without ACTH therapy.SignificanceThis study demonstrated that the rate of the SWI (typical vs. atypical ESES) and the maximum amplitude of the ESES pattern (anterior vs. posterior) have no significant correlation with seizure control and reduction of the SWI on the EEG in children with ESES syndrome.     

Sulthiame add-on therapy in children with focal epilepsies associated with encephalopathy related to electrical status epilepticus during slow sleep (ESES)

Purpose: In children with symptomatic or idiopathic focal epilepsies, their disease may evolve into an epileptic encephalopathy related to continuous spike and wave during slow sleep (CSWS) or electrical status epilepticus during slow sleep (ESES). ESES syndrome implies serious risks of neuropsychologic impairment, and its treatment has frequently been disappointing. The aim of this study is to present our experience using sulthiame as add‐on treatment in 53 patients with ESES syndrome that was refractory to other antiepileptic drugs (AEDs). Methods: Neurologic examinations, cerebral magnetic resonance imaging (MRI), and repeated prolonged sleep electroencephalography (EEG) studies were performed in all cases. Data about school achievements and or neuropsychological evaluations were obtained repeatedly during the follow‐up of 1.5–16 years. Sulthiame was added in doses ranging between 5 and 30 mg/kg/day. Key Findings: Since add‐on of sulthiame, 10 of 28 patients in the symptomatic group became seizure free: 4 patients with normal EEG studies and 6 with residual spikes. Nine of 28 patients showed a significant reduction in number of seizures and presented spikes but no ESES on EEG. The other nine cases showed neither clinical nor EEG improvement. A striking result was that 3 of 11 children with unilateral polymicrogyria and ESES syndrome became seizure free, and in another six a significant improvement in frequency of seizures and in EEG abnormalities seemed to be related to the add‐on of sulthiame. Twenty‐one of the 25 patients in the idiopathic group became seizure free and without ESES in <3 months after add on of sulthiame. In two of the patients the changes were seen in a few days. Significance: We understand that sulthiame may be effective as add‐on treatment in children with ESES syndrome.     

抗癫癎药物对儿童临床下癎性电持续状态及认知功能的影响

目的：探讨抗癫?药物（AED）对临床发作已控制,但脑电图（EEG）上仍存在癫?性电持续状态ESES患者的认知功能的影响。方法：收集2013年3月～2015年11月本院门诊、住院治疗的儿童癫?患者,用日本光电9000型长程录像脑电图（V‐EEG）监测到的16例临床下ESES患者,临床无发作均超过半年,随访观察,调整治疗方案前后均再进行神经心理学评估和V‐EEG监测。结果：16例应用卡马西平（CBZ）、奥卡西平（OXC）临床发作均已得到控制,V‐EEG提示仍存在ESES现象,神经心理学评估均存在不同程度的认知功能障碍,治疗方案调整为丙戊酸钠／丙戊酸镁、左乙拉西坦／托吡酯,3个月后复查V‐EEG提示ESES消失,脑功能状态得到改善（P＜0．05）。结论：AED的治疗目的,不仅要控制临床发作,也要控制临床下?样放电,特别是ESES现象。     

Electrical status epilepticus in sleep

Electrical status epilepticus in sleep (ESES) describes an electroencephalographic pattern showing significant activation of epileptiform discharges in sleep. The terms continuous spike wave in slow-wave sleep (CSWS) and Landau-Kleffner syndrome (LKS) describe the clinical epileptic syndromes seen with ESES. Although there is an overlap between these 2 syndromes, children with CSWS present with a more global regression have more problematic epilepsy and have EEG foci located predominantly in frontotemporal or frontocentral regions. In contrast, children with LKS present with an acquired auditory agnosia, fewer seizures, and EEG foci in the posterotemporal regions. ESES requires a high degree of clinical suspicion because slow-wave sleep must be recorded to confirm this diagnosis. Treatment of ESES extends beyond just control of the seizures; amelioration of the continuous epileptiform discharge must occur to improve neuropsychological outcome. Although there is little evidence to guide treatment, conventional antiepileptic drugs play only a minimal role. Steroid therapy and high-dose benzodiazepines are most commonly used, but other therapies including intravenous gamma-globulin, the ketogenic diet, and surgical therapy with multiple subpial transaction have shown efficacy in small case series. Although epilepsy resolves with time in most cases, many children are left with significant cognitive or language impairment. Longer duration of ESES appears to be the major predictor of poor outcome; markedly abnormal neuronal activity during a critical period for synaptogenesis may result in aberrant synapse formation, explaining the poorer neuropsychological outcome. Early recognition and effective therapy are necessary to improve long-term prognosis in this condition.     

Cognition and Paroxysmal EEG Activities: From a Single Spike to Electrical Status Epilepticus during Sleep

Summary:  Epileptic EEG paroxysms can interfere with cognitive processes producing transitory effects, such as those related to a single spike, as well as long-lasting effects, such as in electrical status epilepticus during slow-wave sleep (ESES). Focal spike-related disruption of cortical functions can produce transitory cognitive impairment, with neuroanatomical specificity between the site of the epileptic focus and the impaired cognitive tasks. ESES represents a model of the long-lasting effects of continuous spike-wave activity on higher cortical functions. The duration of ESES and the localization of interictal foci seem to play a major role in influencing the degree and type of cognitive dysfunction, suggesting that the ESES clinical picture results from a localized disruption of EEG activity caused by focal epileptic activity during sleep. Recently, Giulio Tononi's group reported that a local increase of slow-wave activity (SWA) during sleep after learning is associated with improved performance of the learned task after sleep (Huber et al., Nature 2004;430:78–81). On the basis of these findings, we can speculate that prolonged focal epileptic activity during sleep (as occurring in ESES) interferes with local SWA at the site of the epileptic focus, impairing the neural processes and, possibly, the local plastic changes associated with learning and other cognitive functions.     

The effect of surgery in encephalopathy with electrical status epilepticus during sleep

Purpose: We analyzed clinical and electroencephalography (EEG) outcomes of 13 patients with pharmacoresistant encephalopathy with electrical status epilepticus during sleep (ESES) following epilepsy surgery. Methods: All patients had symptomatic etiology of ESES and preoperative neuropsychological deterioration. Ten patients had daily atypical absences. Clinical outcome was assessed at 6 months and at 2 years after surgery. Clinical and EEG data were reviewed retrospectively. The spike propagation pattern and area and source strength in source montage were analyzed from preoperative and postoperative EEG studies. Key Findings: Preoperative sleep EEG showed electrical status epilepticus during sleep (SES) with one‐way interhemispheric propagation in nine patients and with two‐way interhemispheric propagation in four. The age of the patients at the time of surgery ranged from 3.6–9.9 years. Focal resection (two patients) or hemispherotomy (one patient with postoperative EEG) either terminated SES or restricted the discharge to one region. Either reduced SES propagation area or source strength was found in four of eight callosotomy patients with postoperative EEG. Of patients who had seizures preoperatively, Engel class I–II seizure outcome was observed in two of three children after focal resection or hemispherotomy and in two of eight children after callosotomy. None of these patients with Engel class I–II outcome had SES with two‐way interhemispheric propagation on preoperative EEG. Cognitive deterioration was halted postoperatively in all except one patient. Cognitive catch‐up of more than 10 IQ points was seen in three patients, all of whom had shown a first measured IQ of >75. Significance: Patients with pharmacoresistant ESES based on symptomatic etiology may benefit from resective surgery or corpus callosotomy regarding both seizure outcome and cognitive prognosis.     

Sleep Microstructure and EEG Epileptiform Activity in Patients with Juvenile Myoclonic Epilepsy

Clinical and EEG manifestations of juvenile myoclonic epilepsy (JME) occur in a strict relationship to the sleep-wake cycle, particularly to transition phases (awakening, falling asleep, afternoon relaxation after work). JME manifestations are deactivated during sleep. Because arousal fluctuations during NREM sleep may be controlled by the same neurophysiologic mechanisms regulating awakening, we studied the relationship between the cyclic alternating pattern (CAP) and JME manifestations. All-night polysomnographic recordings of 10 JME patients were analyzed for variations of epileptiform EEG abnormalities in relation to sleep stages and to different microstructural variables (NCAP, CAP, phases A and B). CAP rates (ratio between total CAP duration and total NREM sleep duration) were also calculated. Average CAP rate was 46.70%, significantly higher than that (23%) of an age-matched control group. Macrostructural analysis showed only a trend toward a slight predominance of EEG epileptiform activity during slow wave sleep but no significant correlation between spiking rates and sleep stages. Microstructural analysis confirmed the CAP modulation of EEG epileptiform activity, with maximum appearance of epileptiform abnormalities during phase A CAP (normalized spiking rate = 4.00 +/- 0.98) and strong inhibition during phase B (0.06 +/- 00.6). Intermediate values were noted during NCAP (0.54 +/- 0.27). No correlation was noted between spiking rates during NREM sleep and CAP rates, possibly indicating that in JME patients the increased CAP rate may be partially independent of epileptiform EEG activity. Our data suggest that in JME patients CAP may be a neurophysiologic oscillator organizing expression of the epileptiform discharges independent of the tendency of the individual patient to produce epileptiform EEG discharges.     

睡眠中癎样放电对睡眠的影响

目的：观察不同睡眠时相中?样放电的情况,以及对不同发作类型患者生活品质（QOL ）的评价,探讨?样放电对癫?患者睡眠的影响以及睡眠对其Q O L的影响。方法：对132例癫?患者进行24 h录像脑电图（V‐EEG）及多项睡眠监测（PSG）检查,检测?样放电及分析睡眠结构。运用癫?患者生活质量量表‐31（QOLIE‐31）对不同发作类型患者进行QOL评估。结果：在全部132例患者中,非?性异常为32例（25．8％）,出现?样放电为52例（40．9％）,觉醒期及睡眠期?样放电检出率比较差异有显著意义（P＜0．05）。?样放电组和对照组相比NREM Ⅰ－Ⅱ期明显延长[分别为65．93（±9．1）％和58．67（±5．7）％],NREM Ⅲ期明显缩短[分别为17．78（±5．2）％和26．06（±8．2）％],差异均有统计学意义（P ＜0．05）;睡眠参数中?样放电组REM潜伏期明显延长,同时觉醒次数也增多。而非?性异常组REM 潜伏期、觉醒次数与正常对照组相比均有增加,但差异无统计学意义。不同发作类型睡眠结构差异无统计学意义。各种发作类型的患者各 QOL 指标均低于正常人群,差异有统计学意义（ P＜0．01）;全面性发作患者除药物影响外各指标均低于其他发作类型患者,差异有统计学意义;不同发作类型患者受到药物的影响无明显差异。结论：联合应用 V‐EEG及PSG可以更好地发现睡眠中?样放电,从而有助于确诊临床工作中难以发现的癫?。分析?样放电与睡眠时相之间的关系,以便指导临床癫?治疗,更好地控制癫?发作,改善患者QOL。     

CSWS-related autistic regression versus autistic regression without CSWS

Continuous spike-waves during slow-wave sleep (CSWS) and Landau-Kleffner syndrome (LKS) are two clinical epileptic syndromes that are associated with the electroencephalography (EEG) pattern of electrical status epilepticus during slow wave sleep (ESES). Autistic regression occurs in approximately 30% of children with autism and is associated with an epileptiform EEG in approximately 20%. The behavioral phenotypes of CSWS, LKS, and autistic regression overlap. However, the differences in age of regression, degree and type of regression, and frequency of epilepsy and EEG abnormalities suggest that these are distinct phenotypes. CSWS with autistic regression is rare, as is autistic regression associated with ESES. The pathophysiology and as such the treatment implications for children with CSWS and autistic regression are distinct from those with autistic regression without CSWS.     

Expanding the clinical and EEG spectrum of CNKSR2-related encephalopathy with status epilepticus during slow sleep (ESES)

ObjectiveTo investigate the clinical and EEG features of Encephalopathy with Status Epilepticus during slow Sleep (ESES) related to CNKSR2 pathogenic variants.MethodsDetailed clinical history, repeated wakefulness/overnight sleep EEGs, brain MRI were collected in five patients, including one female, with CNKSR2-related ESES.ResultsNeurodevelopment in infancy was normal in two patients, delayed in three. Epilepsy onset (age range: 2–6 years) was associated with appearance or aggravation of cognitive impairment, language regression and/or behavioral disorders. Worsening of epilepsy and of cognitive/behavioral disturbances paralleled by enhancement of non-rapid eye movement (NREM) sleep-related, frontally predominant, EEG epileptic discharges [spike-wave-index (SWI): range 60–96%] was consistent with ESES. In three patients, episodes of absence status epilepticus or aggravation of atypical absences occurred, in this latter case associated with striking increment of awake SWI. Speech/oro-motor dyspraxia was diagnosed in four patients. In two patients, long-term follow-up showed epilepsy remission and persistence of mild/moderate cognitive disorders and behavioral disturbances into adulthood.ConclusionsNovel findings of our study are occurrence also in females, normal neurodevelopment before epilepsy onset, epilepsy aggravation associated with enhanced awake SWI, mild/moderate evolution in adulthood and language disorder due to speech/oro-motor dyspraxia.SignificanceOur findings expand the phenotypic spectrum of CNKSR2-related ESES.     

When should a sleep‐deprived EEG be performed following a presumed first seizure in adults?

Gandelman‐Marton R, Theitler J. When should a sleep‐deprived EEG be performed following a presumed first seizure in adults?
Acta Neurol Scand: 2011: 124: 202–205.
© 2010 John Wiley & Sons A/S. Objectives – To evaluate the effect of the interval between the seizure and the EEG recording on the yield of early sleep‐deprived EEG (SD‐EEG) in patients admitted following a presumed first seizure. Materials and methods – We retrospectively reviewed the EEG recordings and medical records of patients admitted to the Neurology Department in Assaf Harofeh Medical Center because of a presumed first seizure during a 3‐year period between 2006 and 2009 and who had a SD‐EEG following a first routine EEG without epileptiform discharges (EDs). Results – The study group included 78 patients aged 18–78 years (mean 35 ± 17). Previous seizures were recognized through repeated history in 32 (41%) patients. EDs were recorded in the SD‐EEG in 16 (21%) patients: 13/46 (28%) with a SD‐EEG performed within 3 days following the seizure and 3/32 (9%) with a later SD‐EEG (P = 0.042) and in 10/32 (31%) patients in whom previous seizures were recognized and 6/46 (13%) with a first seizure (P = 0.05). Conclusions – EDs in the SD‐EEG following a first diagnosed seizure occur more commonly when the test is performed within 3 days following a first seizure or when previous seizures are recognized.