Nonconvulsive status epilepticus and coma

Nonconvulsive status epilepticus (NCSE) in a comatose patient cannot be diagnosed without electroencephalography (EEG). In many advanced coma stages, the EEG exhibits continuous or periodic EEG abnormalities, but their causal role in coma remains unclear in many cases. To date there is no consensus on whether to treat NCSE in a comatose patient in order to improve the outcome or to retract from treatment, as these EEG patterns might reflect the end stages of a dying brain. On the basis of EEG, NCSE in comatose patients may be classified as generalized or lateralized. This review aims to summarize the ongoing debate of NCSE and coma and to critically reassess the available literature on coma with epileptiform EEG pattern and its prognostic and therapeutic implications. The authors suggest distinguishing NCSE proper and comatose NCSE, which includes coma with continuous lateralized discharges or generalized epileptiform discharges (coma‐LED, coma‐GED). Although NCSE proper is accompanied by clinical symptoms suggestive of status epilepticus and mild impairment of consciousness, such as in absence status or complex focal status epilepticus, coma‐LED and coma‐GED represent deep coma of various etiology without any clinical motor signs of status epilepticus but with characteristic epileptiform EEG pattern. Hence coma‐LED and coma‐GED can be diagnosed with EEG only. Subtle or stuporous status epilepticus and epilepsia partialis continua–like symptoms in severe acute central nervous system (CNS) disorders represent the borderland in this biologic continuum between NCSE proper and comatose NCSE (coma‐LED/GED). This pragmatic differentiation could act as a starting point to solve terminologic and factual confusion.     

Persistent Nonconvulsive Status Epilepticus After the Control of Convulsive Status Epilepticus

Summary: Purpose: Convulsive status epilepticus (CSE) is a major medical and neurological emergency that is associated with significant morbidity and mortality. Despite this high morbidity and mortality, most acute care facilities in the United States cannot evaluate patients with EEG monitoring during or immediately after SE. The present study was initiated to determine whether control of CSE by standard treatment protocols was sufficient to terminate electrographic seizures. Methods: One hundred sixty-four prospective patients were evaluated at the Medical College of Virginia/VCU Status Epilepticus Program. Continuous EEG monitoring was performed for a minimum of 24 h after clinical control of CSE. SE and seizure types were defined as described previously. A standardized data form entry system was compiled for each patient and used to evaluate the data collected. Results: After CSE was controlled, continuous EEG monitoring demonstrated that 52% of the patients had no after-SE ictal discharges (ASIDS) and manifested EEG patterns of generalized slowing, attenuation, periodic lateralizing epileptiform discharges (PLEDS), focal slowing, and/or burst suppression. The remaining 48% demonstrated persistent electrographic seizures. More than 14% of the patients manifested nonconvulsive SE (NCSE) predominantly of the complex partial NCSE seizure (CPS) type (2). These patients were comatose and showed no overt clinical signs of convulsive activity. Clinical detection of NCSE in these patients would not have been possible with routine neurological evaluations without use of EEG monitoring. The clinical presentation, mortality, morbidity, and demographic information on this population are reported. Conclusions: Our results demonstrate that EEG monitoring after treatment of CSE is essential to recognition of persistent electrographic seizures and NCSE unresponsive to routine therapeutic management of CSE. These findings also suggest that EEG monitoring immediately after control of CSE is an important diagnostic test to guide treatment plans and to evaluate prognosis in the management of SE.     

Nonconvulsive status epilepticus following cardiac arrest—are we missing the beginning?

Background

Status epilepticus (SE) is a common complication in patients surviving a cardiac arrest, but little is known about the frequency of nonconvulsive status epilepticus (NCSE).

Objectives

To compile the first the evidence from the literature of the overall frequency of NCSE in adults with persistent coma following cardiac arrest. Secondarily, to assess the emergence of NCSE in comatose resuscitated patients within the first hours of the return of spontaneous circulation (ROSC) and before inducing target temperature management.

Material and methods

The medical search engine PubMed was screened to identify prospective and retrospective studies in English reporting on the frequency of NCSE in comatose post-resuscitated patients. Study design, time of EEG performance, detection of SE and NCSE, outcomes, and targeted temperature management were assessed.

Results

Only three cohort studies (one prospective and two retrospective) reported on the EEG evaluation describing NCSE during ongoing sedation and target temperature management. Overall, we identified 213 patients with SE in 18–38% and NCSE in 5–12%. Our review found no study reporting NCSE in resuscitated adult patients remaining in coma within the first hours of ROSC and prior to targeted temperature management and sedation.

Conclusion

Studies of NCSE after ROSC in adults are rare and mostly nonsystematic. This and the low proportion of patients reported having NCSE following ROSC suggest that NCSE before target temperature management and sedation is often overlooked. The limited quality of the data does not allow firm conclusions to be drawn regarding the effects of NCSE on outcome calling for further investigations. Clinicians should suspect NCSE in patients with persistent coma before starting sedation and targeted temperature management.

     

No, some types of nonconvulsive status epilepticus cause little permanent neurologic sequelae (or: « The cure may be worse than the disease »)

Nonconvulsive status epilepticus (NCSE) is characterized by a cognitive or behavioral change which lasts for at least 30 minutes, with EEG evidence of seizures. Although there is little argument that generalized nonconvulsive status epilepticus (GNSE) does not cause lasting deficits, there is still debate regarding the morbidity of complex partial status epilepticus (CPSE). Because the EEG is used for diagnosis, a strong argument can be made that NCSE is significantly under-recognized and diagnosed. Furthermore, since the documented cases of permanent neurologic sequelae are few, the potential permanent morbidity from CPSE may be significantly exaggerated. The literature indicates that comatose patients have a poor prognosis largely as a result of comorbid conditions and coma, whereas lightly obtunded or slightly confused patients with NCSE have little or no sequelae. Patients with NCSE may suffer (hypotension and respiratory suppression) from iatrogenic 'aggressive' treatment with intravenous anti-epileptic drugs (IV-AEDs), and the findings in the literature indicate that subjects treated with benzodiazepines may have a worse prognosis. The clinician must balance the potential but rare neurologic morbidity associated with NCSE against the not infrequent morbidity caused by IV-AEDs. Better stratification of the level of consciousness and comorbid conditions is needed when evaluating outcomes so as to clearly distinguish among the deficits due to: comorbid conditions; the effects of treatment and the effects of status epilepticus (SE) proper.     

Non-convulsive status epilepticus; the rate of occurrence in a general hospital

BackgroundNon-convulsive status epilepticus (NCSE) has been increasingly recognized as a cause of impaired level of consciousness in the ICU and emergency rooms. The diagnosis can be easily missed without an electroencephalogram (EEG) given the paucity of overt clinical signs in this condition. Recently few published data estimated the prevalence to be between 3% and 8%.ObjectiveTo assess the rate of occurrence of NCSE among patients with various degrees of impaired consciousness referred to the Neurophysiology Laboratory at Vancouver General Hospital.MethodWe conducted a retrospective analysis of 451 adult patients (>16 years of age) with a question of NCSE or with an unknown cause of impaired level of consciousness between the years 2002 and 2004. NCSE was defined according to the Young's criteria of electrographic status epilepticus. NCSE was categorized into focal and generalized epileptic activity based on the continuous EEG monitoring (CEEG). Further analysis of age, gender and etiology was performed.ResultsOf 451 patients, EEG demonstrated electrographic status epilepticus with no overt clinical signs in 42 patients (9.3%). Median age was 61.8 years (range 21–94). According to etiology, 38.1% of patients with NCSE had hypoxic–anoxic injury, 19% had intracerebral hemorrhage (including trauma), 11.9% had the diagnosis of idiopathic or cryptogenic epilepsy, 7.1% had ischemic stroke, 4.8% were secondary to tumors and 4.8% to viral encephalitis.ConclusionThe rate of occurrence of NCSE in patients with decreased level of consciousness was 9.3%. The cohort represented a group of patients who were comatose and required assisted ventilation or had altered level of consciousness. Hypoxic brain injury was the most responsible etiology of NCSE in the cohort studied.     

Nonconvulsive status epilepticus

Nonconvulsive status epilepticus (NCSE) is a heterogeneous disorder with multiple subtypes. Although attempts have been made to define and classify this disorder, there is yet no universally accepted definition or classification that encompasses all subtypes or electroclinical scenarios. Developing such a classification scheme is becoming increasingly important, because NCSE is more common than previously thought, with a bimodal peak, in children and the elderly. Recent studies have also shown a high incidence of NCSE in the critically ill. Although strong epidemiological data are lacking, NCSE constitutes about 25-50% of all cases of status epilepticus. For the purposes of this review, we propose an etiological classification for NCSE including NCSE in metabolic disorders, NCSE in coma, NCSE in acute cerebral lesions, and NCSE in those with preexisting epilepsy with or without epileptic encephalopathy. NCSE is still underrecognized, yet potentially fatal if untreated. Diagnosis can be established using an electroencephalogram (EEG) in most cases, sometimes requiring continuous monitoring. However, in comatose patients, diagnosis can be difficult, and the EEG can show a variety of rhythmic or periodic patterns, some of which are of unclear significance. Although some subtypes of NCSE are easily treatable, such as absence status epilepticus, others do not respond well to treatment, and debate exists over how aggressively clinicians should treat NCSE. In particular, the appropriate treatment of NCSE in patients who are critically ill and/or comatose is not well established, and large-scale trials are needed. Overall, further work is needed to better define NCSE, to determine which EEG patterns represent NCSE, and to establish treatment paradigms for different subtypes of NCSE.     

EEG im Status epilepticus und bei Enzephalopathie

Status elepiticus is a medical emergency and requires immediate treatment. Clinically pragmatic reasons argue for a division into convulsive status (CSE) and nonconvulsive status (NCSE). The EEG is essential for diagnosis of NCSE. If distinct clinical symptoms are lacking, the EEG can assist in the diagnosis of status epilepticus. A special challenge is the presentation of comatose patients. The spectrum of the EEG in encephalopathies is very broad and can be divided into slow and rhythmic EEG coma patterns. Typical patterns depending on the severity of the encephalopathy are presented.     

Which EEG patterns in coma are nonconvulsive status epilepticus?

Nonconvulsive status epilepticus (NCSE) is common in patients with coma with a prevalence between 5% and 48%. Patients in deep coma may exhibit epileptiform EEG patterns, such as generalized periodic spikes, and there is an ongoing debate about the relationship of these patterns and NCSE. The purposes of this review are (i) to discuss the various EEG patterns found in coma, its fluctuations, and transitions and (ii) to propose modified criteria for NCSE in coma.Classical coma patterns such as diffuse polymorphic delta activity, spindle coma, alpha/theta coma, low output voltage, or burst suppression do not reflect NCSE. Any ictal patterns with a typical spatiotemporal evolution or epileptiform discharges faster than 2.5 Hz in a comatose patient reflect nonconvulsive seizures or NCSE and should be treated. Generalized periodic diacharges or lateralized periodic discharges (GPDs/LPDs) with a frequency of less than 2.5 Hz or rhythmic discharges (RDs) faster than 0.5 Hz are the borderland of NCSE in coma. In these cases, at least one of the additional criteria is needed to diagnose NCSE (a) subtle clinical ictal phenomena, (b) typical spatiotemporal evolution, or (c) response to antiepileptic drug treatment. There is currently no consensus about how long these patterns must be present to qualify for NCSE, and the distinction from nonconvulsive seizures in patients with critical illness or in comatose patients seems arbitrary.The Salzburg Consensus Criteria for NCSE [1] have been modified according to the Standardized Terminology of the American Clinical Neurophysiology Society [2] and validated in three different cohorts, with a sensitivity of 97.2%, a specificity of 95.9%, and a diagnostic accuracy of 96.3% in patients with clinical signs of NCSE. Their diagnostic utility in different cohorts with patients in deep coma has to be studied in the future.This article is part of a Special Issue entitled “Status Epilepticus”.     

Standards of care for non-convulsive status epilepticus: Belgian consensus recommendations

Non-convulsive status epilepticus (NCSE) makes up around one-third of all cases of SE, affecting approximately 1,000 to 4,000 individuals per year in Belgium. Compared with convulsive SE, NCSE has received considerably less attention, is underdiagnosed and undertreated. However, if recognised, NCSE can however be treated successfully. A workshop was convened by neurologists from major Belgian centres to review the latest information on NCSE and to make recommendations on diagnosis and treatment. These recommendations are not only intended for neurologists, but also for primary care physicians and physicians in intensive care units. NCSE should be suspected whenever cases of fluctuating consciousness or abrupt cognitive or behavioural changes are noted. Confirmation of diagnosis by EEG should be obtained wherever possible. In view of the often subtle clinical signs, EEG is also vital for monitoring treatment outcome. Non-comatose patients should generally be treated in a neurology ward since referral to an ICU is unnecessary. First-line treatment should be an intravenous benzodiazepine. For many patients who fail to respond to benzodiazepines, intravenous valproate will successfully abrogate seizure activity. Intravenous phenytoin can be used in patients with focal NCSE in whom valproate is contraindicated or ineffective. Time and care should be spent in identifying an appropriate and effective antiepileptic drug regimen without recourse to anaesthesia. For comatose patients, treatment intensity should be graded according to epilepsy history, general medical state and prognosis. In some patients, intensive remedial measures may allow rapid resolution of NSCE, whereas in more vulnerable patients, such treatment may be counterproductive.     

脑炎后癫痫持续状态进展为难治性癫痫持续状态及超级难治性癫痫持续状态的早期预测因素

目的 探讨脑炎后癫痫持续状态(SE)进展为难治性SE(RSE)及超级RSE(SRSE)的早期预测因素.方法 根据疾病进展情况将89例脑炎后SE患者分为非RSE组、RSE组及SRSE组.比较各组临床资料.结果 非RSE组、RSE组及SRSE组年龄、SE严重程度评分量表(STESS)评分、基于流行病学SE病死率评分(EMS...     

Generalized Convulsive Status Epilepticus in the Adult

Summary: Status epilepticus (SE) is denned as recurrent epileptic seizures without full recovery of consciousness before the next seizure begins, or more-or-less continuous clinical and/or electrical seizure activity lasting for more than 30 min whether or not consciousness is impaired. Three presentations of SE are now recognized: recurrent generalized tonic and/or clonic seizures without full recovery of consciousness between attacks, nonconvulsive status where the patient appears to be in a prolonged "epileptic twilight state," and continuous/repetitive focal seizure activity without alteration of consciousness. Generalized convulsive status epilepticus (GCSE) encompasses a broad spectrum of clinical presentations from repeated overt generalized tonic-clonic seizures to subtle convulsive movements in a profoundly comatose patient. Thus, GCSE is a dynamic state that is characterized by paroxysmal or continuous tonic and/or clonic motor activity, which may be symmetrical or asymmetrical and overt or subtle but which is associated with a marked impairment of consciousness and with bilateral (although frequently asymmetrical) ictal discharges on the EEG. Just as there is a progression from overt to increasingly subtle clinical manifestations of GCSE, there is also a predictable sequence of progressive EEG changes during untreated GCSE. A sequence of five patterns of ictal discharges has been observed: discrete electrographic seizures, waxing and waning, continuous, continuous with flat periods, and periodic epileptiform discharges on a relatively flat background. A patient actively having seizures or comatose who exhibits any of these patterns on EEG should be considered to be in GCSE and should be treated aggressively to stop all clinical and electrical seizure activity to prevent further neurological morbidity and mortality.     

Falsely pessimistic prognosis by EEG in post-anoxic coma after cardiac arrest: the borderland of nonconvulsive status epilepticus

Background. Prognostication following anoxic coma relies on clinical assessment and is assisted by neurophysiology. A non-evolving EEG spike burst/isoelectric suppression pattern after the first 24 hours almost invariably indicates poor outcome, while an evolving pattern implies nonconvulsive status epilepticus (NCSE) that may "hide" surviving brain activity and is amenable to treatment. Case study. We present the case of a 53-year-old woman who had a witnessed out-of-hospital ventricular fibrillation cardiac arrest, was resuscitated by paramedics, but remained comatose. An EEG, performed 36 hours post-insult, showed an unremitting, non-evolving, unresponsive 2-6?Hz high-voltage spike burst/isoelectric suppression pattern, which remained unchanged at 96 hours post-insult, following therapeutic hypothermia. During this period, she was completely off sedation and taking triple antiepileptic treatment, without systemic confounding disorders. Although the initial pattern was indicative of poor neurological outcome, she eventually made meaningful functional recovery; the last EEG showed satisfactory background rhythms and stimulus-induced epileptiform discharges without seizures. Conclusion. In post-anoxic coma, non-evolving >2?Hz spike burst/isoelectric suppression pattern may still reflect NCSE and therefore should be considered in the diagnostic EEG criteria for NCSE. Such borderline patterns should not dissuade physicians from intensifying treatment until more confident prognostication can be made.     

An observational electro-clinical study of status epilepticus: from management to outcome

Status epilepticus (SE) is a neurological emergency associated with a high morbidity and mortality. A prospective 3-year study was conducted in our hospital on 56 consecutive inpatients with SE. Demographic and clinical data were collected. EEG and clinical SE features were considered for the SE classification, both separately and together. The etiology of SE was determined. Patients were treated according to international standardized protocols of guidelines for the management of epilepsy. Response to treatment was evaluated clinically and electrophysiologically. Outcome at 30 days was considered as good, poor or death. Convulsive SE (CSE) was observed in 35 patients and non-convulsive SE (NCSE) in 21. Patients with CSE, in particular focal-CSE, were older than those with NCSE. As regards etiology, patients with SE secondary to cerebral lesions were the oldest, followed by patients with anoxic SE and those with toxic dysmetabolic SE. A first-line treatment was usually sufficient to control seizure activity in lesional and epileptic SE, while more aggressive treatment was necessary in all anoxic SE patients. Outcome was good in 35 patients, poor in 12, while 9 died. A prompt neurophysiological EEG evaluation, combined with the clinical evaluation, helps to make a rapid prognosis and take therapeutic management decisions. First-line treatments may be sufficient to control electro-clinical status in lesional and epileptic SE, while intensive care unit management, a more aggressive therapeutic approach and continuous EEG monitoring are recommended for refractory SE.     

Frequency and Timing of Nonconvulsive Status Epilepticus in Comatose Post-Cardiac Arrest Subjects Treated with Hypothermia

Background  

Therapeutic hypothermia (TH) improves outcomes in comatose patients resuscitated from cardiac arrest. However, nonconvulsive status epilepticus (NCSE) may cause persistent coma. The frequency and timing of NCSE after cardiac arrest is unknown.     

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。     

Aborted and refractory status epilepticus in children: a comparative analysis

PURPOSE: The aims of this retrospective study were: (1) to compare the demographics, clinical characteristics, etiology, and EEG findings of status epilepticus aborted with medication (ASE) and refractory status epilepticus (RSE), (2) to describe the treatment response of status epilepticus (SE), and (3) to determine predictors of long-term outcome in children with SE. METHODS: Medical records and EEG lab logs with ICD-9 diagnostic codes related to SE were reviewed. Patients younger than 18 years of age, hospitalized in 1994-2004 at the Mayo Clinic, Rochester, were included. RESULTS: One hundred fifty-four children had SE; 94 (61%) had ASE, and 60 (39.0%) had RSE. Family history of seizures, higher seizure frequency score, higher number of maintenance antiepileptic drugs (AEDs), nonconvulsive SE, and focal or electrographic seizures on initial EEG were associated with RSE by univariate analysis. In-hospital mortality was significantly higher in RSE (13.3%) than in ASE (2.1%). In the long term, survivors with RSE developed more new neurological deficits (p < 0.001) and more epilepsy (p < 0.004) than children with ASE. Children treated in a more aggressive fashion appeared to have better treatment responses (p < 0.001) and outcomes (p = 0.03). Predictors of poor outcome were long seizure duration (p < 0.001), acute symptomatic etiology (p = 0.04), nonconvulsive SE (NCSE) (p = 0.01), and age at admission <5 years (p = 0.05). DISCUSSION: Several patient and clinical characteristics are associated with development of RSE and poor outcome. Prospective, randomized trials that assess different treatment protocols in children with SE are needed to determine the optimal sequence and timing of medications.     

Non-convulsive status epilepticus: usefulness of clinical features in selecting patients for urgent EEG

BACKGROUND: Non-convulsive status epilepticus (NCSE) is status epilepticus without obvious tonic-clonic activity. Patients with NCSE have altered mental state. An EEG is needed to confirm the diagnosis, but obtaining an EEG on every patient with altered mental state is not practical. OBJECTIVE: To determine whether clinical features could be used to predict which patients were more likely to be in NCSE and thus in need of an urgent EEG. METHODS: Over a six month period, all patients for whom an urgent EEG was ordered to identify NCSE were enrolled. Neurology residents examined the patients and filled out a questionnaire without knowledge of the EEG results. The patients were divided into two groups, NCSE and non-NCSE, depending on the EEG result. The clinical features were compared between the two groups. The sensitivity and specificity of the features were calculated. RESULTS: 48 patients were enrolled, 12 in NCSE and 36 not in NCSE. Remote risk factors for seizures, severely impaired mental state, and ocular movement abnormalities were seen significantly more often in the NCSE group. The combined sensitivity of remote risk factors for seizures and ocular movement abnormalities was 100%. CONCLUSIONS: There are certain clinical features that are more likely to be present in patients in NCSE compared with other types of encephalopathy. Either remote risk factors for seizures or ocular movement abnormalities were seen in all patients in NCSE. These features may be used to select which patients should have an urgent EEG.     

Clinical and EEG features of status epilepticus in comatose patients.

We retrospectively evaluated the clinical and EEG features of status epilepticus (SE) in 47 comatose adult patients in whom SE was suspected clinically or because the EEG revealed repetitive electrographic seizures or continuous spike-and-wave activity. Three groups of patients were identified. Group-1 patients (n = 33) had SE both clinically and on EEG. They usually had subtle, clonic movements restricted to the eyes, face, and upper extremities, and the EEG most commonly showed repetitive electrographic seizures or continuous spike-and-wave activity. Group-2 patients (n = 9) also had subtle motor manifestations of seizures, but the EEG was not that of SE, consisting of either irregular slowing with frequent spikes and sharp waves, an irregular mixed-frequency background with episodic accentuation, or diffuse slowing; one patient also had an intermittent burst-suppression pattern. The five patients in Group 3 lacked any clinical signs of seizures, but the EEG showed repetitive electrographic seizures or continuous spike-and-wave activity. There were no significant differences between groups in etiology of SE, response to therapy, or outcome, and there was no obvious relationship between the EEG findings and duration of SE. We conclude that recognition of SE in comatose patients may require both clinical and EEG evaluation since either approach by itself may fail to establish the diagnosis. Furthermore, the EEG findings in established SE do not necessarily progress through the series of defined stages suggested by some authors.     

Nonconvulsive status epilepticus of frontal origin

OBJECTIVES: To determine the electroclinical characteristics and causative factors of nonconvulsive status epilepticus (NCSE) of frontal origin. METHODS: The authors conducted a 5-year prospective study. RESULTS: Ten patients were studied (seven men, three women; mean age, 56.4 years). Six patients did not have previous epilepsy. The mean diagnostic delay was 48 hours (range, 3 to 96 hours). Two types of frontal NCSE were identified. In type 1 (n = 7), mood disturbances with affective disinhibition or affective indifference were associated with subtle impairment of cognitive functions without overt confusion. EEG showed a unilateral frontal ictal pattern and normal background activity. In type 2 (n = 3), impaired consciousness was associated with bilateral, asymmetric frontal EEG discharges occurring on an abnormal background. Ictal and postictal 99mTc hexamethyl propylene amine oxime (HMPAO) SPECT was performed in five patients and showed unilateral or bilateral frontal HMPAO uptake that aided localization, especially in type 2 NCSE of frontal origin. Etiologies included a focal frontal lesion in six patients (three of which were tumors), neurosyphilis, and nonketotic hyperglycemia. Eight patients did not respond to initial IV benzodiazepine (BZ), but IV phenytoin controlled six patients successfully. The immediate outcome was favorable in all patients. There was no long-term recurrence of SE in seven patients. CONCLUSIONS: NCSE of frontal origin is a heterogeneous syndrome. Some cases are best described as simple partial NCSE, others as complex partial SE, and there are forms that overlap with absence SE. Emergency EEG and neuropsychological assessment are diagnostic, and SPECT may be useful. Many patients may not respond to IV BZ.