You are on page 1of 8

Clinical Neurophysiology 123 (2012) 244–251

Contents lists available at ScienceDirect

Clinical Neurophysiology
journal homepage: www.elsevier.com/locate/clinph

Nonconvulsive status epilepticus in adults: Electroclinical differences
between proper and comatose forms q
José L. Fernández-Torre a,e,f,⇑, Mariano Rebollo b, Agustín Gutiérrez c, Francisco López-Espadas d,
Miguel A. Hernández-Hernández d,f
a

Department of Clinical Neurophysiology, Marqués de Valdecilla University Hospital, Santander, Cantabria, Spain
Department of Neurology, Marqués de Valdecilla University Hospital, Santander, Cantabria, Spain
Department of Radiology, Marqués de Valdecilla University Hospital, Santander, Cantabria, Spain
d
Department of Intensive Medicine, Marqués de Valdecilla University Hospital, Santander, Cantabria, Spain
e
Department of Physiology and Pharmacology, University of Cantabria (UNICAN), Santander, Cantabria, Spain
f
Instituto de Formación e Investigación Marqués de Valdecilla (IFIMAV), Santander, Spain
b
c

a r t i c l e

i n f o

Article history:
Accepted 23 June 2011
Available online 19 July 2011
Keywords:
Nonconvulsive status epilepticus
Absence status epilepticus
Complex partial status epilepticus
Coma
Electroencephalogram
Prognosis

q

h i g h l i g h t s 
This study supports the utility of differentiating between proper and comatose nonconvulsive status epilepticus (NCSE). 
De novo absence status epilepticus (ASE) induced by nonpsychotropic drugs occurs in a well-defined
clinical scenario. 
Comatose NCSE occurs mainly in individuals with acute symptomatic cerebral pathology.

a b s t r a c t
Objective: Nonconvulsive status epilepticus (NCSE) represents an important percentage of status epilepticus in adults, but detailed studies of both NCSE proper and comatose NCSE are lacking. We retrospectively analyzed a prospectively collected series of 50 adult patients with a diagnosis of NCSE whose
electroencephalograms (EEGs) have been interpreted for a period of 10 years by the same investigator.
Methods: Two groups, NCSE proper and comatose NCSE were considered. All clinical, EEGs, neuroimaging
data, antiepileptic treatment and outcome were analyzed.
Results: Thirty-two patients (64%) had NCSE proper and 18 patients (36%) comatose NCSE. The mean age
was 56 years (range 19–89 years). Fourteen (44%) were diagnosed with absence status epilepticus (ASE),
one had simple partial status epilepticus (SPSE) and 17 (53%) had complex partial status epilepticus
(CPSE). The mean episode duration (33.2 ± 13.9 versus 60.6 ± 34.0), mean number of antiepileptic drugs
(AEDs) (1.46 ± 0.5 versus 2.77 ± 1.39) and neuroimaging anomalies (50% versus 16%) was significantly
greater in the partial/focal NCSE proper subgroup than in the ASE subgroup. The mean age (56.0 ± 19.9
versus 69.4 ± 12.1), number of elderly individuals (46% versus 77%), mean duration of the episode
(49.1 ± 30.4 versus 153.3 ± 142.6), mortality rate (6% versus 61%) and admission at ICU (18% versus
83%) was significantly higher in the comatose NCSE group than in the NCSE proper group (p < .05).
Conversely, a previous history of chronic epilepsy was significantly more frequent (62% versus 5.6%) in
the NCSE proper group. The mean duration of comatose NCSE was significantly greater in the surviving
subgroup (102.5 ± 29.1 versus 233.1 ± 65.3; p < .05).
Conclusions: Our study demonstrates that there are sufficient differences regarding age of onset, history
of previous epilepsy, episode duration, mortality rate and clinical presentation between NCSE proper and
comatose NCSE to recommend adoption in clinical practice. These results should be taken into account
when developing future classifications and therapeutic trials on NCSE.
Significance: A distinction between NCSE proper (ambulatory forms of NCSE) and comatose NCSE is useful
in the clinical practice and, therefore, it should taken in account in the design of future investigations on
this heterogeneous epileptic condition.
Ó 2011 International Federation of Clinical Neurophysiology. Published by Elsevier Ireland Ltd. All rights
reserved.

This investigation was partially presented as poster at the Innsbruck Colloquium on Status Epilepticus, April 2009.

⇑ Corresponding author at: Department of Clinical Neurophysiology, Marqués de Valdecilla University Hospital, Avda. Valdecilla, s/n, 39008 Santander, Cantabria, Spain.
Tel.: +34 942 202520x72674; fax: +34 942 315095.
E-mail addresses: jlfernandez@humv.es, ftorrenfc@hotmail.com (J.L. Fernández-Torre).
1388-2457/$36.00 Ó 2011 International Federation of Clinical Neurophysiology. Published by Elsevier Ireland Ltd. All rights reserved.
doi:10.1016/j.clinph.2011.06.020

2.L. In addition.. three subjects in this group (Cases 33.. 2000). 2000). and those with de novo ASE induced by nonpsychotropic drugs. a secondary hospital providing adult neurophysiologic service to 350. none has been analyzed regarding the criteria and standpoint of this study. Bauer and Trinka. lasting more than 30 min.-T.) during the period 1999–2002 at Cabueñes Hospital (Gijón. 1990.. we prospectively identified all those patients with a definitive diagnosis of proper and comatose NCSE. The majority of these patients were diagnosed in the ICU. (ii) atypical ASE (or spike-wave stupor). 2001.1...L. 2000. 2. 2006a.). (ii) Comatose NCSE (Bauer and Trinka.b. 1994). 2010). 28. Thomas and Andermann. It is the only neurophysiology department in the area. FernándezTorre and Leno. Krumholz et al. Baseline demographic data (age. 34 and 44) remained on the hospital ward. Comatose NCSE group Among comatose patients. vegetative disturbances or reduced level of consciousness (Drislane. 2. 2010). the subjects were divided into: (i) NCSE proper and. 2004. and immediate transfer to the intensive care unit (ICU) was unnecessary. (ii) continuous CPSE (type II) showing continuous seizure activity. (ii) focal. 2. in which continuous or recurrent electrographic seizure activity was responsible for diverse clinical symptoms including altered mental state. Kaplan.. 2004). Drislane. (iii) situation-related ASE and. 1994. there has been a push to consider this patient group as a different type of NCSE (Kaplan. Drislane. those with de novo ASE of late onset (Thomas et al. 2010).2. Williamson. 2004. All EEGs in comatose NCSE patients were assessed and found to fit into three patterns: (i) generalized. All were ambulatory and came to the emergency department with relatives. 2008. 2003. however. those criteria for the diagnosis of NCSE proposed by Young and colleagues (1996). Fernández-Torre and Martínez-Martínez.. EEG reports and protocols. Particular interest was focused on accurately determining the level of consciousness and patient’s mental status. However. sensory and verbal stimulation in awake and comatose subjects. the full description of all patients may be found in Spanish as a Doctoral Thesis elsewhere (Fernández-Torre. 3.3. lobe) were analyzed. Brenner. Between 1999 and 2008.. 2001). behavioral and perception abnormalities. Comatose NCSE included all subjects with severe and profound impairment of consciousness (coma state). 1994). Definition and diagnostic criteria NCSE was defined as a pleomorphic and heterogenous epileptic condition.J. Introduction Nonconvulsive status epilepticus (NCSE) represents one of the great challenges in neurology (Meierkord and Holtkamp. focal or localization-related NCSE. 1996. six patients (Cases 2.F. 2002. 2007. 1992. Resolution of the clinical and EEG anomalies after treatment with antiepileptic drugs (AEDs) was considered necessary to determine definite NCSE (Kaplan. past medical history. 2009. Data collection This investigation is a retrospective analysis of a prospectively collected series. Celesia et al. 1988. 2007). 1995) of the term ‘‘subtle generalized convulsive status epilepticus’’ (SGCSE). and partial. which was also divided into simple partial (SPSE) and complex partial status epilepticus (CPSE) (Treiman. Kaplan. Bauer and Trinka. 2002. distribution (generalized or focal) and localization (hemisphere. and the response to the acute administration of intravenous benzodiazepines (IVBZDs) when used for diagnosis. located in the north of Spain. Continuous EEG or video-EEG was obtained for at least 30 min including photic. (1984) and Treiman (1993.. emergency) were recorded. Kaplan. and the description of different states of continuous electrographic activity associated with minimal or absent motor manifestations in severely ill and comatose patients (Simon and Aminoff. Privitera et al. 2007a. Fernández-Torre et al. 2003a. All tracings were reviewed by one board- 245 certified clinical neurophysiologist (J. Since the introduction by Treiman et al. Meierkord and Holtkamp. Fernández-Torre et al. 2. we distinguished two subtypes of situation-related ASE. 2006). The purpose of our study was to describe the electroclinical differences between non-comatose and comatose forms of NCSE in adults. Treiman et al. 2007. NCSE proper group ASE was further subdivided into four categories: (i) typical ASE (or petit mal status epilepticus). NCSE proper included patients with generalized NCSE or absence status epilepticus (ASE).2. were also included. 1996. gender). 2000.b.c. and resident sign-out notes.. 1995. Differential diagnosis and confirmation of NCSE can be difficult and depends to a large degree on electroencephalography (Brenner. Young et al. and controversy regarding intensity of. Not all patients were treated with acute IVBZDs due to physiologic considerations. 2000. partial or lateralized. The clinical effect of IVBZDs was evaluated during the EEG recording for 5–10 min after its administration. 2009). 1990. 1983. toxics.. electroconvulsive therapy or metabolic disturbances. precipitated by the use or withdrawal of psychotropic drugs. 23. 1999. All these symptoms occurred without major convulsive activity. Electroencephalograms (EEGs) were performed with 21 electrodes placed according to the International 10–20 system. Fujikawa. Patients and methods 2. 2. frequency. All patients older than 16 years who between 2002 and 2008 were diagnosed as having NCSE were included in the study and followed clinically until April 2009. In addition.b. 1986. 2003.886 inhabitants in an urban and rural area of the region of Cantabria. 1997): (i) cyclic CPSE (type I) with recurrent complex partial seizures without recovery of consciousness between seizures and. 2006. All patients and recordings were examined by the same neurophysiologist .1. Maganti et al. 1988. and subsequently modified by Chong and Hirsch (2005) were used. In addition. ICU.L.3.F. 1996.3. Lowenstein and Aminoff. 2008. and approaches to treatment (Walker. Classification In practical terms. discharge summaries. Patients The Department of Clinical Neurophysiology at Marqués de Valdecilla University Hospital provides adult neurophysiologic service to 591. 1992. 2009). 32 and 44) diagnosed by the first author (J. and (iii) focal secondarily generalized (FSG). (iv) ASE with focal features (Thomas et al. because of its frequently missed diagnosis (Kaplan. Fernández-Torre et al. / Clinical Neurophysiology 123 (2012) 244–251 1. NCSE proper patients remained in this group for analysis despite being transferred to the ICU because of refractory NCSE.4. Fernández-Torre and Rebollo. Eighteen of the patients included in this series have been previously published in detail individually as case reports (Fernández-Torre.-T. and the discharge type. All clinical data were gathered from chart review. Asturias). 2005).000 habitants. 2005. Fernández-Torre and Díaz-Castroverde. and the location of the patient at the time of the EEG (hospital floor. CPSE was also subclassified into two subtypes (Ballenger et al. Drislane and Schomer.

2. alcohol Brain infarct GTCS GTCS Occipital CPSE Occipital CPSE Temporal CPSE Frontal CPSE Frontal CPSE Temporal CPSE Temporal CPSE CT: normalb MR: left hypocampal sclerosis MR: hyperintense lesions in corona radiata/right temporal lobe Temporal CPSE Fronto-temporal CPSE Parietal CPSE MR: white matter lesions CT: left basal ganglia ischemic infarct Indeterminate CPSE Parieto-temporal CPSE Parietal CPSE Frontal CPSE Parietal CPSE MR: right parietal ischemic infarct. sleep deprivation GTCS AED low levels. An advantage. Fernández-Torre et al. . diffuse cerebral atrophy MR: diffuse cerebral atrophy MR: left parietal cavernous angioma CT: left parietal ischemic infarct MR: normal MR: right parietal meningioma AED: antiepileptic drugs. When we had 50 consecutive patients. LZP. The onset of NCSE was considered as being the moment at which the first EEG confirmed the presence of ongoing seizures. Statistical analysis Data were analyzed using commercially available statistical software SPSS 10. / Clinical Neurophysiology 123 (2012) 244–251 Table 1 Demographic. CJD: Creutzfeldt–Jakob disease. ND: no done. LZP: lorazepam. PME: Progressive Myoclonus Epilepsy. disphasia Stupor Yes No Cefepime Alcohol – AED low levels. sleep deprivation. metamorphosia Confusion Yes CJD 29 SPP M/50 Slowed thinking Yes 30 TBM 31 TRD 32 VMS M/74 F/20 F/81 Confusion Slowed thinking Confusion No Yes No GTCS. In all patients the termination of the episode of NCSE was confirmed with EEG. clinical characteristics. GTCS AED low levels Brain infarct 27 MVL F/23 Yes Brain infarct 28 PFM F/75 Confusion. (Chicago.0.L. In all cases subsequent follow-up EEGs were done. b There was a previous history of left frontal hemorrhage. classification and neuroimaging features of patients with NCSE proper. IL). a There was no previous diagnosis of epilepsy but there was history of seizures in infancy.L. SPSE: simple partial status epilepticus. CPSE: complex partial status epilepticus. however. Morfine PME Lafora type AED low levels.246 J.F. In comatose patients. The grade of agreement or congruence was performed using a Pearson correlation coefficient. MR: magnetic resonance. alcohol – Levofloxacin. is that the assessed period by EEG corresponds to ‘‘definite’’ NCSE. Values of p < . This protocol was approved by the local Ethics Committee. GTCS GTCS. periventricular hypodense lesions CT: right temporo-parietal atrophy CT: left parieto-occipital atrophy MR: left temporal atrophy MR: left hyperintense frontal/insular lesions 22 JMG 23 LGD 24 LMF F/53 F/47 M/66 Confusion/mutism Slowed thinking Confusion Yes Yes No 25 MCA 26 MHM M/67 F/89 Confusion.-T. Chi-square and Fisher’s Exact tests were used for categorical data. we retrospectively analyzed all our data. infection PB intoxication GTCS Alcohol withdrawal. NCSE duration may have been underestimated because in some cases several hours may precede EEG evaluation. the Mann–Whitney U test was performed. GTCS: generalized tonic–clonic seizures.05 for these tests were considered statistically significant. For comparison of means between non-normally distributed variables.) who determined the patient neurologic status at the time of diagnosis. the number of hours taken to control NCSE was defined as the lapsed time from diagnosis of ictal epileptiform discharges (EDs) on the patient’s EEG until a followup EEG showed seizure resolution with or without changes in the level of consciousness.5. (J. GTCS GTCS None Alcohol withdrawal. Duration of NCSE could not be determined precisely because none of our patients had continuous EEG monitoring throughout the illness. Patients Sex/ age Clinical presentation Epilepsy history Precipitating factors NCSE type Neuroimaging 1 AAB 2 BDG 3 EAR M/43 F/79 F/74 No No Yes Cefepime LZP withdrawal – De novo De novo Typical CT: parietal ischemic infarct CT: normal CT: normal 4 FPR M/76 Yes – Typical CT normal 5 JGT 6 JTM F/74 M/29 No Yes Cefepime – De novo Atypical CT: normal ND 7 JTR M/50 Yes AED low levels Typical CT: normal 8 MCR 9 PCG 10 POO 11 RRA F/39 M/57 F/27 M/33 Mutism/stupor Confusion/incontinence Somnolence/slowed thinking GTCS/slowed thinking/ stupor Mutism/myoclonias Slowed thinking/ myoclonias Slowed thinking/ desorientation Slowed thinking/stupor GTCS/confusion GTCS/mutism GTCS/confusion No No Yes Yes De novo De novo Typical Typical MR: normal MR: white matter lesions ND CT: normal 12 RSV 13 USV F/68 M/73 GTCS/slowed thinking GTCS/slowed thinking Yesa No Typical De novo MR: white matter lesions MR: white matter lesions 14 YRG 15 PGR F/19 M/44 GTCS/confusion/stupor Posturing Yes Yes Atypical Frontal SPSE MR: diffuse cortical atrophy CT: right hemispheric atrophy 16 ARL 17 CSV M/69 F/67 Slowed thinking Stupor No Yes Parietal CPSE Temporal CPSE 18 19 20 21 DPC ESV FOF JCM M/48 M/80 F/43 M/55 Stupor Stupor Slowed thinking Confusion Yes Yes Yes No CT: bilateral parietal atrophy CT: diffuse atrophy. The end-point of NCSE was determined to be when the mental state normalized and the EEG changes regressed. The number of EEGs studies ranged from one to 34 records. CT: computerized tomography.

Several years before the episode of atypical ASE a diagnosis of JME has been established. All AEDs used in these patients are given in Supplementary Table S1. (d) six (Cases 18.1. 16. Fernández-Torre et al.9 years (range 19–79 years). clinical characteristics. The mean duration of ASE was 33. 25. / Clinical Neurophysiology 123 (2012) 244–251 247 3. 3. All patient characteristics are shown in Table 1 and Supplementary Table S1. sensitivity: 100 lV/cm. In two (Cases 6 and 10) neuroimaging was not performed (Table 1). there was a previous misdiagnosis of Juvenile Myoclonic Epilepsy (JME). 27. LF: 0. a significant diminution of EDs was observed. 1997). All these patients had significant medical antecedents such as epilepsy.53 Hz. All characteristics of these patients are summarized in Table 1 and Supplementary Table S1. Absence status epilepticus (ASE) Fourteen patients were included in this category. In all subjects except for one (Case 15). There was a previous diagnosis of epilepsy in 12 patients (66%). duration of the episode. 27. 3. (A) EEG of patient 10 (POO). 29.1. The syndromic classification included: (a) six patients (Cases 3. 13 and 14). there was previous history of epilepsy. 3. Myoclonias were observed at onset or during the picture of NCSE in three (Cases 5.5%). 20 and 31) had mental retardation. 22. and 29) with symptomatic partial epilepsy (SPE). Results In all. one with Progressive Myoclonus Epilepsy (PME) of Lafora type (Case 14) and other with sporadic Creutzfeldt–Jakob disease (sCJD) (Case 28) died during the episode of NCSE. 6. one or several generalized tonic–clonic seizures (GTCSs) occurred at the onset of the episode. CNS surgery. The mean age was 56 years (range 19–89 years). There were seven men and seven women. 1a. EDs were completely abolished and in one (Case 20) the attenuation was solely transient. Seventeen patients were categorized as CPSE and only one (Case 15) was classified as SPSE. valvular cardiac surgery and Parkinson disease. The mean age was 52. All patients except for one (Case 14) with typical or atypical ASE had a previous diagnosis of epilepsy. ictal discharges (SIRPIDs). 7. generalized EDs were only abolished Fig. lupus erythematosus. The mean duration of NCSE was 49. SD. 3. 28 and 31) with probably symptomatic/ cryptogenic partial epilepsy and. In one patient (Case 14). 10 and 14) accounting for 57%. In 20 patients (62. The mean age was 58 years (range 20– 89 years). 24.9%) were elderly (age P 65 years). Note the presence of continuous polyspikewave (PSW) and spike-wave complexes (SW) in keeping with the diagnosis of typical ASE. The mean age was 59 years (range 20–89 years). 9. HF: 70 Hz. 9. All ictal EEG features. 20. 4.The localization of the onset of NCSE is summarized in Table 1. 30 and 32) a cyclic variety of CPSE was identified (Williamson. 17. Recurrence of NCSE occurred in 10 patients (31%).1.1 h (range 12– 20 h).2. 20. ASE occurred as late complication of an unrecognized picture of IGE (Fernández-Torre and Rebollo. 18. Ictal EEG features are summarized in Supplementary Table S1. There were 16 men and 16 women. 20 and 31). 25. In four patients.1. 19. In eight patients (Cases 2. 6 and 14). In all subjects with continuous CPSE. Five patients (Cases 14. 28 and 32). alcoholism. 2009). she finally developed Progressive Myoclonus Epilepsy (PME) of Lafora type. 8. Two patients.L. speed: 30 mm/s. 15. No of subjects with situationrelated ASE had history of previous seizures. 50 patients were identified with both clinical and EEG evidence of NCSE. 13. IVBZDs were administrated during the EEG. There were nine men and nine women. and in five (Cases 4. Thirty-two patients (64%) had NCSE proper and 18 patients (36%) comatose NCSE. 9. LF: 0. 23. (B) EEG of patient 14 (LRG). speed: 15 mm/s. treatment and outcome are summarized in Supplementary Table S1. 22. All demographic. 14. The data from the patient with PME of Lafora type were excluded for this statistical analysis because of the exceptional long duration in this case (86 days). 1.53 Hz.J. 19. frank EDs consisting of spikes (S) and spike-wave complexes (SW) were seen from the onset of EEG recording. In one patient (Case 12). All patients were mentally normal except for two (Cases 6 and 14). Neuroimaging was normal in seven patients and revealed diverse abnormalities in other five (Cases 1. In 11 individuals (Cases 16. classification and neuroimaging features are summarized in Table 1.5%). There were nine women and eight men in this group. periodic. There was recurrence in five patients (Cases 3. An example of characteristic EEG is shown in Fig. Partial. NF: 50 Hz. HF: 70 Hz. In 12 patients (37. 11. . In four patients (Cases 17. Fifteen patients (46. NF: 50 Hz. during profound sedation with propofol (PPF) and thiopental (THP). In all of them. 20. 12. However. 21. IVBZDs were administrated during the EEG recording.1. focal or localization-related NCSE There were 18 patients in this group. and in only one (Case 32) was clinical improvement seen. 10 and 14) there was clinical improvement (Supplementary Table S1). 4.9). In three of them (Cases 17. 10. 22 and 29) were transferred to the ICU by refractory NCSE. 5. 3.1. (b) one (Case 6) with symptomatic generalized epilepsy (SGE). 7. Ictal EEG features are summarized in Supplementary Table S1. All patients were mentally normal except for three subjects (Cases 15.2. 8 and 11). 8. dementia and cerebrovascular disease. sensitivity: 150 lV/cm.2 h (range 24–72 h. IVBZDs were administrated during the EEG recording. In the patient with PME of Lafora disease. In 17 (53%). and 14) with diagnosis of idiopathic generalized epilepsy (IGE). NCSE proper Thirty-two patients were included in this group. the clinical presentation was an alteration in mental status. Complex partial status epilepticus (CPSE). 28 and 32) IVBZDs were administrated during the EEG. Observe as a tactile stimulus (black arrow) elicited a burst of epileptiform discharges (EDs) in keeping with the definition of stimulus-induced rhythmic. (c) six (Cases 15. Five of these patients (Cases 6.

abolition was only transient.9 versus 69. 45 and 49). 20.5 versus 2. In two patients follow-up data were unavailable. mean number of AEDs (1.05) (Supplementary Table S5). epilepsy OH None ACVD ACVD. OH Hepatopathy. SD. 44 and 46) (Table 2). All of them were neurologically and intellectually normal. GTCS Anoxia CNS infection ACVD. and in two (Cases 40 and 47) motor partial seizures occurred. a Necropsy finding.7).3 ± 142. Discussion This investigation offers the unusual possibility of comparing 50 patients with ambulatory and comatose forms of NCSE in a homogeneous diagnostic. CVD: cerebrovascular disease. therapeutic and follow-up setting. The association between etiology and type of comatose NCSE. cardiopathy Hypertension.05) (Supplementary Table S4).1). hepatopathy Lung transplant Hypertension. 49 and 50). There was a statistically increased tendency to administer IVBZDs during the EEG (57% versus 22%) in the ASE subgroup.248 J. SD.5 h (range 24–120 h.3 h (range 24–480 h. Fifteen subjects (83%) were diagnosed in the ICU. GTCS Sepsis. 24. In six patients (34%). 23.0 ± 19. This group was treated with an average of 2. GTCS Anoxia Anoxia Subdural hematoma. Multiple medical problems were frequent and are summarized in Table 2. 37. cardiopathy CVD. Recurrence occurred in five subjects (Cases 16. Unfortunately. three had a central nervous system infection (17%). In three patients (Cases 16. NLEa Right parietal infarcta ND CT: left infarct in corona radiata CT: bilateral subdural hematoma CT: normal CT: subcortical atrophy.6).5 ± 29. None had significant changes in mental status. Neuroimaging was normal in only two subjects (Cases 22 and 31) (Table 1). SD. 41. In the majority of patients a combination of several AEDs was used (Supplementary Table S1). a previous history of chronic epilepsy (62% versus 5.1 versus 233. 32.6%) was significantly more frequent in the NCSE proper group. GCSE: generalized convulsive status epilepticus.6). one or several GTCSs preceded or were associated with the symptoms. FSG: focal secondarily generalized. cerebral infarcts CT: normal CT: bilateral occipital infarct CT: left parieto-temporo-occipital hematoma CT: congenital ventriculomegaly CT: cerebral edema ACG CGC EAM EMP JFG JGL JPJ JRG JRU JSL JTS MGC MGF MRM MTJ PHE SCR YIS ACVD: acute cerebrovascular disease.3. and number of AEDs and etiology may be found in Supplementary Fig. mortality rate (6% versus 61%) and admission to the ICU (18% versus 83%) was significantly higher in the comatose NCSE group than in the NCSE proper group (p < . ND: no done. 3. However.9 versus 60. we observed that the mean duration was significantly greater in the surviving subgroup (102. NCSE types and neuroimaging features in comatose NCSE.77 ± 1. GTCS: generalized tonic–clonic seizures. 47 and 48) had significant sequelae. two had a favorable outcome. Patients Sex/age Medical history Precipitating factors NCSE type Neuroimaging 33 34 35 36 37 38 39 40 41 42 43 44 45 46 47 48 49 50 F/88 M/65 M/79 M/65 M/70 M/69 M/55 M/75 M/74 M/73 F/73 F/80 M/85 F/75 M/56 F/75 M/54 F/39 Hypertension Lung tumor Cardiopathy Cardiopathy.3). 4. and patients were treated with an average of 2. OH: alcoholism. 41 and 44). Eleven patients (61%) died and seven (39%) survived to hospital discharge. Conversely. number of elderly individuals (46% versus 77%).1 ± 30.46 ± 0. S1. CLL: chronic lymphoid leukemia. CT: computerized tomography.7 drugs (range 1–6. leukoariosis Hypertension. OH Cardiopathy Leukemia (CLL) Aortic aneurysm Hypertension.1 ± 65. 44. 43. Four patients (Cases 16. When we analyzed patients with comatose NCSE. Only one patient (5%) had a previous history of epilepsy. PMS: partial motor seizures. mean duration of the episode (49.L. CVD Hypertension. Neuroimaging was normal in only three patients (Cases 35.4 versus 153.7 drugs (range 1–5.4 years (range 39–88 years). 49 and 50).6 ± 34. Statistical analysis The clinical.39) and neuroimaging anomalies (50% versus 16%) were significantly greater in the partial/focal NCSE proper subgroup than in the ASE subgroup (Supplementary Table S3). PMS ACVD GCSE. When we compared our patients according to the clinical scenario (NCSE proper versus comatose NCSE). EDs were completely abolished and in other three (Cases The mean episode duration (33. All ictal EEG features. In all subjects. focal or lateralized comatose NCSE. neurophysiologic and neuroimaging characteristics of the 18 patients with comatose NCSE are summarized in Table 2 and Supplementary Table S2. 1. seven (39%) had generalized comatose NCSE and three (17%) had a FSG comatose NCSE.2 ± 13. Two patients died during the follow-up. and 31). None of the patients in this group had recurrence on follow-up. 44. 142. The mean duration of NCSE was 63. 41. parkinsonism CVD. The mean age was 69. 48. 1. In three (Cases 35. The mean duration of NCSE was 153. PMS Anoxia ACVD Subdural hematoma GCSE CNS infection. two (11%) had SGCSE and one (5%) was diagnosed with sepsis (Table 2). the mean age (56. SD. In five patients (Cases 34. Comatose NCSE 3. Fernández-Torre et al. 22 and 29) anesthetic management of NCSE was needed. alcohol deprivation CNS infection FSG Focal Generalized Focal Focal Generalized Generalized Focal FSG Focal Focal Generalized Generalized Focal Focal FSG Generalized Generalized CT: intraventricular hemorrhage Infarct in territory both mid cerebral arteriesa CT: normal ND CT: subdural hematoma ND CT: right hypodensity in basal ganglia. the cause or precipitating factor was acute cerebrovascular disease (ACVD). p < . 22 and 29) were transferred to the ICU as consequence of refractory NCSE. / Clinical Neurophysiology 123 (2012) 244–251 Table 2 Demographic. treatment and outcome are summarized in Supplementary Table S2. IVBZDs were administrated during the EEG recording.4 ± 12. 48.3). Of these seven patients.0). There were 12 men (66%) and six women (34%). NLE: necrotizing leukoencephalopathy. the request for an EEG was made because of significant alteration in consciousness.2. Antiepileptic treatment was varied. two (11%) had subdural hematoma. hepatic failure ACVD. multivariate analysis was not applied. four (22%) had cerebral anoxia.3. In six patients (Cases 35. CNS: central nervous system. five out seven (Cases 33. duration of the episode. There are few studies including more than 50 patients collected consecu- . clinical antecedents. Eight patients (44%) had partial. 20. Fourteen patients (78%) were elderly.

The difference was statistically significant in comparison with the NCSE proper group. However. Indeed. this diagnostic approach seems to play a more important role in those patients with CPSE showing continuous EDs. It is therefore not surprising that patients with diagnosis of comatose NCSE have a dismal prognosis. antiepileptic treatment was highly variable. In 10 of our patients one or several GTCSs preceded the episode of CPSE. Some authors avoid including anoxic causes of comatose NCSE. Narayanan and Murthy. A previous history of chronic epilepsy was observed in only one patient (5%). We believe this to be the first report of refractory atypical ASE in a subject with PME of Lafora type in which stimulus-induced rhythmic.. Drislane et al. Fernández-Torre et al. Drislane et al. 2006). 249 In our study. 1986.. eLorenzo et al. 1999). HF: 70 Hz.. Similar results have been published by other authors (Jaitly et al. mean duration. the demonstration of recurrent partial seizures may be sufficient to reach a diagnosis in the cyclic variant of CPSE. 2003). In our study. 2). an additive negative impact of ongoing EDs to the underlying lesion cannot be excluded (Waterhouse et al. our results replicate the findings also obtained by others authors (Scholtes et al. ictal discharges (SIRPIDs) have been described (Fig. 1992. However. Alroughani et al. 2006. Agathonikou et al... Rossetti et al. 1998). sensitivity: 100 lV/cm. Therefore.. Fagan and Lee... speed: 15 mm/s. 1992) who emphasized the high prevalence of this partial type of NCSE. 1993. 1982.. 2000. 1998). 2003).. 1998.1 versus 233. Guberman et al..... With cyclic CPSE it is important to remember that it may be necessary to extend the recording duration so as to increase the change of capturing a partial seizure.. EEG of patient 50 (YIS). 1972. If we consider only the ambulatory group. . Mortality rate (61%) was notably higher than in the NCSE proper group (6%). 2..5–3 Hz in keeping with the diagnosis of generalized comatose NCSE. Towne et al. Thus.. severity of illness was also the major determinant of poor outcome. 2008). Tomson et al. slightly more than ASE rate (44%). This result was expected because the gravity of etiology in these patients. This therapeutic diversity agrees with the conclusions of a recent investigation on the management of refractory SE. In a previous similar study. 2008.. however. In all patients with typical and atypical subtypes.. which included CPSE (Holtkamp et al. ASE can generally be detected from the onset of the EEG recording. Guberman et al. NF: 50 Hz. 1986. Ballenger et al. it seems that comatose NCSE occurs in individuals with acute symptomatic cerebral pathology or exacerbation of a chronic pre-existing neurologic process that only in a small percentage includes epilepsy.53 Hz. We conclude that Fig. 1998. 2003).. others have concentrated their efforts in comatose and critically ill individuals (Young et al. a recent investigation on duration of refractory SE and outcome.. LF: 0. Interestingly. 2010). Therefore. 1996. 1996. This result is not surprising since dead patients may have an abbreviated stay. One of these patients with cryptogenic encephalitis (Case 50) fulfilled criteria in keeping with a malignant variant of SE (Holtkamp et al. Litt et al.. existence of recurrence. 1994. clinical presentation. The most frequent cause of comatose NCSE in our series was an ACVD (34%). situation-related ASE was triggered by intravenous cefepime. 1996. In three cases. Moreover. this number reached 53%. she died as consequence of bowel ischemia which has recently been described as a complication of prolonged treatment with THP (Cereda et al.. Pandian et al. 1996. Seventeen out of 50 patients (34%) were diagnosed with CPSE. most cases of comatose NCSE are acute symptomatic with underlying acute brain disorders and. 2008).. Thus. cancer and infection. 1986.5 ± 29. 1996. Towne et al. 1998). 1990.1 ± 65. which was statistically significant. NCSE is a rare complication in Lafora’s disease (Corkill and Hardie. the patients with de novo ASE induced by nonpsychotropic drugs had severe concomitant disorders such as leukemia. 1986. / Clinical Neurophysiology 123 (2012) 244–251 tively (Shneker and Fountain. The patient experienced an exceptionally prolonged episode of refractory atypical ASE that proved fatal. 1992.. Kaplan 1996. Logroscino et al. 2005) (Fig.J. a prolonged in-hospital stay (P10 days) in three survivors contributed to this result. 1994. 2010).. 2002... 2008). Camacho et al.L. 2008). while some authors have focused their attention on ambulatory forms of NCSE (Andermann and Robb.. and precipitating factors were similar to those described in previous series (Andermann and Robb. Scholtes et al. these episodes of ASE occurred in different clinical scenarios from those classically seen with de novo ASE of late onset (Thomas et al. None of our 10 patients was comatose.. The patient 14 (YRG) was initially misdiagnosed as JME. Drislane et al. in the group of situation-related ASE there was a predominance of sharp-slow wave complexes (SSW) and biphasic sharp waves (Sws) at 2–2. 2000. López-Mesa et al. 2009). Agathonikou et al. However.. NCSE in comatose subjects is often unsuspected and difficult to diagnose (Drislane et al. Litt et al. It is important to emphasize that an excessively long postictal period following a GTCS may occur in either ASE or CPSE. 2001) supporting the observations reported by Tomson’s group (Tomson et al. After 2-year-follow-up the neurological examination is unremarkable. lymphoma. Most studies of NCSE have analyzed the two principal categories independently.. generalized polyspike-wave complexes (PSW) and SW ranging from 2 to 6 Hz were observed.5 Hz. 1997. 2004. 1998.05). SE outcome is mainly determined by etiology and age (Towne et al. Litt et al.. 1999. renal failure. Others authors have obtained similar numbers (Young et al. Neurologic examination and an EEG obtained several months after hospital discharge were completely normalized. 1983. The mean duration of comatose NCSE was significantly longer in the surviving subgroup (102. 2009). This issue has been recently reviewed (Shorvon and Trinka. 2009). Bauer and Trinka. Thomas and Andermann.. Note the presence of continuous epileptiform discharges (EDs) consistent of rhythmic sharp waves (Sws) and sharp-slow wave complexes (SSW) at 2. 2009). Scholtes et al.. Although traditionally ASE has been considered more frequent than CPSE. and her EEG is completely normalized. 1972. NCSE may occur following GTCSs or controlled convulsive status epilepticus (SE) (Bauer et al. p < . suggested that the prognostic effect of duration was strongly influenced by etiology (Drislane et al. 1b). 2007. This problem is not rare in patients with GTCSs and myoclonus (Striano et al. Koutroumanidis.. Both ACVD and anoxia were the two more frequent causes in the present investigation. The administration of IVBZDs is considered important in making a ‘‘definitive’’ diagnosis of NCSE (Kaplan. (1998) did not found differences in mortality relative to the mean number of hours from diagnosis to control of SE.3. In general in the ASE group. Three out four CPSE subjects in whom IVBZDs were administered during the EEG had a continuous type of CPSE.. periodic.

Eur J Neurol 1999.L. Clin Neurophysiol 2004. Oterino A. Mayr U. Agirre Z. Status epilepticus no convulsivo: experiencia en 33 pacientes. Similarly Shneker and Fountain (2003) analyzed 100 patients with NCSE and they did not observe any association between EEG pattern and mortality. Supplementary data Supplementary data associated with this article can be found. J Clin Neurophysiol 2008. King DW.39:833–40. Solar DM. Giannakodimos S.22:79–91. Persistent nonconvulsive status epilepticus after the control of convulsive status epilepticus. Fernández-Torre JL. Berger MM. Nagayama et al. USA) by his kind revision of the manuscript and invaluable comments and suggestions. Corkill RG. Prolonged confusion following convulsions due to generalized nonconvulsive status epilepticus. González-Mandly A. association between generalized patterns and mortality rate (Litt et al. The two faces of electrographic status epilepticus: the waking wounded and the ictally comatose. 2006).21:411–9.. González-Rato J. Schomer DL.19:111–21. the authors attributed it to the different etiologies. Fernández-Torre JL. Neurology 1983. at doi:10. Seizure 2003b. Rebollo M.21:319–31. Mechanisms and management. Partial complex status epilepticus. and that an accurate electroclinical correlation and EEG monitoring are the clue to reach a definitive diagnosis. An unusual case of Lafora body disease.37:215–8. Sánchez JM.2011. Acebes A. et al. Ictal generalized EEG patterns (generalized and FSG) were more frequent.. However. Fagan KJ. Bowel ischemia: a rare complication of thiopental treatment for status epilepticus. Martínez-Martínez M. Status epilepticus. Drislane FW. Rev Neurol 2000.50:1566–71. Clinical implications of generalized electrographic status epilepticus. Nonconvulsive generalized status epilepticus: clinical features. Alroughani R. nonanoxic patients Drislane et al. et al. Therefore. Cephalosporin-induced nonconvulsive status epilepticus: clinical and electroencephalographic features. Ko D. Gallagher BB. Hardie RJ. Treiman DM. Waterhouse EJ.39:1265–76. Aichner F. Trinka E. Clin EEG Neurosci 2006b.33:1545–52. London: The MIT Press. Cereda C. Fernández-Torre JL. Martínez-Martínez M. Functional and cognitive outcome in prolonged refractory status epilepticus. Robakis and Hirsch. Martínez-Martínez M. de la Peña P. Arch Neurol 1988. Schomer DL. Among treated. Velasco-Zarzosa M. 2009. DeLorenzo RJ. Doctoral thesis. González C. Maestro I. Antiepileptic treatment was heterogeneous.43(Suppl. Bauer G.38:57–60. found that the patients with evidence of focal onset in their seizures responded better to AEDs that did those with generalized EDs. Epileptic Disord 2007. Martínez-Martínez M. Broughton R. Drislane FW. Acknowledgments Dr. Drislane FW. Fernández-Torre JL. Lee SI. J Neurol 2006c. Figols J.30:1040–4.020. A reappraisal following review of thirtyeight patients. Rabinstein AA. S2).18:82–3. Clinical and electroencephalographic characteristics of nonconvulsive status epilepticus in adults. Neurología 2001. the rate of occurrence in a general hospital. Stuss D. Nonconvulsive status epilepticus following generalized tonic-clonic seizures. Guberman A.37:744–52.14:e14–5. Interestingly. Villarejo A. Hirsch LJ. Neurology 2008. Estado epiléptico no convulsivo. Drislane FW. and treatment of nonconvulsive status epilepticus. J Clin Neurophysiol 2004. (2008). Leno C. episode duration. 1998). Fernández-Guinea O. Rossetti AO. Casariego Pola F..6:245–71. In conclusion. Javidan M. Fernández-Torre JL.25:181–6. Gutiérrez-Pérez R. Epilepsy Res 1994.9:134–9. Gautam S. J Clin Neurophysiol 2005. Epilepsia 2010. Epilepsia 1998. Marco de Lucas E. Absence status. Fernández-Torre JL. Is it status? Epilepsia 2002.18:38–42. Typical absence status in adults: diagnostic and syndromic considerations. 2009.12:245–8. Fernández-Torre JL. and long-term follow-up. Calleja J. Robb JP. Díaz-Castroverde A-G. Eur J Neurol 2007. Subacute encephalopathy with seizures (SESA syndrome) in alcoholics: report of an unusual case. evaluation. Fernández-Torre JL. Cereceda R. Fernández-Torre JL. Fernández-Torre et al. Simple partial frontal status epilepticus with recurrent asymmetric tonic seizures. Cantu-Reyna G. Alonso I.66:1505–9. Chong DJ. Complex partial status epilepticus of extratemporal origin in a patient with systemic lupus erythematosus.10:355–8.clinph. González-Rato J. Non-convulsive status epilepticus in elderly individuals: report of four representative cases. history of previous epilepsy. Hernández-Hernández JL. Jiménez-Bonilla J. Seizure 2009. Pérez-Martínez D. Neurology 1986. et al. Floriach-Robert M. Ballenger CE. Lopez MR. Rev Neurol 2003a.36:1284–91. De novo absence status of late onset following withdrawal of lorazepam: a case report. Creutzfeldt–Jakob disease and nonconvulsive status epilepticus: a clinical and electroencephalographic follow-up study. Epilepsia 2010. Seizure 2009. González-Rato J.18:306–7.1:301–14. Age Ageing 2004. SESA syndrome: a subtype of localisation-related non-convulsive status epilepticus. 2009. Arch Neurol 2009. Presentation. our findings suggest that we do not have to be excessively dogmatic in the interpretation of determined EEG patterns.70:e30–1. . Fernández-Torre JL. Fernández-Torre JL. Qasem A. Epilepsia 2005. Fernández-Torre is indebted with Professor Peter W. Grigg MM. Panayiotopoulos CP. 3):103–13. Infante J. mortality rate and clinical presentation between NCSE proper and comatose NCSE to recommend adoption in clinical practice. Fernández-Torre.1016/j. EEG in convulsive and nonconvulsive status epilepticus. Generalized status myoclonicus in acute anoxic and toxic-metabolic encephalopathies. in contrast to the EEG criteria proposed by Chong and Hirsch (2005) that required the second criterion (clinical improvement or appearance of normal EEG) when EDs occurred at frequency <3 Hz. Camacho A. Blum AS. Boggs JG. Typical absence status epilepticus as late presentation of idiopathic generalised epilepsy in an elderly patient. Schomer DL. In: Wasterlain CG.250 J. and the mean number of AEDs employed (2. Brenner RP. p. Eur Neurol 1982. Parrilla G. Brenner RP..16:394–8. Which EEG patterns warrant treatment in the critically ill? Reviewing the evidence for treatment of periodic epileptiform discharges and related patterns. Lopez MR.13:177–87. Nonconvulsive status epilepticus and coma. Blum AS. Fernández-Torre JL.51:177–90. Puchades R. Fernández-Torre JL. Detection and treatment of refractory status epilepticus in the intensive care unit.37:50–3. our study demonstrates that there are sufficient differences regarding age of onset. Complex partial status epilepticus is an unrecognised feature in SESA syndrome: new insights on its pathophysiology. Calatayud MT. Kaplan (Baltimore. Fernández-Torre JL. Estado epiléptico no convulsivo de origen frontal. DeLorenzo GA. Astudillo A. Arce F. Alotaibi N. Agirre Z. Epilepsia 2009. Nonconvulsive status epilepticus causing prolonged stupor after intraventricular hemorrhage: report of a case. Cooper AD.253:392–5. Spain: University of Cantabria. Drislane et al. 109–12. Duration of refractory status epilepticus and outcome: loss of prognostic utility after several hours. Fernández-Torre JL. Fernández-Torre JL. Appendix A.33:78–81. Seizure 2009. editors. Epilepsy Behav 2000. Epilepsia 1998. Fernández-Torre JL. Fujikawa DG. Britton JW. Seizure 2001. Localisation-related nonconvulsive status epilepticus.45:781–4.115:316–9. Presentación de un caso. Neurology 1990.40:1689–94. neuropsychological testing. Ross E. Calleja J.7) was identical to the study by Litt and colleagues (1998). 2005. Bauer G. Prognostic utility of duration in refractory nonconvulsive status epilepticus. Fernández-Torre would like to thank all staff of the Department of Clinical Neurophysiology of Marqués de Valdecilla University Hospital (Santander) and Cabueñes Hospital (Gijón) for your collaboration in the evaluation of some of the patients included in this study. 2010. We did not find as others have. Nonconvulsive status epilepticus as an unrecognised cause of acute confusion in alcoholics. Clin EEG Neurosci 2007. Conflict of interest None of the authors has any conflict of interest to disclose. Epilepsia 1972. Agirre-Arrizubieta Z. Fernández-Torre JL. Clin EEG Neurosci 2006a. several of the unequivocal cases of generalized and FSG comatose NCSE reported here had a frequency of EDs < 3 Hz (Supplementary Table S2 and Fig.51:319. Koutroumanidis M.06. Rodríguez E. Towne AR. Martínez-Martínez M. Dr. Sánchez JM. Further evidence of permanent cerebral damage. Non-convulsive status epilepticus. / Clinical Neurophysiology 123 (2012) 244–251 exceptionally prolonged episodes of NCSE should not be regarded as hopeless in terms of successful clinical recovery (Cooper et al. Celesia GC. Rodrigo E.10:433–7. These results should be taken into account when developing future classifications and therapeutic trials on NCSE. Neurocrit Care 2009. References Agathonikou A. 2006. González-Mandly A.46:1550–2. Andermann F. Necrotizing leukoencephalopathy associated with nonconvulsive status epilepticus and periodic short-interval diffuse discharges: a clinicopathological study. in the online version. González C.

Kopec-Garnett L. et al. Cervasio M. Holtkamp M. Meinardi H. Status epilepticus. 1997. Persistent but reversible coma in encephalitis. Towne AR.12:343–62. Garnett LK. Pellock JM.26:329–39. Manno E. A progressive sequence of electroencephalographic changes during generalized convulsive status epilepticus. Assessment of acute morbidity and mortality in nonconvulsive status epilepticus. Rossetti AO. Privitera M. Neurology 2000. Aminoff MJ. Epilepsy: a comprehensive textbook. Towne AR. Hurwitz S. Clinical and EEG features of status epilepticus in comatose patients. A ‘‘malignant’’ variant of status epilepticus. Tomson T. Nonconvulsive status epilepticus. Stern BJ. Andermann F. London: John Libbey and Company Ltd. Marescaux C. Kaplan PW. Idiopathic generalized epilepsies. Doig GS. Outcome from coma after cardiopulmonary resuscitation: relation to seizures and myoclonus. editors.77:611–5. p. Epilepsy Behav 2002.61:1090–4. London: The MIT Press. 145–66.61:1066–73. Literature review. The management of refractory generalised convulsive and complex partial status epilepticus in three European countries: a survey among epileptologists and critical care neurologists. Striano P.4:106–11. Young GB. Shinohara Y. diagnosis. J Clin Neurophysiol 1995. Genton P. Epilepsy Behav 2010.29:175–83. Neurology 1990. Neurology 1992. Epilepsia 2007. Assessing the outcomes in patients with nonconvulsive status epilepticus: nonconvulsive status epilepticus is underdiagnosed. Mullen PD. Meierkord H. Masuhr F. Absence status. / Clinical Neurophysiology 123 (2012) 244–251 Holtkamp M.74:1095–9.11:348–61. Narayanan JT.12:572–86. Epilepsia 1998. Alanis-Guevara IM. Brown AJ. Towne AR. Chung S. J Neurol Neurosurg Psychiatry 2006. Subtle generalized status epilepticus. age. and prognosis of nonconvulsive status epilepticus. Nagayama T. Chatel M. Hirsch E. In: Engel Jr J. Neurocrit Care 2006. 91–108. Treiman DM. Dolisi C.14:326–34. Jaitly R. So EL. Kaplan PW. and confounded by comorbidity. 2009. p. Sgro JA. Non-convulsive status epilepticus: causes. Kendrick C. Annegers JF. Nonconvulsive status epilepticus: high incidence of complex partial status. Lebrun C.L. 681–99. Bernasconi R. Behavioral manifestations of nonconvulsive status epilepticus. Pandian JD. Shneker BF. Young GB. Nat Clin Pract Neurol 2008. Logroscino G. Clinical features and outcome. Simon RP. Epilepsy Res 1990. Meierkord H. Ko D. et al.25:653. Fernández-Torre et al.47:83–9. Treiman DM.2:185–93. Ryan DD. Williamson PD.48:900–6. Fulgham JR. Neurologist 2005. Svanborg E. Broglin D.5:49–60. Epilepsy Res 1998. Othman J. Weiss H. Diagnosis and treatment of nonconvulsive status epilepticus. Gilbert JJ. p. Weiss HD. Nonconvulsive status epilepticus and the postictal state. Determinants of mortality in status epilepticus. Waterhouse EJ. Gerber P.42:100–4. Zifkin B. Wickboldt C. Hauser WA. Einhäupl KM. Epilepsia 1996. Litt B. Robakis TK.19:172–5. Typical progression of myoclonic epilepsy of the Lafora type: a case report. Epilepsia 1993. Digital videoelectroencephalographic monitoring in the neurological–neurosurgical intensive care unit. Bagiella E. Nonconvulsive status epilepticus in a neurological intensive care unit: profile in a developing country. Epilepsia 1992. and outcome in 65 patients. Ann Neurol 1986. Nonconvulsive status epilepticus. Kaplan PW. Arch Neurol 2004.61:1035–6. Holtkamp M. Andermann F. Tomson T. case report. Koutroumanidis M. Vaughan JK. Barnes TY. Neurology 1996. Epileptic Disord 2000. Wityk RJ. et al. Logroscino G. Daijin K. Salisbury S. Mechanisms and management. Moore JL.37:643–50. Treiman DM. New York: Demos Medical Publishing. Epilepsia 1993. Wedlund J-E. Hertz SH. In: Wasterlain CG. Longterm mortality after a first episode of status epilepticus. Jordan KG. 251 Scholtes FB. Philadelphia: Lippincott-Raven Publishers. ‘De novo’ absence status of late onset: report of 11 cases. Buchheim K. 1):S2–S11. Nonconvulsive status epilepticus in adults: thirty-two consecutive patients from a general hospital population. Thomas P. In: Malafosse A. Fernández González-Aragón MC.16:341–52.40:1843–8. Boggs JG. Non-convulsive status epilepticus in adults: clinical forms and treatment. Epilepsia 1986. Kaplan PW. Zara F. J Clin Neurophysiol 1999. editors. Cascino GD. Neurology 2003. Girard JM. Epilepsy Behav 2008. treatment. Cerda-Téllez F.18:155–66. De novo absence status as a benzodiazepine withdrawal syndrome. Krumholz A. Shorvon S. Schielke E. J Neurol Neurosurg Psychiatry 1996. . Pedley TA. Cascino GD. Genton P. DeGiorgio CM. Towne AR. EEG detection of nontonic–clonic status epilepticus in patients with altered consciousness. Masuhr F.54:340–5.3:122–39. Walton NY. Synergistic effect of status epilepticus and ischemic brain injury on mortality. Prognosis of status epilepticus: role of aetiology. Generalized status epilepticus in the adult.33:829–35. The significance of myoclonic status epilepticus in postanoxic coma. Epilepsia 1984. Absence status epilepticus. Trinka E. Estado epiléptico no convulsivo asociado a Enfermedad de Lafora: presentación de dos casos. Lindbom U. 1994. Neurology 2003. Thomas P.35:27–34. Late-onset absence status epilepticus is most often situation-related. An assessment of nonconvulsive seizures in the intensive care unit using continuous EEG monitoring: an investigation of variables associated with mortality.37:945–7..61:93–5.34(Suppl. Nilsson BY. Treiman DM. and consciousness impairment at presentation. Ruano-Calderón MA. 2006. editors. Zochodne DW. Prevalence of nonconvulsive status epilepticus in comatose patients.58:537–41.2:252–7. Epilepsia 1994.4:35–46. Complex partial status epilepticus.20:351–5. Pronostic value of EEG monitoring after status epilepticus: a prospective adult study. Prognosis in nonconvulsive status epilepticus. Walker MC.39:1194–202. J Neurol Neurosurg Psychiatry 2003. CNS Drugs 2001.42:104–10. Electrographic status epilepticus in fatal anoxic coma. Maganti R. Thomas P. Lowenstein DH. Matsushima K. Nagayama M. Harms L. Buchheim K. J Clin Neurophysiol 1997. Neurology 2002. Nonconvulsive status epilepticus in the critically ill elderly. Drees C. Kaplan PW. Fountain NB.15:931–9. Rev Neurol 2003. Hesdorffer DC. DeLorenzo RJ. Aminoff MJ. and expert discussion of prolonged refractory status epilepticus. Treiman DM. potentially overtreated. Chatel M. Thomas P. DeLorenzo RJ. Turnbull J. Arch Neurol 2005. Neurology 1992. et al. Electroclinical features of status epilepticus. Renier WO. Neurocrit Care 2005.J.27:276–85.38:401–5. Drislane FW.34:355–8. Waterhouse EJ. editors. Bromfield EB. Nonconvulsive status epilepticus.62:1428–31. Beaumanoir A. Jester D. Murthy JMK. The clinical features. Epilepsy Res 1994. Hirsch LJ. Hoffman M. Lancet Neurol 2007. 95–109. Ackerley CA. Neurology 1988. In: Kaplan PW. Meierkord H. Smith Jr JR. Kaplan PW. Nonconvulsive status epilepticus in the emergency room. p. López-Mesa EG. Boggs JG.