Generalized Periodic Epileptiform Discharges Research Articles

Transition dynamics and optogenetic controls of generalized periodic epileptiform discharges

This paper aims to analyze possible mechanisms underlying the generation of generalized periodic epileptiform discharges (GPEDs), especially to design targeted optogenetic regulation strategies. First and foremost, inspired by existing physiological experiments, we propose a new computational framework by introducing a second inhibitory neuronal population and related synaptic connections into the classic Liley mean field model. The improved model can simulate the basic normal and abnormal brain activities mentioned in previous studies, but much to our relief, it perfectly reproduces some types of GPEDs that match the clinical records. Specifically, results show that disinhibitory synaptic connections between inhibitory interneuronal populations are closely related to the occurrence, transition and termination of GPEDs, including delaying the occurrence of GPEDs caused by the excitatory AMPAergic autapses and regulating the transition process of GPEDs bidirectionally, which support the conjecture that selective changes of synaptic connections can trigger GPEDs. Additionally, we creatively offer six optogenetic strategies with dual targets. They can all control GPEDs well, just as experiments reveal that optogenetic stimulation of inhibitory interneurons can suppress abnormal activities in epilepsy or other brain diseases. More importantly, 1:1 coordinated reset stimulation with one period rest is concluded as the optimal strategy after taking into account the energy consumption and control effect. Hope these results provide feasible references for pathophysiological mechanisms of GPEDs.

A rare case of partially empty sella with epileptiform discharges presenting with first episode of mania.

Sir, Busch described the condition empty sella syndrome (ESS) in 1951 where the sella turcica is filled with cerebrospinal fluid (CSF) causing displacement or flattening of the normal pituitary gland.[1] It is reported to occur in 5.5%–23.5% of the population[2] which is pathophysiologically characterized by either anatomic abnormalities in the diaphragma sellae (primary ESS) or damage to the pituitary by irradiation/surgery, or autoimmunity leading to the availability of “empty” space in the sella (secondary ESS).[1] The common signs and symptoms includes headache, papilledema due to raised intracranial pressure, leakage of CSF through nose and weight gain.[1] It can also present as decreased libido, galactorrhea, amenorrhea and secondary infertility.[3] Psychiatric manifestations of ESS are rare but can occur in the form of behavioral disturbances and psychotic symptoms.[4,5] A 25-year-old male presented to us with violent behavior towards family members, reduced need for sleep, elevated self-esteem and grandiose delusions claiming himself to be the prime minister of India. It was associated with one episode of tonic–clonic movements two nights back, with urinary incontinence. Patient also complained of jerky movements in his left arm occasionally about two to three times a day following this. All the symptoms started abruptly for past 10 days, this being his first such episode in his lifetime. There was no history of any febrile illness, head injury, substance abuse; blood parameters that included serum electrolytes, serum prolactin, vitamin B12 levels, and serum osmolality were all within normal limit. He was diagnosed to be in mania as per Diagnostic and Statistical Manual of Mental Disorders (DSM 5). Young’s Mania Rating Scale (YMRS) score was 24. The patient was subjected to magnetic resonance imaging (MRI) scan which revealed empty sella [Figure 1]. 10–20 electroencephalogram findings revealed generalized periodic epileptiform discharges (GPED). The patient was placed on sodium valproate 1000mg, haloperidol 10 mg and trihexyphenidyl 4 mg in divided dosages. The symptoms reduced in severity and YMRS score came 12 on day 5 of admission and EEG was normal. This was his first episode of mania that coexisted with first lifetime episode of seizure. GPEDs results in kindling of neuronal pathways, leading to psychiatric manifestations such as mania. Lateral hypothalamic kindling can induce manic-like behavior in a rat model.[5]Figure 1: MRI scan showing empty sellaThere are reports of atypical presentations of ESS in the form of acute psychosis, sinus bradycardia, herniation of anterior cerebral artery.[5–7] The presentation of empty sella as seizure episode has been reported rarely.[8] Moreover, it is even more rare to be presenting with both seizure episode and mania.[9] In one case report mania was precipitated by hyponatremia in a patient with ESS[10] whereas in our case sodium and other electrolytes level were in normal range. The possible mechanism of such is still a gray area.[9] Even there is also a dilemma of seizure precipitating mania or vice-versa. More sample based studies is needed to establish the neurochemical events leading to the same for better diagnosis and management. Ethical concerns Proper consent was taken from the patient regarding publication of the case without revealing patient’s identity Financial support and sponsorship Nil. Conflicts of interest There are no conflicts of interest.

Partially empty sella with generalized epileptiform discharges presented as manic episode in an elderly female: A case with diagnostic dilemma - Causation or coincidence?

Partially empty sella with generalized epileptiform discharges presented as manic episode in an elderly female: A case with diagnostic dilemma - Causation or coincidence?

Topography of generalized periodic epileptiform discharges in postanoxic nonconvulsive status epilepticus.

SummaryWe studied slow (≤2.5 Hz) nonevolving generalized periodic epileptiform discharges (GPEDs) in the electroencephalogram (EEG) of comatose patients after cardiac arrest (CA) in search of evidence that could assist early diagnosis of possible hypoxic nonconvulsive status epilepticus (NCSE) and its differentiation from terminal brain anoxia (BA), which can present with a similar EEG pattern. We investigated the topography of the GPEDs in the first post‐CA EEGs of 13 patients, using voltage‐mapping, and compared findings between two patients with NCSE and GPEDs > 2.5 Hz (group 1), and 11 with GPEDs ≤ 2 Hz, of whom six had possible NCSE (group 2) and five had terminal BA (group 3). Voltage mapping showed frontal maximum for the negative phase of the GPEDs in all patients of groups 1 and 2, but not in any of the patients of group 3, who invariably showed maximization of the negative phase posteriorly. Morphology, amplitude, and duration of the GPEDs varied across the groups, without distinctive features for possible NCSE. These findings provide evidence that, in hypoxic coma after CA with slow GPEDs, anterior topography of the maximum GPED negativity on voltage mapping may be a distinctive biomarker for possible NCSE contributing to the coma.

Clinical outcome of generalized periodic epileptiform discharges on first EEG in patients with hypoxic encephalopathy postcardiac arrest.

The EEG, alongside clinical examination, imaging studies, and SSEPs, is used to determine the prognosis following hypoxic encephalopathy postcardiac arrest. Generalized periodic epileptiform discharges (GPEDs) are recognized as a "malignant" EEG pattern associated with very poor outcome with previous studies reporting no or few survivors. We looked at our database of cardiac arrest patients who subsequently developed GPEDs to determine clinical outcome and profile any survivors. We identified all cardiac arrest patients treated at King's College Hospital between 2011-2014 who developed hypoxic encephalopathy associated with GPEDs, BiPLEDs (bilateral periodic lateralized epileptiform discharges), and periodic discharges on first EEG. We collected clinical data including age, gender, downtime, EEG reactivity, presence of seizures or myoclonus, and outcome. Survivors were defined as patients who were discharged from the hospital to home or a neurorehabilitation unit. Thirty-six postcardiac arrest patients with hypoxic encephalopathy were identified, 24/36 with GPEDs, and 12/36 with BiPLEDs on first EEG. The mean age of patients was 62.8 ± 14.5 years old, with 27 males (75%) and 9 females (25%). Ten of thirty-six patients survived, which is slightly higher than previously reported. Statistical tests to compare clinical characteristics between survivors and nonsurvivors demonstrated no significant differences except for trend to significance for the presence of reactivity on first EEG (p = 0.0794). On discharge, one survivor had good functional outcome (and subsequently became independent), but all others were dependent for all ADLs (activities of daily living). Generalized periodic epileptiform discharges carry a grave clinical prognosis following cardiac arrest. This study did identify a higher number of survivors compared to previous studies, but most were severely disabled at hospital discharge. Reactivity of the first EEG might predict better prognosis and merit further evaluation. This article is part of a Special Issue entitled "Status Epilepticus".

LP31: EEG and MEG source localization of the epileptogenic foci in tuberous sclerosis complex: a pediatric case report

LP31: EEG and MEG source localization of the epileptogenic foci in tuberous sclerosis complex: a pediatric case report

Prognostic EEG patterns in patients resuscitated from cardiac arrest with particular focus on Generalized Periodic Epileptiform Discharges (GPEDs).

We assessed clinical and early electrophysiological characteristics, in particular Generalized Periodic Epileptiform Discharges (GPEDs) patterns, of consecutive patients during a 1-year period, hospitalized in the Intensive Care Unit (ICU) after resuscitation following cardiac arrest (CA). Consecutive patients resuscitated from cardiac arrest (CA) with first EEG recordings within 48hours were included. Clinical data were collected from hospital records, in particular therapeutic hypothermia. Electroencephalograms (EEGs) were re-analyzed retrospectively. Sixty-two patients were included. Forty-two patients (68%) were treated with therapeutic hypothermia according to international guidelines. Global mortality was 74% but not significantly different between patients who benefited from therapeutic hypothermia compared to those who did not. All the patients who did not have an initial background activity (36/62; 58%) died. By contrast, initial background activity was present in 26/62 (42%) and among these patients, 16/26 (61%) survived. Electroencephalography demonstrated GPEDs patterns in 5 patients, all treated by therapeutic hypothermia and antiepileptic drugs. One of these survived and showed persistent background activity with responsiveness to benzodiazepine intravenous injection. Patients presenting suppressed background activity, even when treated by hypothermia, have a high probability of poor outcome. Thorough analysis of EEG patterns might help to identify patients with a better chance of survival.

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Introduction: We compared the sensitivity of intermittent electroencephalography (iEEG) and continuous electroencephalography (cEEG) in malignant pattern (MP) detection in post-cardiac arrest patients, and described the delay in time to detection. Methods: IRB approved, retrospective cohort study of post-cardiac arrest subjects treated with therapeutic hypothermia (TH) and monitored with cEEG from 4/1/2010 to 6/4/2013. We extracted demographic and EEG data from subjects who demonstrated MP, defined as generalized periodic epileptiform discharges (GPEDs), myoclonic status epilepticus (MSE) and nonconvulsive status epilepticus (NCSE), during the first 48 hours after application of EEG. Post cardiac arrest category (PCAC) was determined on hospital arrival. The results were compared with simulated iEEG sampling intervals of 6, 8, and 12 hours post EEG initiation and twice daily at 9 am and 5pm, with each spot check lasting 20 minutes. The primary outcome was sensitivity of MP detection. The secondary outcome was time delay in MP detection. Data were analyzed with ANOVA and Mann-Whitney U test. Results: In 380 subjects included, mean age was 57 (SD 17), most were male (N=236, 62%) and experienced out-of-hospital cardiac arrest (N=289, 76%). The predominant primary rhythm was ventricular fibrillation (N=116, 30%), and PCAC IV (N=203, 61%). A total of 110 (29%) subjects survived in the cohort, with 7 (6%) surviving after MP development. MPs were detected in 111 (30%) subjects with 62 (56%) developing GPEDs, 67 (60%) developing MSE, and 28 (25%) developing NCSE. Median duration of MP was 26 hours (IQR 13, 39; range 1–48). MP detection sensitivity varied with iEEG sampling intervals of 6, 8, and 12 hours and twice daily at 9am and 5pm, with corresponding overall detection sensitivities of 94.3% (151/160), 90.6% (145/160), 90.6% (145/160), and 83.1% (133/160) [p=0.0068]. Similarly, average delay in detection varied by sampling interval (1.2 hours (IQR 0, 2.5), 1.7 hours (IQR 0, 3), 2.6 hours (IQR 0, 4.8) and 6.2 hours (IQR 2.4, 8.8), p=0.0001). Conclusions: MP detection sensitivity decreased and delay to MP recognition increased with prolonged iEEGs sampling interval. Survivorship following development of malignant EEG patterns remains low.

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Introduction: Therapeutic hypothermia (TH) for comatose survivors after cardiac arrest (CA) has been proven to improve neurological outcomes. However, the clinical examination, as well as other tests such as neuron specific enolase (NSE), somatosensory evoked potentials (SSEP), electroencephalography (EEG) has not been extensively validated on these patients. American Academy of Neurology (AAN) 2006 has published guidelines for prognostication after cardiac arrest. The data did not included TH patients. Methods: After IRB approval, we retrospectively reviewed the clinical, laboratory, and neurophysiological data of a prospective series of CA patients treated with TH at Mayo Clinic Florida, from January 2006 to January 2012. TH was established at core temperature values of 32 to 340C for 12 to 24 hours per American Heart Association (AHA) guidelines. Clinical outcome was defined by the Cerebral Performance Category (CPC) scale by death or hospital discharge, and dichotomized into standard definitions as either good outcome (CPC 1–2), or poor outcome (CPC 3–5). Glasgow coma scale (GCS) less than 8 was used to define coma. Results: Over the 6 year period we identified 85 CA patients treated with TH, of which 15 (17.6%) died within 3 days. Of the remaining 72 patients, the median age was 63 years. (SD 17.4, range: 25 - 93), with 50% being male. About 35% (n=25) of patients had an initial ventricular fibrillation/ventricular tachycardia (VF/VT) arrest, the rest being pulseless electrical activity/asystole arrest (PEA/asys). Those with PEA/asys arrest showed worse outcome compared to VF/VT, 73% vs. 27% respectively (P value = 0.02). By day 1 pupil was reactive on 88% of CPC 1–2 patients and 66% of CPC 3–5 patients. At day 3 pupil reactivity was present in 100 % of patients with good outcome. A Glasgow coma scale (GCS) >8 by day 3 was associated with 82 % chance of good outcome (P= <0.001). When GCS motor subcomponent by day 3 was more than 4, it predicted 94% good outcome (false positive rate 35%). NSE values > 33mcg/L had specificity of 87% to predict poor outcome (false positive rate 13%). When median nerve SSEP N20 values were absent poor outcome was predicted in 100% of patients which was similar finding with AAN. EEG was also 100% specific for poor outcome when it showed either suppression-burst (S-B) pattern or generalized periodic epileptiform discharges (GPEDS). Compared with our study AAN 2006 looked at myoclonus and status epilepticus on EEG who had poor outcome. We could not establish direct comparison. Conclusions: Therapeutic hypothermia-treated cardiac arrest patients may have different NSE values than those not treated with hypothermia. By day 1–3 NSE values > 33 had poor outcome with a false positive rate of 13% compared to AAN 2006 which was 0%. Based on the above data we suggest a ‘multicomponent prognostic approach’ incorporating clinical variables as well as other testing for the most accurate prediction.

Generalized periodic epileptiform discharges in critically ill children: Clinical features, and outcome

Generalized periodic epileptiform discharges (GPDs) are a specific periodic EEG pattern, reported as having a poor clinical outcome. The incidence and clinical implications of this EEG pattern in children are not known. In this study, we examined the clinical features of children with GPDs. EEG-video monitoring reports of children with critical illness in the intensive care unit were retrospectively reviewed to detect GPDs. The clinical history, hospital course and seizure characteristics were reviewed and outcome was based on the clinical findings at hospital discharge. Twenty one children (age 2-18 years) were identified with GPDs. The most common underlying etiology was encephalitis (N=11). At the time of EEG, a continuous intravenous infusion (cIV) of an anticonvulsant drug was used to treat refractory status epilepticus (RSE). Non-convulsive seizures (NCS) were identified in 15, and clinical seizures in 13 children after GPDs were detected. GPDs occurred after a dose reduction in the cIV in 43%. Neuroimaging done in 16 children showed an acute change in 13/16 (81%) and chronic changes in 2/16 (13%). Five children (23%) died. Seven (33%) children had a favorable outcome, whereas the remaining children had a moderate to severe disability at the time of hospital discharge. GPDs are seen during the course of RSE in critically ill children and are associated with seizure recurrence. A lower mortality rate occurs in children with GPDs compared to adult counterparts, likely related to different etiologies. Although the significance of GPDs must be determined within the context of the clinical situation, GPDs suggest a still active epileptic process.

Continuous EEG predictors of outcome in patients with altered sensorium

PurposeTo evaluate EEG predictors of outcome in patients with altered sensorium suspected to have seizure and to assess whether short term EEG is as effective as long term continuous EEG (cEEG) in predicting the outcome of patients with altered sensorium due to neurological causes. MethodsWe identified 99 consecutive critically ill patients with altered sensorium in whom nonconvulsive seizures were suspected. They underwent cEEG. Functional outcome was assessed with the modified Rankin Scale (mRS) at 4 weeks, discharge or death. We compared efficacy of short term EEG and long term continuous EEG in recording the abnormal patterns on EEG. Logistic regression analysis was performed to identify EEG findings associated with poor outcome, defined as mRS 4–6 (dead or moderately to severely disabled). ResultsPoor outcome was associated with nonconvulsive seizures (NCS), nonconvulsive status epilepticus (NCSE), periodic lateralized epileptiform discharges (PLEDS), PLEDS plus, generalized periodic epileptiform discharges (GPEDS) and abnormal EEG background. Short term EEG can detect seizure activity and other electrographic markers of poor outcome but the values are statistically insignificant. ConclusioncEEG monitoring provides independent prognostic information in patients with altered sensorium and suspected seizures. Unfavorable findings include nonconvulsive seizures, periodic epileptiform discharges and abnormal background. Short term EEG is ineffective in detecting seizures on EEG in patients with altered sensorium and should not be used as substitute for Long term EEG

Abstract 53: Abnormal Continuous Electroencephalography Recordings Are Not Predictive of Survival Outcomes Following Cardiac Arrest

Background: Cerebral anoxia following cardiac arrest can lead to poor neurological outcomes. Post-arrest therapeutic hypothermia (TH) has been shown to be neuroprotective in this setting. Early prognostication of survival outcomes is important for patient care and resource management. The use of continuous electroencephalography (cEEG) may be an important tool for prognostication of survival outcomes after cardiac arrest. Objectives: To determine if abnormal cEEG recordings are associated with survival outcomes following cardiac arrest. Methods: Retrospective study of all patients who suffered an in- or out-of-hospital cardiac arrest and were entered into the post-arrest management protocol (PAMP) at a single academic institution between May 2011 and May 2012. As part of the PAMP, cEEGs are recorded during TH, during the rewarming phase, and at normothermia. All cEEG reports were assessed for routinely described abnormal patterns: severe suppression, burst suppression, status epilepticus, intermittent epileptiform discharges (IED), generalized periodic epileptiform discharges (GPED), either α,β, or [[Unable to Display Character: ▵]] coma, or diffuse intermixed slowing. Descriptive statistics were analyzed. Results: Ninety-one patients were admitted to the ICU after cardiac arrest and 42 patients had PAMP and TH initiated. Of these, 36 (86%) received a neurologic consultation and 27(64%) had a cEEG placed. 24/27 (89%) survived to 24 hours and 7/27 (26%) survived to hospital discharge. Of the 7 survivors to discharge, 1 had severe suppression, 3 demonstrated α,β, or [[Unable to Display Character: ▵]] coma, and 3 demonstrated diffuse intermixed slowing during MTH. During early rewarming and normothermia, 3 had diffuse intermixed slowing, 2 demonstrated either α,β, or [[Unable to Display Character: ▵]] coma, and 1 demonstrated IEDs. Conclusion: Abnormal cEEG during MTH and early rewarming is not predictive of survival outcomes following cardiac arrest in this small, retrospective study. This study is limited by the small number of enrolled patients who have completed the protocol to date.

Generalized periodic discharges

Continuous EEG monitoring (cEEG) is increasingly employed to detect nonconvulsive seizures (NCSz) and nonconvulsive status epilepticus (NCSE) in critically ill patients. A recent international survey of 338 neurologists found that 83% use cEEG at least monthly.1 The growth in cEEG utilization has led to an increase in the recognition of EEG patterns of uncertain diagnostic and prognostic implications. Generalized periodic discharges (GPDs), formerly referred to as generalized periodic epileptiform discharges (GPEDs), represent one such pattern. GPDs are defined as the repetition of frontal- or occipital-dominant, synchronous, relatively symmetric discharges.2 They have relatively uniform morphology and duration with a definable and quantifiable interval between consecutive waveforms, with recurrence …

Periodic electroencephalographic patterns: usefulness of definition and classification

identified a peri-odic and lateralized pattern, which they described as periodic lateralized epilepti-form discharges (PLEDs). The acronym encapsulates the essential characteristics of PLEDs, namely, wide distribution, polymorphism, one or more sharp components in a repeti-tive way (usually at the rate of one to two seconds), and localization over the hemisphere. Subsequent studies have described other variable periodic patterns as two independent PLED types in the same EEG (BIPLEDs), multifocal PLEDs, generalized periodic epileptiform dis-charges (GPEDs), and stimulus-induced rhythmic, periodic, or ictal discharges (SIRPIDs)

Centromedian thalamic nuclei deep brain stimulation in refractory status epilepticus

Refractory status epilepticus (RSE) is associated with high mortality. We report a potential treatment alternative. Deep brain stimulation (DBS) of the centromedian thalamic nuclei (CMN) can be effective in the treatment of RSE. Report of the evolution of RSE after DBS of the CMN in a 27-year-old man. In the course of an encephalopathy of unknown origin, and after a cardiac arrest, the patient developed RSE with myoclonic jerks and generalized tonic-clonic seizures. The EEG showed continuous generalized periodic epileptiform discharges (GPEDS). Five weeks after RSE onset, bilateral DBS of the CMN was started. This treatment was immediately followed by disappearance of tonic-clonic seizures and GPEDS, suggesting a resolution of RSE. The patient continued having multifocal myoclonic jerks, probably subcortical in origin, which resolved after 4 weeks. The patient remained clinically stable for 2 months in a persistent vegetative state. The remission of RSE, the abolition of GPEDS, and the patient survival suggest that DBS of the CMN may be efficacious in the treatment of refractory, generalized status epilepticus.

Generalized Periodic Epileptiform Discharges in Critically Ill Children

Generalized periodic epileptiform discharges (GPEDs) are a specific periodic EEG pattern, reported with status epilepticus (SE) or a metabolic or an anoxic encephalopathy in critically ill patients. In this study, we examined the clinical course and evolution of EEG findings associated with GPEDs in children with refractory convulsive SE. The EEG reports of 279 children with SE diagnosed between 2002 and 2010 were reviewed to detect GPEDs. Ten children were identified with GPEDs on continuous EEG recording. The entire EEG recording was available for review in only six children. In the clinical course, seizure characteristics and evolution of EEG findings were analyzed. Six children (age, 5 to 17 years) were admitted to the intensive care unit with refractory convulsive SE. All had acute symptomatic SE except for one child with a history of epilepsy and developmental delay. Intravenous anesthetic agents were used to treat convulsive SE in five children. After tapering the intravenous anesthetic agents, GPEDs were seen on the continuous EEG recording, nonconvulsive seizures occurred in five, and nonconvulsive SE in four children. None of the children returned to baseline, and three children died. Generalized periodic epileptiform discharges are seen during the treatment course of convulsive SE in children and heralded seizure recurrence. We found a sequential evolution of the EEG patterns after the control of convulsive SE, with GPEDs occurring in a dynamic fashion in a continuum along with burst suppression and electrographic seizures. Recognizing that GPEDs represent a still active epileptic state after the control of convulsive SE with intravenous anesthetic agents and modifying the treatment regimen to control GPEDs may prevent immediate seizure recurrence.

How useful is EEG and EEG monitoring in the acutely ill and how to interpret it?

How useful is EEG and EEG monitoring in the acutely ill and how to interpret it?

Assessment of hairline EEG as a screening tool for nonconvulsive status epilepticus: Response to Bubrick et al.

To the Editors: We thank Dr. Bubrick and her colleagues for interest in our paper. In their letter to Epilepsia (Bubrick et al., 2007), they raise some interesting points for discussion. Overall, they disagree with our conclusions because they feel the sensitivity and specificity for detection of nonconvulsive status epilepticus (NCSE) with a hairline electroencephalogram (EEG) is adequate, and that waiting to obtain a standard EEG will needlessly delay treatment decisions. Moreover, they routinely use this practice and have found it useful (Milligan & Bromfield, 2005). Since the impetus for our study was the delay in obtaining urgent and emergent EEG, we agree that a more rapid assessment would be preferable. Bubrick et al. suggest that the sensitivity and specificity of hairline EEG is adequate for this purpose. In our study, the sensitivity for detecting electrographic seizures was 72% and for periodic lateralized epileptiform discharges (PLED) was only 54% (Kolls & Husain, 2007). Certainly the detection of PLED is very important, since in certain situations it may represent an ictal or interictal pattern. Additionally, a review of the misinterpretations reveals that 33 seizure and 42 PLED patterns were misinterpreted as diffuse slowing (see Figs 3 and 4 in Kolls & Husain, 2007). Moreover, seven patterns with diffuse slowing were misinterpreted as seizures, PLED, or generalized periodic epileptiform discharges (GPED). These are significant errors that may gravely impact patient care. It should also be noted that samples in our study were interpreted by experience neurophysiologists; interpretation by neurology residents resulted in even lower sensitivities and specificities (unpublished data). Consequently, we maintain that a hairline EEG is inadequate for diagnosing NCSE. Bubrick et al. note that patterns of NCSE were not studied. The patterns that were selected, such as electrographic seizures, PLED, and GPED, were not random, and are very likely to be present in patients in NCSE. Identification of these patterns would warrant an emergent EEG and possibly treatment of NCSE. Knowledge of the clinical situation, while always helpful, would be only of marginal additional utility. Bubrick et al. also noted that they have taught the hairline EEG technique to their residents and have found it useful (Milligan & Bromfield, 2005). Unfortunately, the reference cited to support this claim of usefulness includes a single patient who was found to be in NCSE with a hairline EEG. We do not dispute that for the occasional patient, hairline EEG may reveal the correct diagnosis. However, anecdotal studies and case reports cannot establish the utility of this technique. Indeed, it was our belief that this technique would be adequate for and expedite the diagnosis of NCSE, However, our data has shown otherwise. Bubrick et al. are encouraged to evaluate their data in a prospective manner and publish their results. Emergent EEG is time consuming and not universally available. Though quicker and easier to obtain, hairline EEG does not appear to be an adequate substitute. Further research on this and other alternatives is needed to determine the best method for quickly and accurately determining whether a patient is in NCSE.

Nonconvulsive Seizures in the Pediatric Intensive Care Unit: Out of Sight, Out of Mind?

Nonconvulsive Seizures in the Pediatric Intensive Care Unit: Etiology, EEG, and Brain Imaging Findings. Saengpattrachai M, Sharma R, Hunjan A, Shroff M, Ochi A, Otsubo H, Cortez MA, Carter Snead O III. Epilepsia 2006;47(9):1510–1518. PURPOSE: To determine the occurrence of nonconvulsive seizures (NCS) in the Pediatric Intensive Care Unit (PICU); to ascertain the relationship of NCS to past medical history, etiology, EEG, and brain imaging; and to determine the concordance between abnormal EEG findings and neuroimaging abnormalities. METHODS: A retrospective review was conducted of all pediatric patients who were admitted or transferred to the PICU from January 2000 to December 2003 with an unexplained decrease in level of consciousness, no overt clinical seizures, and EEG recordings performed within the 24 hours of onset of an altered state of consciousness. RESULTS: Twenty-three of 141 patients who met criteria for inclusion in the study (16.3%) were found to have NCS. The male-to-female ratio was 1.9:1. The largest group of patients (43%) had no preexisting neurological condition prior to the onset of NCS. In the remainder, the etiology of NCS included: acute structural brain lesion (48%), acute nonstructural brain lesion (22%), epilepsy-related seizure (13%), and others (17%). Epileptic foci were lateralized to the right side in 39.2%, the left side in 30.4%, and were bilateral in 30.4%. Of 23 patients with NCS, 18 (78.3%) demonstrated abnormal neuroimaging. In 10 of 18 of these patients (55.6%), the findings on neuroimaging were concordant with the lateralization found on EEG ( p &lt; 0.05, Fisher's exact test). CONCLUSIONS: NCS are not uncommon in pediatric patients with an altered state of consciousness. Almost half of the patients were previously healthy especially if they were under 6 months of age. This report highlights the importance of clinical awareness of NCS in the PICU. Nonconvulsive Status Epilepticus in Children: Clinical and EEG Characteristics. Tay SK, Hirsch LJ, Leary L, Jette N, Wittman J, Akman CI. Epilepsia 2006;47(9):1504—1509. BACKGROUND: Nonconvulsive status epilepticus (NCSE) is a highly heterogeneous clinical condition that is understudied in the pediatric population. OBJECTIVE: To analyze the epidemiological, clinical, and electroencephalograpic features in pediatric patients with NCSE. METHODS: We identified 19 pediatric patients with NCSE from the epilepsy database of the Comprehensive Epilepsy Center at Columbia University between June 2000 and December 2003. Continuous EEG monitoring was analyzed and chart review was performed. RESULTS: The patients ranged from 1 month old to 17 years of age. Five patients developed NCSE following convulsive status epilepticus (CSE), and a further 12 patients developed NCSE after brief convulsions. Two developed NCSE as the first manifestation during a comatose state following hypoxic events. Acute hypoxic-ischemic injury was the most frequent etiology of NCSE in our population (5 of 19; 26%), followed by exacerbation of underlying neurometabolic disease (4 of 19; 21%), acute infection (3 of 19; 16%), change in antiepileptic drug regimen (3 of 19; 16%), refractory epilepsy (2 of 19; 11%), and intracranial hemorrhage (2 of 19; 11%). Six patients had associated periodic lateralized epileptiform discharges (PLEDs), one had generalized periodic epileptiform discharges (GPEDs). Five (5 of 19; 26%) patients died of the underlying acute medical illness. Periodic discharges were associated with worse outcome. CONCLUSIONS: The majority of our patients with NCSE had preceding seizures in the acute setting prior to the diagnosis of NCSE, though most of these seizures were brief, isolated convulsions (12 patients) rather than CSE (five patients). Prolonged EEG monitoring to exclude NCSE may be warranted in pediatric patients even after brief convulsive seizures. Prompt recognition and treatment may be necessary to improve neurological outcome.

Nonconvulsive Status Epilepticus in Children: Clinical and EEG Characteristics

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