Benign Epileptiform Transients Of Sleep Research Articles

Normal variants and artifacts: importance in EEG interpretation.

Overinterpretation of EEG is an important contributor to the misdiagnosis of epilepsy. For the EEG to have a high diagnostic value and high specificity, it is critical to recognize waveforms that can be mistaken for abnormal patterns. This article describes artifacts, normal rhythms, and normal patterns that are prone to being misinterpreted as abnormal. Artifacts are potentials generated outside the brain. They are divided into physiologic and extraphysiologic. Physiologic artifacts arise from the body, and include EMG, eyes, various movements, EKG, pulse, and sweat. Some physiologic artifacts can be useful for interpretation such as EMG and eye movements. Extraphysiologic artifacts arise from outside the body, and in turn can be divided into the environments (electrodes, equipment, cellphones) and devices within the body (pacemakers, neurostimulators) Normal rhythms can be divided into awake patterns (alpha rhythm and its variants, mu rhythm, lambda waves, posterior slow waves of youth, HV-induced slowing, photic driving, photomyogenic response) and sleep patterns (POSTS, vertex waves, spindles, K complexes, sleep-related hypersynchrony, frontal arousal rhythm). Breach can affect both awake and sleep rhythms. Normal variants or variants of uncertain clinical significance include variants that may have been considered abnormal in the early days of EEG but are now considered normal. These include wicket spikes and wicket rhythms (the most common normal pattern over-read as epileptiform), small sharp spikes (aka benign epileptiform transients of sleep), rhythmic midtemporal theta of drowsiness (aka psychomotor variant), Cigánek rhythm (aka midline theta), 6 Hz phantom spike-wave, 14&6 Hz positive spikes, subclinical rhythmic epileptiform discharges of adults (SREDA), slow fused transients, occipital spikes of blindness, and temporal slowing of the elderly. Correctly identifying artifacts and normal patterns can help avoid overinterpretation and misdiagnosis. This is an educational review paper addressing a learning objective of the International League Against Epilepsy (ILAE) curriculum.

WS1.3. Normal EEG: Drowsiness and Sleep, and Normal Variants

The EEG in the normal awake child and adult is well known and needs to be known for proper reading and reporting and identifying an abnormal transient or pattern. The following are points of emphasis: Alpha rhythm seen after age of 5 years, Significant theta activity (4–7 Hz) is present in the EEG of children and adolescents. Delta activity in the awake tracing is rarely seen after the age of 5 years. Beta rhythm is seen anteriorly. All these will be discussed in details with traces. In the evaluation of abnormalities in the EEG, one needs to be constantly aware that there are many EEG transients that morphologically resemble epileptiform discharges and that need to be distinguished from diagnostically crucial epileptiform abnormalities to avoid overdiagnosis or misdiagnosis. These include: Artifacts: for example, electrode pop, muscle potentials, eye movements, electrocardiogram (EKG), chewing, electrical, etc. Normal components of ongoing background activity: for example, vertex sharp transients of sleep, f waves, slow wave sleep, POSTs, mu rhythm, lambda waves, drowsy activity during sleep in children that may often be associated with sharp components, etc. Epileptiform variants of dubious clinical significance: there are a large number of benign epileptiform variants that must be recognized, lest they be misinterpreted. Although morphologically similar, they are nonepileptogenic as they have no established relationship with the process responsible for generating epileptic seizures. Such sharp transients include 14 to 6 per second positive spikes, small sharp spikes or benign epileptiform transients of sleep, 6 Hz spike wave or phantom spike wave, wicket spikes, psychomotor variant pattern or rhythmic midtemporal discharges, breach rhythm, etc. Sleep not only activates diagnostically useful epileptiform EEG patterns, but also unmasks several types of nonepileptogenic sharp transients. It is necessary that anyone dedicating a career in epilepsy be well aware of these. Often reading EEG requires eyeballing and identifying patterns. The more the number of EEGs reviewed the more the possibility of not missing out normal patterns and rhythms. These will be demonstrated in various EEG epochs in the workshop.

Electromagnetic evidence that benign epileptiform transients of sleep are traveling, rotating hippocampal spikes

ObjectiveBenign epileptiform transients of sleep (BETS) have a unique voltage topography and a posteriorly propagating, inferiorly rotating diphasic EEG pattern. The source generators of BETS have not been definitively identified. We aimed to clarify the cerebral localization of BETS using MEG and electromagnetic source imaging (EMSI). MethodsWe analyzed BETS recorded with simultaneous MEG and EEG in four patients with epilepsy. Magnetic source imaging (MSI) and EMSI using equivalent current, single moving and rotating dipole inverse models was performed on averaged BETS potentials. MEG beamforming was performed in one case with abundant BETS. ResultsMSI and EMSI revealed hippocampal dipole source maxima in all cases, with current flow direction rotating from inferomedial to superomedial or superolateral between the first and second BETS peaks. Moving dipole analyses revealed spatiotemporal propagation along the anterior-posterior hippocampal axis and concomitant electromagnetic field rotation. Beamformer source reconstruction revealed an identical hippocampal localization. ConclusionsConverging evidence from different electromagnetic inverse modeling methods indicates that BETS are traveling, rotating hippocampal spikes, whose diphasic waveform is due to back and forth propagation along the anterior-posterior axis of the hippocampus. SignificanceThe hippocampal localization and longitudinal, rotating propagation pattern of BETS raises the possibility of a sleep-related functional role for these hippocampal spikes.

T160. Magnetoencephalography findings of benign epileptiform transients of sleep on scalp EEG in three patients with temporal lobe epilepsy

Introduction Benign epileptiform transients of sleep (BETS) is a finding on electroencephalography, defined as monophasic or diphasic transients with low amplitude ( μ V) and short duration ( Methods Patient 1, a 37-year-old right-handed male, was diagnosed with left TLE. Complex partial seizures started from age 15 years. Video-EEG (VEEG) showed interictal left anterior and posterior temporal sharp waves, and left temporal seizure onset was suggested. Magnetic resonance (MR) imaging revealed a mass lesion in the left lateral temporal lobe, suspected to be dysembryoplastic neuroepithelial tumor. Patient 2, a 38-year-old right-handed male, was diagnosed with left TLE. Complex partial seizures started from age 20 years. VEEG showed interictal bilateral independent temporal spikes, and left temporal seizure onset was suggested. MR imaging showed no abnormalities. Patient 3, a 33-year-old right-handed female, was diagnosed with right TLE. Complex partial seizures with oral automatism started from age 20 years. VEEG showed interictal right anterior temporal spikes, and right temporal seizure onset was suggested. MR imaging showed no abnormalities. All three patients underwent simultaneous EEG-MEG recording. EEG electrode placement used the 10–10 system with additional anterior temporal electrodes. MEG used a 200 channel whole-head system (MEGvision PQA160C, Ricoh Company, Ltd., Tokyo, Japan). The study investigated MEG activities correlated with EEG findings concordant with BETS. Results In Patient 1, MEG spikes correlated with BETS in the left temporal lobe had epileptic form, with high amplitude spike activity followed by slow wave activity. The source as evaluated with equivalent current dipoles was estimated around the left temporal lesion. In Patient 2, MEG spikes correlated with BETS in the right temporal lobe had epileptic form, with high amplitude spike activity followed by slow wave activity. No activity fulfilling the definition of BETS was detected in the left hemisphere. In Patient 3, no apparent MEG activity correlated with BETS was seen in the right temporal lobe. Conclusion The present study demonstrated variations in MEG findings correlated with EEG BETS in patients with TLE. These results may indicate heterogeneous background of BETS, so that only some BETS have an epileptic mechanism.

Electroencephalography Findings in Healthy and Finnish Spitz Dogs with Epilepsy: Visual and Background Quantitative Analysis

Background: Qualitative and quantitative electroencephalography (EEG) parameters of healthy and Finnish Spitz dogs with epilepsy have not been determined.Objective: To determine if EEG can provide specific characteristics to distinguish between healthy dogs and dogs with epilepsy.Animals: Sixteen healthy and 15 Finnish Spitz dogs with epilepsy.Methods: A prospective clinical EEG study performed under medetomidine sedation. Blinded visual and quantitative EEG analyses were performed and results were compared between study groups.Results: Benign epileptiform transients of sleep and sleep spindles were a frequent finding in a majority of animals from both groups. The EEG analysis detected epileptiform activity in 3 Finnish Spitz dogs with epilepsy and in 1 healthy Finnish Spitz dog. Epileptiform activity was characterized by spikes, polyspikes, and spike slow wave complexes in posterior‐occipital derivation in dogs with epilepsy and with midline spikes in control dog. The healthy dogs showed significantly less theta and beta activity than did the dogs with epilepsy (P< .01), but the only significant difference between healthy dogs and dogs with untreated epilepsy was in the alpha band (P< .001). Phenobarbital treatment increased alpha, beta (P< .001), and theta (P< .01), and decreased delta (P< .001) frequency bands compared with dogs with untreated epilepsy.Conclusions and Clinical Importance: Benign epileptiform transients of sleep could be easily misinterpreted as epileptiform activity. Epileptiform activity in Finnish Spitz dogs with epilepsy seems to originate from a posterior‐occipital location. The EEG of dogs with epilepsy exhibited a significant difference in background frequency bands compared with the control dogs. Phenobarbital treatment markedly influenced all background activity bands. Quantitative EEG analysis, in addition to visual analysis, seems to be a useful tool in the examination of patients with epilepsy.

Electroencephalography Findings in Healthy and Finnish Spitz Dogs with Epilepsy: Visual and Background Quantitative Analysis

Qualitative and quantitative electroencephalography (EEG) parameters of healthy and Finnish Spitz dogs with epilepsy have not been determined. To determine if EEG can provide specific characteristics to distinguish between healthy dogs and dogs with epilepsy. Sixteen healthy and 15 Finnish Spitz dogs with epilepsy. A prospective clinical EEG study performed under medetomidine sedation. Blinded visual and quantitative EEG analyses were performed and results were compared between study groups. Benign epileptiform transients of sleep and sleep spindles were a frequent finding in a majority of animals from both groups. The EEG analysis detected epileptiform activity in 3 Finnish Spitz dogs with epilepsy and in 1 healthy Finnish Spitz dog. Epileptiform activity was characterized by spikes, polyspikes, and spike slow wave complexes in posterior-occipital derivation in dogs with epilepsy and with midline spikes in control dog. The healthy dogs showed significantly less theta and beta activity than did the dogs with epilepsy (P < .01), but the only significant difference between healthy dogs and dogs with untreated epilepsy was in the alpha band (P < .001). Phenobarbital treatment increased alpha, beta (P < .001), and theta (P < .01), and decreased delta (P < .001) frequency bands compared with dogs with untreated epilepsy. Benign epileptiform transients of sleep could be easily misinterpreted as epileptiform activity. Epileptiform activity in Finnish Spitz dogs with epilepsy seems to originate from a posterior-occipital location. The EEG of dogs with epilepsy exhibited a significant difference in background frequency bands compared with the control dogs. Phenobarbital treatment markedly influenced all background activity bands. Quantitative EEG analysis, in addition to visual analysis, seems to be a useful tool in the examination of patients with epilepsy.

Benign Epileptiform Transients of Sleep (BETS) Are Not Associated with Symptoms of Sleep Disorders

ABSTRACT.One hundred patients with benign epileptiform transients of sleep (BETS) seen on their electroencephalograms (EEGs) were compared with 100 control patients without BETS in reference to their sleep habits, sleep disruptions, and daytime sleepiness. No statistically significant differences between the two groups were observed. We believe that BETS are not markers of subjective sleep abnormalities.

Sharp transients in the sleep EEG of healthy adults: a possible pitfall in the diagnostic assessment of seizure disorders

The use of sleep EEG recordings is a routine procedure in the diagnostic work up of patients with suspected epilepsy. With respect to the diagnostic significance of paroxysmal EEG phenomena it is of importance to be informed about the incidence of such paroxysms in EEG's of healthy subjects. Several benign paroxysmal EEG phenomena during drowsiness or sleep have been identified (benign epileptiform transients of sleep (BETS), 14 and 6 positive spikes). Recent studies have shown that other, apparently aspecific, paroxysmal sharp transients may be recorded during drowsiness or sleep in healthy subjects. In order to obtain more data on such paroxysmal EEG phenomena during sleep, a qualitative and semi quantitative analysis was performed on full night sleep recordings from 60 carefully selected healthy volunteers. Only 4 recordings were completely without the studied phenomena, all others showed some suspicious paroxysmal transients and some rare yet true specific epileptiform discharges were recorded in 8 subjects (13%), predominantly during transient periods of light non-REM sleep in the first two sleep cycles. The presence of some sharp transients during drowsiness or light sleep thus should be considered as a non-specific and non-pathological finding. Moreover these findings indicate the limited diagnostic specificity of the presence of a few epileptiform discharges during sleep, especially in patients with an ambiguous clinical history of epilepsy.

Are benign epileptiform transients of sleep (BETS) associated with symptoms of sleep disordres?

Are benign epileptiform transients of sleep (BETS) associated with symptoms of sleep disordres?

Epileptiform activity during opioid anesthesia

The proconvulsant properties of exogenously administered opioids in man are not established. We prospectively evaluated relationships between epileptiform activity and opioid dose in 20 patients undergoing coronary artery revascularization. Baseline electroencephalograms were performed before surgery. Ten subjects were given fentanyl and 10 sufentanil, at 100 μg/kg and 10 μg/kg, respectively, in 4 divided doses, 3 min apart. Midazolam (4 mg) was given 3 min after the last dose of narcotic. Serum opioid concentrations were measured by radioimmunoassay. Within 3 min of the first opioid dose, 19 of 20 patients developed epileptiform activity, characterized by generalized single and multiphasic, low-to-moderate voltage spike discharges, similar in appearance to benign epileptiform transients of sleep (BETS). Despite continuously increasing serum concentrations of opioid, the number of spike discharges initially increased during the first and second dose intervals and then declined during the third and fourth dose intervals. This dissociation between epileptiform discharges and measured serum opioid concentration was unexpected and remained unexplained. Spike activity was consistently attenuated ( P = 0.000003) within 20 sec of midazolam administration. Abrupt cessation of discharges after administration of the anticonvulsant, midazolam, suggests an epileptogenic mechanism for the opioid-induced activity.

Effect of Epilepsy and Sleep Deprivation on the Rate of Benign Epileptiform Transients of Sleep

Seventy-eight individuals with EEG records containing benign epileptiform transients of sleep (BETS) were identified among 7,400 records reviewed in our laboratory in a 6-year period. The records contained no other abnormality in 51 patients (65%). Genuine epileptiform discharges were found in the records of 19 patients; 14 had a history of epilepsy. Thirty-five patients (45%) had a proven history of epilepsy with antiepileptic drug (AED) therapy. In the records of these patients, the mean number of BETS per unit of time was significantly higher (11.88 +/- 2) than in the record of the rest of the laboratory population with BETS (6.89 +/- 0.9) (p less than 0.02). Among five conventional surface montages, ipsilateral ear referential montage (IERM) showed a significantly higher number of BETS per unit of time than did any other surface montage used in the study. Thirty-nine records (50%) were performed after sleep deprivation (SD). When only IERM was considered, SD records showed a significantly higher number of BETS per unit of time (7.36 +/- 1.1) than did non-SD records (3.89 +/- 0.69) (p less than 0.01). Our findings support the general consensus that individual BETS may be normal variants, but a high occurrence of BETS in the record should raise suspicion of underlying epilepsy.

Clinical implications of benign epileptiform transients of sleep

One hundred electroencephalograms (EEGs) with benign epileptiform transients of sleep (BETS) were reviewed. The incidence of epileptic seizures, syncope, headaches, transient ischemic attacks (TIAs), dizziness and psychiatric complaints was determined. The incidence of these symptoms was similarly ascertained for another group of patients whose sleep EEGs had preceded (96 patients) or followed (96 patients) each of the BETS EEGs. These patients formed 2 separate internal control groups. No significant differences in the demographic composition of the 3 groups or in the incidence of symptoms or diagnoses were noted. The patients with BETS were also divided into 2 groups according to whether their EEGs were otherwise normal or abnormal. Each of these 2 groups was compared with their respective control group (pre- or post-BETS patients with normal or abnormal EEGs). No significant differences in the incidence of seizures were noted. Benign temporal epileptiform transients of sleep appear to be an occasional but clinically unimportant finding in sleep tracings.

Benign epileptiform transients of sleep. Clarification of the small sharp spike controversy.

Electroencephalograms were performed on 120 normal subjects sleep deprived for 24 hours. Twenty-four percent of the volunteers exhibited one or more epileptiform transients during stages 1 or 2 of non-rapid eye movement sleep. These potentials usually appeared as monophasic or diphasic spikes unaccompanied by sharp waves or focal slowing. When abundant, they occurred sporadically and independently over both hemispheres but were best developed in the anteromesial temporal regions. A 20 percent incidence of similar spikes was found in 599 consecutively referred patients recorded under the same conditions. We conclude that these epileptiform transients of sleep, which have been called "small sharp spikes," are normal and are of no diagnostic value in the evaluation of patients with seizures.