Epileptiform Electroencephalogram Research Articles

Epileptiform electroencephalogram discharges increase seizure recurrence risk in patients with acute symptomatic seizure due to a structural brain lesion

ObjectiveThe risk factors for seizure recurrence after acute symptomatic seizure due to a structural brain lesion are not well established. The aim of this study was to analyze possible associations between demographic, clinical, and electroencephalographic variables and epilepsy development in patients with acute symptomatic seizure due to an acute structural brain lesion. MethodsWe designed an observational prospective study of patients with acute symptomatic seizure due to an acute structural brain lesion (hemorrhagic stroke, ischemic stroke, traumatic brain injury, or meningoencephalitis) who underwent EEG during their initial admission between January 2015 and January 2020. We analyzed prospectively recorded demographic, clinical, electroencephalographic (EEG), and treatment-related variables. All variables were compared between patients with and without seizure recurrence during 2 years of follow up. ResultsWe included 194 patients (41.2 % women; mean [SD] age, 57.3 [15.8] years) with acute symptomatic seizure due to an acute structural brain lesion. They all underwent EEG during admission and were followed for at least 2 years. The identifiable causes were hemorrhagic stroke (44.8 %), ischemic stroke (19.5 %), traumatic brain injury (18.5 %), and meningoencephalitis (17 %). Fifty-six patients (29 %) experienced a second seizure during follow-up. Seizure recurrence was associated with epileptiform discharges on EEG (52% vs 32 %; OR 2.3 [95 % CI, 1.2–4.3], p = 0.008) and onset with status epilepticus (17% vs 0.05 %, OR 4.03 [95 % CI 1.45–11.2], p = 0.009). ConclusionsEpileptiform discharges on EEG and status epilepticus in patients with acute symptomatic seizure due to an acute structural brain lesion are associated with a higher risk of epilepsy development.

GRP-DNet: A gray recurrence plot-based densely connected convolutional network for classification of epileptiform EEG

BackgroundThe classification of epileptiform electroencephalogram (EEG) signals has been treated as an important but challenging issue for realizing epileptic seizure detection. In this work, combing gray recurrence plot (GRP) and densely connected convolutional network (DenseNet), we developed a novel classification system named GRP-DNet to identify seizures and epilepsy from single-channel, long-term EEG signals. New methodsThe proposed GRP-DNet classification system includes three main modules: 1) input module takes an input long-term EEG signal and divides it into multiple short segments using a fixed-size non-overlapping sliding window (FNSW); 2) conversion module transforms short segments into GRPs and passes them to the DenseNet; 3) fusion and decision, the predicted label of each GRP is fused using a majority voting strategy to make the final decision. ResultsSix different classification experiments were designed based on a publicly available benchmark database to evaluate the effectiveness of our system. Experimental results showed that the proposed GRP-DNet achieved an excellent classification accuracy of 100 % in each classification experiment, Furthermore, GRP-DNet gave excellent computational efficiency, which indicates its tremendous potential for developing an EEG-based online epilepsy diagnosis system. Comparison with existing methodsOur GRP-DNet system was superior to the existing competitive classification systems using the same database. ConclusionsThe GRP-DNet is a potentially powerful system for identifying and classifying EEG signals recorded from different brain states.

Effect of dexmedetomidine on sevoflurane anesthesia-induced cortical epileptiform electroencephalogram activity in neonatal rats

Objective To evaluate the effect of dexmedetomidine on sevoflurane anesthesia-induced cortical epileptiform electroencephalogram (EEG) activity in the neonatal rats. Methods Forty clean-grade healthy Sprague-Dawley rats, aged 4-6 days, weighing 8-15 g, were divided into 5 groups (n=8 each) using a random number table method: control group (C group), sevoflurane group (S group), dexmedetomidine plus sevoflurane group (D+ S group), dexmedetomidine plus alpha 2-adrenoceptor antagonist atipamezole plus sevoflurane group (D+ A+ S group), and atipamezole plus sevoflurane group (A+ S group). After the electrode was correctly placed, the EEG was continuously monitored, and normal saline 5 μl/g was intraperitoneally injected at 58 min of monitoring in group C, dexmedetomidine 25 μg/kg was intraperitoneally injected in group D+ S, dexmedetomidine 25 μg/kg and atipamezole 250 μg/kg were intraperitoneally injected in group D+ A+ S, and atipamezole 250 μg/kg was intraperitoneally injected in group A+ S.Anesthesia was induced by inhaling 6% sevoflurane for 3 min starting from 60 min of monitoring and then maintained by inhaling 2.1% sevoflurane for 1 h. The total duration, the number and average duration of epileptic waves were recorded during anesthesia.Blood samples were obtained from the left ventricle after the end of anesthesia for blood gas analysis.Rats were then sacrificed and blood samples were collected for measurement of the serum corticosterone concentration. Results No epileptic wave was found in group C. The serum concentration of corticosterone was significantly higher in the other four groups than in group C (P 0.05). Compared with group D+ S, the total duration of epileptic wave was significantly prolonged, the number of epileptic wave was increased, and the serum concentration of corticosterone was increased in D+ A+ S and A+ S groups (P<0.05). Conclusion Dexmedetomidine can inhibit the occurrence of cortical epileptiform EEG activity induced by sevoflurane anesthesia in the newborn rats, and the mechanism may be related to improving the hypothalamus-pituitary-adrenocortical axis hyperfunction mainly through activating the central 2-adrenoceptor. Key words: Dexmedetomidine; Anesthetics, inhalation; Infant, newborn; Electroencephalograpy

Deficiency of aminopeptidase P1 causes behavioral hyperactivity, cognitive deficits, and hippocampal neurodegeneration.

Metabolic diseases affect various organs including the brain. Accumulation or depletion of substrates frequently leads to brain injury and dysfunction. Deficiency of aminopeptidase P1, a cytosolic proline-specific peptidase encoded by the Xpnpep1 gene, causes an inborn error of metabolism (IEM) characterized by peptiduria in humans. We previously reported that knockout of aminopeptidase P1 in mice causes neurodevelopmental disorders and peptiduria. However, little is known about the pathophysiological role of aminopeptidase P1 in the brain. Here, we show that loss of aminopeptidase P1 causes behavioral and neurological deficits in mice. Mice deficient in aminopeptidase P1 (Xpnpep1-/- ) display abnormally enhanced locomotor activities in both the home cage and open-field box. The aminopeptidase P1 deficiency in mice also resulted in severe impairments in novel-object recognition, the Morris water maze task, and contextual, but not cued, fear memory. These behavioral dysfunctions were accompanied by epileptiform electroencephalogram activity and neurodegeneration in the hippocampus. However, mice with a heterozygous mutation for aminopeptidase P1 (Xpnpep1+/- ) exhibited normal behaviors and brain structure. These results suggest that loss of aminopeptidase P1 leads to behavioral, cognitive and neurological deficits. This study may provide insight into new pathogenic mechanisms for brain dysfunction related to IEMs.

Role of NKCC1 in neurons in sevoflurane-induced epileptiform electroencephalogram activity in cortex of neonatal rats

Objective To evaluate the role of Na+ -K+ -2Cl- cotransporter isoform 1(NKCC1)in neurons in sevoflurane-induced epileptiform electroencephalogram(EEG)activity in the cortex of neonatal rats. Methods Twenty-four neonatal Sprague-Dawley rats, aged 4-6 days, weighing 8-15 g, were randomly divided into 3 groups(n=8 each)using a random number table: control group(group C), sevoflurane group(group S), and NKCC1 inhibitor bumetanide + sevoflurane group(group B). After electrodes were placed correctly, EEG was monitored continuously.At 30 min of monitoring, normal saline 3 μl/g was injected intraperitoneally in D and S groups, and bumetanide 10 μg/g was injected intraperitoneally in group B. At 60 min after the end of intraperitoneal administration, anesthesia was induced with inhalation of 6% sevoflurane for 3 min and maintained with inhalation of 2.1% sevoflurane for 1 h in group S and group B. The total duration of seizures, the duration of a single episode, the number of episodes of electroencephalographic seizures, and the amplitude and frequency of spike-and-wave were recorded. Results Seizures were not detected in group C, and no spike-and-wave was found in group B. Compared with group C, the incidence of seizures in S and B groups(75% and 25%, respectively)and incidence of spike-and-wave in group S(100%)were significantly increased(P<0.05). Compared with group S, the incidence of seizures and spike-and-wave was significantly decreased, the total duration of seizures, and duration of a single episode were significantly shortened, and the number of episodes of electroencephalographic seizures was significantly decreased in group B(P<0.05). Conclusion NKCC1 in neurons may be involved in the formation of sevoflurane-induced epileptiform EEG activity in the cortex of neonatal rats. Key words: Anesthetics, inhalation; Infant, newborn; Electroencephalography

Cognitive and electrophysiological characteristics of children with specific language impairment and subclinical epileptiform electroencephalogram

The current study is a preliminary examination of cognitive profiles and cortical distribution of the spectral power of different electroencephalogram (EEG) rhythms in children with specific language impairment and subclinical epileptiform discharges. Although a number of empirical studies point to higher incidence of abnormal EEGs in children with specific language impairment, only a few studies were found examining electrophysiological characteristics, such as locus of discharges and connections with cognitive functioning in this population of children. The sample included 12 children with specific language impairment (SLI) and abnormal EEG who underwent testing of cognitive functioning using the Wechsler Intelligence Scale for Children (WISC). The control sample included 13 children with specific language impairment and regular EEG. Results point to lower scores on several subtests of the performance scale for children with abnormal EEG than for the group with regular EEG. Detailed EEG analysis of cortical distribution of the spectral power of different EEG rhythms partially confirms the results of neuropsychological assessment, pointing to abnormal function of frontal and temporal regions. Higher values of spectral power of the delta brain rhythm in frontal regions are associated with lower results on the WISC performance scale. Results are discussed in the context of subgroups of the population of children with SLI.

Yield of epileptiform electroencephalogram abnormalities in incident unprovoked seizures: a population-based study.

The yield of epileptiform abnormalities in serial electroencephalography (EEG) studies has not been addressed in a population-based setting for subjects with incident epilepsy or a single unprovoked seizure, raising the possibility of methodologic limitations such as selection bias. Our aim was to address these limitations by assessing the yield and predictors of epileptiform abnormalities for the first and subsequent EEG recording in a study of incident epilepsy or single unprovoked seizure in Rochester, Minnesota. We used the resources of the Rochester Epidemiology Project to identify all 619 residents of Rochester, Minnesota, born in 1920 or later with a diagnosis of incident epilepsy (n = 478) or single unprovoked seizure (n = 141) between 1960 and 1994, who had at least one EEG study. Information on all EEG studies and their results was obtained by comprehensive review of medical records. Among subjects with epilepsy, the cumulative yield of epileptiform abnormalities was 53% after the first EEG study and 72% after the third. Among subjects with a single unprovoked seizure, the cumulative yield was 39% after the first EEG study and 68% after the third. Young age at diagnosis and idiopathic etiology were risk factors for finding epileptiform abnormalities across all EEG recordings. Although the cumulative yield of epileptiform abnormalities increases over successive EEG recordings, there is a decrease in the increment for each additional EEG study after the first EEG study. This is most evident in incident epilepsy and in younger subjects. Clinically it may be worthwhile to consider that the probability of finding an epileptiform abnormality after the third nonepileptiform EEG recording is low.

Epileptiform electroencephalogram abnormality in children with congenital sensorineural hearing loss

ObjectivesThis work was designed to study electroencephalogram findings in children with congenital sensorineural hearing loss and correlate these findings with the SNHL parameters as duration, etiology, severity, and type. MethodsNinety children with bilateral congenital sensorineural hearing loss served as the study group. They were free from any neurological disorders or symptoms that are commonly associated with abnormal electroencephalogram as convulsions or loss of consciousness. Twenty children having normal hearing with no history of otological or neurological disorders served as the control group. All children participating in the study were subjected to full medical and audiological history, otological examination, neurological examination, audiological evaluation and electroencephalogram recording. ResultsMean age of the children in the control group was 3.56±2.1 years and mean age of the children in the study group was 3.8±2.2 years. While none of the control children had abnormal electroencephalogram, 38 (42.2%) of children with congenital SNHL had epileptiform electroencephalogram abnormality. The epileptiform abnormality was generalized in 14 children (36.8%), focal temporal in 17 children (44.7%) and focal other than temporal in 7 children (18.4%). According to the hemispheric side affected, the abnormality was right in 14 children (36.8%), left in 10 children (26.3%) and bilateral in 14 children (36.8%). No statistically significant predominance of specific site or side of the epileptiform abnormality was found. Similarly, no statistical significant prevalent of the epileptiform abnormality was found in relation to the age or sex of children, duration of hearing loss or etiology of hearing loss (i.e., genetic vs. neonatal insults). On the other hand, the epileptiform abnormality was statistically prevalent in children with moderate degree of hearing loss, and in children with auditory neuropathy spectrum disorder. ConclusionsThe epileptiform electroencephalogram abnormality is a common finding in children with congenital sensorineural hearing loss especially those with auditory neuropathy spectrum disorder, suggesting the affection of the central nervous system despite the absence of neurological symptoms or signs. These findings raise the question of the requirement of medical treatment for those children and the effect of such treatment in their rehabilitation.

Prediction for relapse and prognosis of newly diagnosed epilepsy

The objective of this study was to investigate the timing of therapy initiation and other clinical factors as potential predictors for relapse and prognosis of epilepsy, based on hospital-based prospective observational data in China. One hundred and seventy-one newly diagnosed patients with one or more seizures were recruited and followed for at least 2 years. Kaplan-Meier survival analysis was used for calculating recurrence and remission rates. Univariate and multivariate analyses for risk factors were performed using Cox proportional hazards model. Among the 171 patients analyzed, more patients had partial (54.4%) than generalized seizures (45.6%). The range of patients' age was 6-70 years, but 70% were under 16 years of age. Multiple seizure types (HR = 2.01; 95% CI, 1.31-3.10), epileptiform electroencephalogram (EEG) abnormality (HR = 1.95; 95% CI, 1.09-3.49), and >1 seizure monthly before treatment (HR = 2.74; 95% CI, 1.69-4.51) were predictors of seizure recurrence. The best negative predictors of remission were as follows: relapse (HR = 0.13; 95% CI, 0.07-0.23) and epileptiform EEG within 1 year of treatment (HR = 0.61; 95% CI, 0.39-0.97). Delayed treatment after three or more seizures did not significantly increase the risk of recurrence (P = 0.70) or remission (P = 0.31) compared with early treatment after one or two seizures. Multiple seizure types, epileptiform EEG abnormality, and >1 seizure monthly before treatment predict seizure recurrence. Relapse and epileptiform EEG within 1 year of treatment predict adverse seizure outcome. Early treatment does not affect relapse or prognosis.

Chronic application of topiramate and carbamazepine differentially affects the EEG and penicillin-induced epileptiform activity in rats

Carbamazepine (CBZ) and topiramate (TPM) are among commonly used antiepileptic drugs. The acute actions of these drugs are well known but the effects of long-term use on partially induced epileptiform characteristics are yet to be clarified. The rats were received CBZ (154 mg/kg/day), TPM (10 mg/kg/day) or tap water by gavage. We investigated penicillin-induced cortical epileptiform activity and electroencephalogram spectral power of rats by using electrocorticogram recordings. Animals were anesthetized with i.p. urethane (1·25 g/kg). Analysis of electroencephalogram recordings prior to epileptiform activity revealed that 3-week treatment of CBZ significantly increased relative power of delta (P<0·01) while reduced alpha (P<0·017) and beta (P<0·017) relative power compared to both control group and TPM group. TPM had no effect on absolute power and relative power of any frequency band. TPM treatment of 21 days significantly reduced the spike frequency (P<0·01). This preventive effect was missing in CBZ-treated rats. Upon the application of the last dose of drugs during ongoing epileptiform activity, the drugs suppressed the epileptiform activity. However, TPM was more rapid and effective than CBZ. In conclusion, our in vivo electrophysiological data suggest that TPM is more effective in animal model of partial epilepsy at the applied doses in this study.

Anesthetic management of a child with Aicardi syndrome undergoing laparoscopic Nissen’s fundoplication: a case report

Aicardi syndrome (AS) is a rare congenital syndrome and is characterized by the triad of infantile spasm, agenesis of the corpus callosum, and anomaly of chorioretinal lacunae. We here report a case of a patient with AS under general anesthesia. Although there is no report in which muscle relaxants were used in AS patients, vecuronium bromide was used for artificial pneumoperitoneum in this case. Careful management is important for AS patients during an operation that significantly affects respiratory function. In addition, it is possible that muscle relaxants be administered safely in AS patients. Careful monitoring such as epileptiform electroencephalogram and bispectral index monitors may be needed for the early detection of epileptic activities.

Epileptiform Asymetries and Treatment Response in Juvenile Myoclonic Epilepsy

Epileptiform electroencephalogram (EEG) asymmetries are not uncommon in juvenile myoclonic epilepsy (JME) and can contribute to the misdiagnosis of this syndrome. The objective of this study is to further characterize patients with focal or asymmetric epileptiform electroencephalographic abnormalities and more specifically in terms of response to treatment. Controversial data exists in the literature concerning this issue. We retrospectively reviewed clinical and EEG data of a group of consecutive JME patients followed at our Epilepsy Service. The first EEG available for each patient was reviewed blindly by two independent electroencephalographers. Twenty-eight patients with JME were identified: 11 (39.3%) were resistant to at least one appropriate anti-epileptic drug (AED), including valproate, lamotrigine, topiramate or levetiracetam. All patients except two had generalized epileptiform abnormalities. Overall, EEG asymmetries were detected in 57.1% of the cases. The proportion of EEG asymmetries between AED-sensitive group (52.9%) and AED-resistant group (63.5%) did not reach statistical significance. Concordance between examiners for identification of EEG asymmetries was good. Analysis of patients with and without asymmetries showed no statistically significant differences in comparisons of age, family history of seizure, presence of polyspike and slow wave, photosensitivity and timing of EEG related to the onset of treatment. Asymmetric electroencephalographic abnormalities are frequent in patients with JME. These features should not be misinterpreted as being indicative of partial epilepsy. In our group, asymmetries were not associated with resistance to treatment.

Lower Bispectral Index Values in Children Who Are Intellectually Disabled

Very few data are available on the use of bispectral index (BIS) monitoring in children who are intellectually disabled. Epileptiform electroencephalogram activity, underlying cerebral pathology, or anticonvulsant/spasmolytic therapy might influence BIS monitoring. Our aim in this exploratory study was to first compare BIS values at 4 different stages of anesthesia between intellectually disabled children and controls. Our second aim was to investigate the discriminative properties of BIS between consciousness and unconsciousness for intellectually disabled children and for controls. Eighteen intellectually disabled children and 35 control children, aged 2-13 yr, were included. BIS values, landmark events, and standard monitoring values of vital functions were recorded throughout the whole procedure. The performance of BIS in distinguishing between a conscious and unconscious state was assessed from receiver operating characteristic curves. Median (interquartile range) BIS values for the intellectually disabled group were significantly lower than those for controls in the awake state (72 [48-77] vs 97 [84-98], P < 0.001), during stable intraoperative anesthesia (34 [21-45] vs 43 [33-52], P = 0.02), and during return of consciousness (59 [36-68] vs 73 [64-78], P = 0.009). The discriminative properties of the BIS monitor for the state of consciousness were comparable between the 2 groups according to the receiver operating characteristic curves. Nevertheless, the optimal cutoff BIS value for discrimination between conscious and unconscious state was 28 points lower for the intellectually disabled group. We advise anesthesiologists to be alert to possible lower BIS values in intellectually disabled children. There is a risk that they will inadvertently misinterpret the state of consciousness in intellectually disabled children. New multicenter studies must find the optimal manner of evaluating (un)consciousness in intellectually disabled patients with documented and confirmed specific etiologies of their intellectual disability.

Dexmedetomidine Does Not Reduce Epileptiform Discharges in Adults With Epilepsy

There are limited data on the effect of dexmedetomidine on epileptiform electroencephalogram (EEG). The aim of this study was to investigate if dexmedetomidine will abolish epileptiform discharges in patients with medically refractory seizure disorders who were candidates for surgery to resect foci of epileptic activity. With approval from the Institutional Review Board and written informed consent, we enrolled 5 patients with medically intractable seizures who were undergoing continuous video/EEG monitoring. EEG and hemodynamic values were recorded from 15 minutes before, during, and for 60 minutes after a 60-minute dexmedetomidine infusion. Epileptiform discharges were counted for each 15-minute epoch during the study. Two of the 5 patients had a discrete spike focus in each hemisphere. Thus, we analyzed the activity of 7 distinct foci. Epileptiform activity did not decrease in any individual focus during dexmedetomidine infusion. Although dexmedetomidine did not have a statistically significant effect on interictal epileptiform activity for the group as a whole, the activity of 4 foci increased during dexmedetomidine infusion. Dexmedetomidine did not reduce seizure focus activity and thus may be a suitable anesthetic adjunct during seizure surgery.

Neurobiological Consequences of Early Stress and Childhood Maltreatment: Are Results from Human and Animal Studies Comparable?

Recent studies have reported an association between exposure to childhood abuse or neglect and alterations in brain structure or function. One limitation of these studies is that they are correlational and do not provide evidence of a cause-effect relationship. Preclinical studies on the effects of exposure to early life stress can demonstrate causality, and can enrich our understanding of the clinical research if we hypothesize that the consequences of early abuse are predominantly mediated through the induction of stress responses. Exposure to early abuse and early stress has each been associated with the emergence of epileptiform electroencephalogram (EEG) abnormalities, alterations in corpus callosum area, and reduced volume or synaptic density of the hippocampus. Further, there is evidence that different brain regions have unique periods when they are maximally sensitive to the effects of early stress. To date, preclinical studies have guided clinical investigations and will continue to provide important insight into studies on molecular mechanisms and gene-environment interactions.

The effects of amount and frequency of pulsed direct current used in water bath stunning and of slaughter methods on spontaneous electroencephalograms in broilers

AbstractThe effectiveness of electrical water bath stunning of broilers (n = 96) for 1 s with a constant average current of 100, 150 or 200 mA delivered using a variable voltage/constant current stunner with 200, 800 or 1400 Hz pulsed direct current (DC), with a mark:space ratio of 1:1, followed by slaughter using a unilateral or ventral neck cutting procedure, was evaluated. The results of a binary logistic model showed that both the electrical frequency and average current had significant effects on the probability of inducing epileptiform electroencephalogram (EEG) and therefore, of effective stunning. The results of univariate analysis showed that only slaughter method had highly significant effects on the power contents in the 13–30 Hz and 2–30 Hz EEG frequency bands. Based on these results, it is recommended that a minimum of 200 mA average (400 mA peak) current per bird should be delivered using 200 Hz pulsed DC, with a mark:space ratio of 1:1, to achieve effective water bath stunning in 80% of broilers. Frequencies of above 200 Hz pulsed DC would presumably require average currents of greater than 200 mA. Electrical water bath stunning of broilers with 200 mA average current of 200 Hz resulted in cardiac arrest in six out of eight broilers that showed epileptiform activity. Two other broilers that had cardiac arrest showed no epileptiform EEGs indicative of effective stunning. Owing to the prevalence of cardiac arrest in conscious broilers, the use of pulsed DC for water bath stunning of broilers could be questioned on ethical and bird welfare grounds.

Three cases of PICU sedation with isoflurane delivered by the ‘AnaConDa®’

Prolonged sedation in the pediatric intensive care unit may be difficult because of tolerance, drug dependence and withdrawal, drug interactions and unwanted drug effects. We present three patients sedated with isoflurane via the Anesthetic Conserving Device, AnaConDa. AnaConDa is a modified heat and moisture exchanger that allows evaporation and delivery of inhalational anesthetics without an anesthesia machine, vaporizer or adapted ventilator. Two patients with abdominal complications and prolonged sedation for mechanical ventilation were converted to isoflurane sedation for several days. The third patient with refractory status epilepticus received isoflurane to treat epileptiform electroencephalogram activity. Patients weighing 40 and 30 kg were treated with AnaConDa placed at the Y-piece, while the patient weighing 20 kg was treated with AnaConDa in the inspiratory limb of the respiratory circuit. Adequate sedation was achieved with endtidal isoflurane concentration of 0.3-0.4%, while antiepileptic effect was achieved at a higher dose, 0.9%. Intravenous sedatives could be reduced or discontinued during isoflurane sedation. Inhaled sedation of isoflurane with AnaConDa was effective in these patients. It may provide an alternative in difficult cases needing prolonged sedation and should be evaluated further.

A Rapid Increase in the Inspired Concentration of Desflurane Is Not Associated with Epileptiform Encephalogram

The large inspired concentration of sevoflurane (S) during mask induction of anesthesia can induce epileptiform electroencephalogram (EEG) associated with tachycardia. Tachycardia is also seen when the concentration of desflurane (D) is abruptly increased. It is not known whether this is associated with epileptiform EEG similar to S. We studied EEG and heart rate (HR) during rapidly increased concentrations of S or D in 31 females during the postintubation period of anesthesia. Anesthesia was induced with propofol and remifentanil, and the tracheas were intubated. Patients were randomized to receive either S or D in nitrous oxide-oxygen mixture after intubation, at a small dose first. After 10 min, S or D vaporizer was advanced to the highest reading of the vaporizer (7% for S, 18% for D) for 5 min. HR and EEG were recorded. Epileptiform EEG activity was recorded in eight of 15 patients in group S and in none in group D (P < 0.05). HR increased in both groups. In group S, HR increased gradually and the highest HR value was 84 bpm at 5 min after the increase in sevoflurane concentration. In group D, HR increased to 93 bpm 2 min after the increase in desflurane concentration (no significant difference, S versus D). A rapid increase in the concentration of S frequently induces epileptiform EEG during normoventilation. Tachycardia during increasing concentrations of D is not associated with epileptiform EEG. A rapid increase in the concentration of sevoflurane induces epileptiform encephalogram (EEG) with tachycardia. A rapid increase in the concentration of desflurane also induces tachycardia but is not associated with epileptiform EEG.

Incidence of Epileptiform Electroencephalogram Activity during Induction of Anesthesia with Sevoflurane or Propofol in Children

Incidence of Epileptiform Electroencephalogram Activity during Induction of Anesthesia with Sevoflurane or Propofol in Children

Retrospective study of febrile seizures: subsequent electroencephalogram findings, unprovoked seizures and epilepsy in adolescents.

A retrospective questionnaire to determine the prevalence of febrile seizures was given to adolescents (16- and 17-year-olds) in the final 2 years of secondary school at the five schools in Alexandroupolis, Greece. Parents were interviewed, and clinical and electroencephalographic examinations were performed in all adolescents with a history of febrile seizures. Of 1708 adolescents, 56 (3.3%) had experienced at least one febrile seizure. Of these, 44 (78.6%) were simple and 12 (21.4%) were complex febrile seizures. Recurrent seizures occurred in 22 cases (39.3%), and the mean age at onset was 25.1 months. There was a positive first-degree family history in eight cases (14.3%) and this increased to 27.3% in cases with recurrent seizures. Two of the adolescents (3.6%) had had one unprovoked seizure before the age of 3 years, and another two children developed epilepsy. Epileptiform electroencephalogram discharges were observed in only one case (1.8%) with generalized tonic-clonic epilepsy.