Search

Competing Interests: Disclosures The authors have no conflicts to disclose.

Background: Atrial fibrillation (AF) and cavotricuspid isthmus (CTI)-dependent atrial flutter (AFL) are 2 separate entities that coexist in a significant proportion of patients. In patients with CTI ablation of AFL, the decision to hold anticoagulation often becomes an issue., Objectives: This study aimed to describe the incidence of the development of AF after CTI ablation in patients without a history of AF and to identify the risk predictors of the occurrence of AF., Methods: The present study included 120 consecutive patients (106 men; mean age 68 ± 12 years) who underwent radiofrequency catheter ablation (RFCA) of typical AFL since 2010. Patients with a history of AF before RFCA were excluded. The P-wave and QRS morphology, characteristics, and duration were evaluated by 12-lead electrocardiography the day after ablation., Results: During 3.6 ± 2.6 years of follow-up after RFCA, 49 patients (41%) developed new-onset AF. A univariate analysis revealed that the presence of fragmented QRS (fQRS) complexes (hazard ratio [HR], 4.63; 95% confidence interval [CI] 2.31-9.29; P < .001) and advanced interatrial block (IAB), defined as P-wave duration > 120 ms and biphasic morphology in the inferior leads (HR 4.44; 95% CI 2.45-8.01; P < .001), were predictors of new-onset AF. A multivariate analysis revealed that fQRS complexes (HR 3.35; 95% CI 1.58-7.10; P = .002) and advanced IAB (HR 2.64; 95% CI 1.38-5.07; P < .004) were independent predictors., Conclusion: The present study indicated that new-onset AF developed in a significant proportion of patients undergoing AFL ablation. The presence of fQRS complexes and advanced IAB were predictors of new-onset AF., (Copyright © 2020 Heart Rhythm Society. Published by Elsevier Inc. All rights reserved.)

Background: Early recurrence of atrial fibrillation (AF) is common following a successful electrical cardioversion (ECV). The purpose of this study was to investigate the hypothesis that AF recurrence is related to atrial electrical inhomogeneity, which may influence the P wave characteristics., Methods: Two hundred ninety-one consecutive persistent AF patients who underwent ECV were enrolled, and evaluated for AF recurrences one month after the ECV. Patients with open-heart surgery, a history of catheter ablation, and an unsuccessful ECV were excluded. The P wave duration, dispersion and P wave morphology were evaluated by 12‑lead ECGs 30 min after the ECV., Results: In total, 141 patients were investigated. One month after the ECV, 60 (43%) patients maintained sinus rhythm. The advanced interatrial block (aIAB; P wave duration >120 ms and biphasic P waves in the inferior leads) (Hazard ratio [HR], 4.51; 95% confidence interval [CI] 1.45-14.01, P = 0.009), P wave dispersion (HR, 1.06; 95%CI 1.02-1.09, P = 0.001), and duration of AF per month (HR, 1.03; 95%CI 1.01-1.04, P = 0.004) were independent predictors of AF recurrence. An aIAB was not associated with structural parameters such as the left atrial volume index or right atrial area. There were no differences in the serum BNP level and frequency of administering anti-arrhythmic drugs between the patients with and without recurrence., Conclusions: The risk of AF recurrence after the ECV can be predicted by the P wave characteristics. A longer P wave dispersion and the duration of AF also had a tendency for recurrence., (Copyright © 2018 Elsevier B.V. All rights reserved.)

Background: Atrial tachycardia (AT) may develop after biatrial surgical ablation of atrial fibrillation. However, the mechanism has not been determined in detail., Objective: We aimed to determine the mechanism and treatment of postoperative AT following biatrial surgical ablation in relation to the design and durability of the surgical lesion sets., Methods: An electrophysiologic study and radiofrequency ablation were performed in 34 consecutive patients (23 male, mean age of 63 ± 9.4 years) who were referred for AT that developed late after biatrial surgical ablation., Results: The mechanism of a total of 53 ATs was macroreentry in 30, a focal mechanism in 20, and localized reentry in 1, and could not be determined in 2. The cause of the macroreentrant AT was residual conduction across a surgical lesion, most of which was located at the annular end of the mitral (n = 18) or tricuspid isthmus incision (n = 7), where cryoablation was applied during the surgery. We did not find any gaps across the cut-and-sew lesions. Radiofrequency (RF) applications to the gap, or an alternative site to transect the circuit, or the earliest activation site of the focus was effective for 48 ATs (91%). After a total of 1.3 ± 0.6 RF sessions, 27 patients (79%) were free of AT (n = 2) or AF (n = 5) during a follow-up period of 50 ± 49 months., Conclusions: Macroreentry due to a gap in a surgical lesion and focal AT were the major mechanisms of AT in patients after biatrial surgical ablation. Radiofrequency ablation of those ATs is feasible., (Copyright © 2016 Heart Rhythm Society. Published by Elsevier Inc. All rights reserved.)

To elucidate attention-deficit/hyperactivity disorder (ADHD)-related factors observed in high-function pervasive developmental disorder (PDD) and their impact on daily life, we classified high-function PDD patients according to the Diagnostic and Statistical Manual of Mental Disorders, Fourth Edition (DSM-IV) criteria for ADHD with the exception of the exclusion criteria (coexistence with PDD), and studied the relationship between ADHD-related aspects and daily behavior problems using the Child Behavior Checklist (CBCL). The subjects were divided into two groups: Group 1, eight patients less than 6 years of age; and Group II, eight patients 6 years of age and older. Six patients in Group II met the criteria for ADHD. Five of them were classified as having the predominantly inattentive type of ADHD, and the remaining patient exhibited the combined type. However, no patient in Group I met the criteria for ADHD, suggesting the low sensitivity of the DSM-IV criteria for assessing the inattentiveness of preschoolers. The analyses of the correlation between corresponding items in the DSM-IV criteria and CBCL scores suggested that ADHD-related symptoms in high-function PDD patients have an impact on their daily lives.

To clarify the relationship between the degree of developmental disturbance and the severity of epilepsy in Angelman syndrome, we investigated 11 patients and measured both clinical outcomes and EEG parameters. Seven patients were followed up until after 8 years of age. Eight patients were found to have 15q11-q13 deletions. All patients experienced epileptic seizures and all but one displayed non-convulsive status epilepticus (NCSE) during the period of observation. Epileptic seizures, including NCSE, disappeared by around 8 years of age. In addition, specific epileptic discharges, as measured by EEG, tended to subside with age. Although development seemed almost normal or only slightly delayed during the first 6 months of life, all patients eventually developed severe retardation. Two patients displayed very severe retardation and were unable to comprehend language or walk independently at the last follow-up. Only one patient was able to speak a few meaningful words. In one of the most severely affected patients, who showed the earliest onset of seizures and NCSE, it is possible that the repetitive bouts of NCSE might be responsible for the severe developmental outcome. However, the other patient with particularly severe retardation did not experience NCSE, while the patient with the most favorable outcome had repetitive episodes of NCSE. Therefore, we conclude that the severity of developmental disturbance in Angelman syndrome is not necessarily related to the degree of epilepsy. However, intensive therapy for NCSE might still be justified because there are some patients in whom NCSE results in a transient and sometimes permanent decline in mental and motor functioning.

Panayiotopoulos syndrome (PS) is a type of benign childhood partial epilepsy, which has a good prognosis despite the fact that it is frequently associated with abundant multifocal spikes on the electroencephalography (EEG). We investigated whether stable dipoles, as seen in rolandic epilepsy, were also present in PS. We performed dipole analysis of the interictal spike discharges seen in the interictal EEGs of eight children with PS. We chose more than 10 spikes for each kind of spike, and investigated whether or not more than three of these spikes showed consistently stable dipole locations. (1) We observed 15 different kinds of spikes in various regions in the EEGs of the eight children. (2) Twelve of the 15 kinds of spikes had dipoles with a high goodness of fit. Furthermore, 14 of the 15 spikes had stable dipoles with similar locations for more than three individual spikes. (3) Fourteen of the 15 spikes, including frontal spikes, showed dense dipole locations in the mesial occipital area. Thirteen of these 14 spikes also showed other dipole locations in the rolandic area and/or the vertex (Cz). Our study revealed that the various types of spikes observed in PS have similar and stable dipole locations. The dipoles showing high stability, were located in the mesial occipital area, and were accompanied by dipoles located in the rolandic area. The stability and location of these dipoles indicate that there may be a pathogenetic link between PS and rolandic epilepsy.

Unlabelled: We report on the successful identification of epileptic foci in two children with partial epilepsy using ictal magnetoencephalography (MEG). Case 1 is a 12-year-old male suffering with simple partial seizures with leftwards nystagmus. Ictal SPECT revealed a hyperperfusion area in the right lateral occipital area, and MRI revealed cortical dysplasia in the same area. Interictal EEG dipoles were concentrated in the right mesial occipital lobe. Both interictal and ictal MEG dipoles were concentrated in the right mesial occipital lobe, which corresponded well with neuroimaging data and his clinical features. Case 2 is a 5-year-old female suffering with simple partial seizures with left-side facial twitching. Interictal EEG dipoles were located in her left motor area, the pre-sylvian fissure, close to the location of the interictal MEG-estimated dipoles. Ictal EEGs showed no remarkable changes associated with her clinical manifestations. However, ictal MEG showed high-voltage slow waves over her left hemisphere, and ictal MEG iso-contour maps revealed a clear dipolar pattern, which suggested that the MEG dipole was located in the area of the sylvian fissure. Ictal SPECT revealed hyperperfusion areas around the left sylvian fissure., Conclusion: Ictal MEG is useful for determining the precise location of epileptic focus in patients with motionless seizures, including children.

Unlabelled: We performed a longitudinal clinico-electroencephalographic study of 23 children who were diagnosed as having absence epilepsy on their initial visits to our facility and we analysed those factors which lead to an unfavourable prognosis., Subjects and Methods: We divided the 23 patients into three groups according to their clinical courses: Group A: eight patients who responded well to the therapy and became seizure free without relapse of epileptic discharges on EEGs; Group B: thirteen patients who suffered from relapse of epileptic discharges on EEGs despite clinical seizure cessation; Group C: two patients who continued to suffer from seizures., Results: (1) Fifty-six percent of all patients had focal epileptic discharges, including a surprising 63% of patients in Group A. (2) "Lead in" in the ictal EEGs and automatisms during seizures were most commonly observed in patients in Group B, although there were no significant differences between the three groups. (3) The epilepsy of one patient in Group C evolved into complex partial seizures or absence status during her clinical course. She seemed to suffer from so-called "frontal absence", despite the fact that her initial EEG did not show any focal abnormalities. (4) Patients in Group B were treated with lower AED dosages than those in Group A. In addition, one patient in Group C was treated irregularly., Conclusion: We conclude that it is not uncommon for patients with absence epilepsy to show focal abnormalities on EEGs and clinical ictal automatisms. Thus, the existence of clinical ictal automatisms and focal signs in electroencephalographic features are not sufficient indicators of the final outcome. Furthermore, it appears that regular and adequate drug therapy is important for a favourable prognosis.

Objectives: Febrile seizures plus (FS+) are attracting attention for their corresponding genetic abnormalities, and are defined as febrile seizures (FS) continuing beyond 6 years of age (late FS) or those associated with afebrile seizures. We tried to elucidate their clinical and EEG characteristics as compared with those of children having only FS., Subjects and Methods: We reviewed clinical records in a pediatric neurology clinic to identify 31 patients with FS+ (group FS+) and 51 with only FS (group FS). Their family history of seizures, clinical features and EEG findings were compared., Results: A family history of seizures was noted in 14 patients (45.2%) of group FS+ and in 24 (47.1%) of group FS. In group FS+, 19 patients had late FS, 11 had afebrile seizures, and the remaining one had both types of seizures. Two patients had seizures induced by TV/video-game as well, and another suffered from absences. Epileptic EEG abnormalities, which included diffuse spike-waves and focal spikes, were noted in 13 patients (41.9%) of group FS+ and 12 (23.5%) of group FS., Conclusions: The clinical and EEG characteristics of the children having FS+ were diverse, without significant differences from those with FS except for the seizures types.

To elucidate the pathophysiology of spasms in series, the distribution and density of spikes on hypsarrhythmia were studied in 13 patients with West syndrome by excluding slow waves from EEG using a digital filter. (1) Interictal spikes were mostly multifocal and dominant over the bilateral posterior head area with very few diffuse discharges. Therefore, spikes on hypsarrhythmia were demonstrated to occur actually depending on the brain regions although they appeared random. (2) The dominant region of interictal spikes did not correspond to the underlying focal cortical lesion in many patients, and was indicated to reflect the general process of cerebral maturation in infancy. (3) There were far fewer inter-spasm spikes, especially during the middle phase of a series of spasms, than interictal spikes. It was implied that the cortical activity of hypsarrhythmia was interfered with by the abnormal subcortical function, which might be related to the generation of spasms. (4) The dominant region of inter-spasm spikes tended to coincide with a focal cortical lesion shown by MRI and the focus of associated partial seizures.

Previous studies suggested that the onset of phenytoin-induced gingival overgrowth depended on serum phenytoin concentration. Cytochrome P450 2C (CYP2C) plays an important role in phenytoin metabolism. Recently, single nucleotide polymorphisms in the coding region of CYP 2C influencing phenytoin metabolism were identified. The purpose of the present study was to see if CYP 2C polymorphisms might relate to the onset and severity of phenytoin-induced gingival overgrowth. Twenty-eight epileptic patients taking phenytoin aged 15 to 75 (mean age: 42.2 years old, 20 males and 8 females) and 56 unrelated healthy subjects aged 30 to 48 (mean age: 36.8 years old, 48 males and 8 females) were examined for CYP 2C polymorphisms. All epileptic subjects were examined for the degree of gingival overgrowth, daily phenytoin dose and serum phenytoin concentration. The results indicated about 7% of the subjects including epileptic and healthy subjects examined were positive for CYP 2C9*3. However, the degree of gingival overgrowth did not directly correlate with CYP 2C polymorphisms. Nevertheless, the subjects with severer gingival overgrowth exhibited significantly higher serum phenytoin concentration, indicating that phenytoin metabolism is an important determinant for the severity of the disease. Additionally, CYP 2C9*3 carriers exhibited significantly higher serum drug concentration to drug dose. Therefore, we concluded although the gene analysis is not directly related to diagnose the disease itself, it can be utilized in estimating serum phenytoin concentration from drug dose, which in turn serves to predict the future development and clinical course of the disease.

The purpose of this study was to clarify the risk factors of relapse following discontinuation of AEDs in patients with childhood-onset cryptogenic localization-related epilepsies. The subjects were 82 patients who fulfilled the following criteria: (1) age at first visit of less than 15 years, (2) follow-up period of more than 5 years, (3) suffering from cryptogenic localization-related epilepsies, and (4) the patient underwent AED withdrawal during the follow-up period. As a basic principle, we decided to start withdrawing AEDs when both of the following two conditions were met: (1) the patient had a seizure-free period of 3 years or more, and (2) there were no epileptic discharges on EEGs just prior to the start of withdrawal. Seizures recurred in eight of the 82 patients (9.8%). Univariate analysis revealed that the following factors were correlated with higher rates of seizure relapse: 6 years of age or higher at onset of epilepsy; 15 years of age or higher at the start of AED withdrawal; 5 years or more from the start of AED treatment to seizure control; five or more seizures before seizure control; and two or more AEDs administered before seizure control. Among these risk factors, 6 years of age or higher at onset and 5 years or more from the start of AED treatment to seizure control were determined by multivariate analysis to be independent risk factors for relapse. Thus, we conclude that the physician should be more careful in discontinuing AEDs in these higher-risk patients groups, and more generous in discontinuing AEDs in lower-risk groups.

We classified 28 patients with severe myoclonic epilepsy in infancy (SME) according to the presence or absence of myoclonic seizures and/or atypical absences. Eleven of the patients had myoclonic seizures and/or atypical absences, and we refer to this condition as 'typical SME (TSME)'. Seventeen of the patients had only segmental myoclonias, and we refer to this condition as 'borderline SME (BSME)'. We then analyzed the electroclinical and genetic characteristics of these two groups. Ten of the 11 TSME patients had a photoparoxysmal response at some time during their clinical course, while none of the BSME patients showed this response. TSME and BSME showed a significant difference in regard to gender ratio: female dominance in TSME and male dominance in BSME (P=0.008). The detection rate of the voltage-gated sodium channel alpha1-subunit (SCN1A) gene mutations was 72.7 and 88.2% in TSME and BSME, respectively. There was no difference in the type or rate of mutation between TSME and BSME. We conclude that TSME and BSME show distinct differences in photoparoxysmal response and gender, which might be caused by some genetic mechanism(s) other than the SCN1A gene mutation.

We report on the electroclinical findings and the results of a molecular genetic study of a patient with typical severe myoclonic epilepsy in infancy (TSME) and three with borderline SME (BSME) who showed paroxysmal movement disorders, such as choreoathetosis, dystonia and ballismus, during their clinical course. BSME was defined as a clinical entity that shares common characteristics with TSME but lacks myoclonic seizures associated with ictal EEG changes. When the paroxysmal movement disorders were first observed, all the patients in this study were being treated with polytherapy including phenytoin (PHT), and these abnormal movements disappeared when PHT was discontinued or reduced. However, on other occasions, two of our cases also showed the same abnormal movements even when not being treated with PHT. One patient with TSME and two of the three patients with BSME had SCN1A gene mutations that lead to truncation of the associated protein. We conclude that paroxysmal movement disorders seen in SME patients were closely related to their AED therapy, especially the use of PHT. It is thought that patients with both TSME and BSME have some predisposition toward paroxysmal movement disorders, and that this predisposition is partly related to sodium channel dysfunction, although some other factors might influence the occurrence of this phenomenon.

To study the electroclinical characteristics of patients with childhood-onset epilepsy who showed polymicrogyria (PMG) on MRI, we classified 15 patients according to the location of PMG on MRI. The composition of the subjects was as follows: four patients with PMG in both hemispheres; three with localized PMG in one hemisphere associated with other lesions such as porencephaly; and eight with only localized PMG in one hemisphere. We investigated the electroclinical characteristics of the epileptic syndromes associated with these different types of PMG. Four patients suffered from infantile spasms during their clinical course. Five patients suffered from epilepsy with electrical status epilepticus during slow sleep (ESES) and ESES-related epilepsy. The other six patients had only localization-related epilepsy throughout their clinical course. Patients with PMG in both hemispheres, and localized PMG in one hemisphere associated with other lesions tended to have early-onset intractable seizures, especially infantile spasms. On the other hand, patients with only localized PMG in one hemisphere had ESES and ESES-related epilepsy or localization-related epilepsy, and their seizure prognosis was relatively favorable. These findings are useful in predicting the outcome of patients with PMG., (Copyright 2002 Elsevier Science B.V.)

To investigate the possible correlation between genotype and phenotype of epilepsy, we analyzed the voltage-gated sodium channel alpha1-subunit (SCN1A) gene, beta1-subunit (SCN1B) gene, and gamma-aminobutyric acid(A) receptor gamma2-subunit (GABRG2) gene in DNAs from peripheral blood cells of 29 patients with severe myoclonic epilepsy in infancy (SME) and 11 patients with other types of epilepsy. Mutations of the SCN1A gene were detected in 24 of the 29 patients (82.7%) with SME, although none with other types of epilepsy. The mutations included deletion, insertion, missense, and nonsense mutations. We could not find any mutations of the SCN1B and GABRG2 genes in all patients. Our data suggested that the SCN1A mutations were significantly correlated with SME (p<.0001). As we could not find SCN1A mutations in their parents, one of critical causes of SME may be de novo mutation of the SCN1A gene occurred in the course of meiosis in the parents., ((c) 2002 Elsevier Science (USA).)

It is important for the fields of child neurology and child public health to clarify the prevalence and incidence rates of West syndrome because this syndrome is a major cause of developmental disorders.However, there have been few reports in Japan on the prevalence rate of West syndrome in the general population. We carried out a population-based survey in Okayama Prefecture, in western Japan in 1994. The population under 2 years of age in Okayama Prefecture in 1994 was 37,085. Six cases of West syndrome were identified. The prevalence rate was 0.16 per 1000.

Although spasms in clusters are one of the major characteristics of West syndrome (WS), there are a significant number of patients who show spasms in clusters but do not fit the standard pattern of WS. It is possible to divide these atypical cases into the following three groups. Group 1: refractory epilepsies beginning in early infancy, associated with atypical electroencephalographic (EEG) features; Group 2: generalized epilepsies with spasms in clusters at ages of 2-3 years or above; and Group 3: localization-related epilepsies with spasms in clusters. Ictal clinical and EEG findings of spasms in clusters in these atypical patients and also those in WS are similar. Patients in Group 1 often suffer from Aicardi syndrome, cortical malformations, early myoclonic encephalopathy and Ohtahara syndrome. Most patients in Group 2 suffer from Lennox-Gastaut syndrome and other generalized epilepsies such as severe epilepsy with multiple independent spike foci. A significant number of them had a history of WS. Small number of patients in Group 2 can be diagnosed as having late-onset WS or long-lasting WS. In Groups 1 and 3 patients, cortical mechanisms play a critical role in their pathophysiology. The presence of older patients with spasms in clusters might indicate not only developing process of the brain but also some selective dysfunction of the brain plays an important role in the occurrence of spasms in clusters. Investigations on these atypical patients can help the understanding of pathophysiological mechanisms of WS and its related epileptic syndromes.

Monitoring brain function by EEG is an important means of preventing cerebral insults in pediatric cardiovascular surgery. We studied intraoperative EEG changes and their regional differences associated with hypothermia and brain ischemia. The subjects of this study consisted of 13 children ranging in age from 4 months to 4 years and 6 months. Multi-channel EEGs were recorded using a portable digital EEG system, and the EEG changes were examined by visual inspection and computerized analyses. The results were as follows. (1) During cooling, a discontinuous EEG pattern was transiently observed in four patients, and this phenomenon indicated rapid suppression of cerebral function and subsequent adaptation. (2) Regarding the patterns of change in equivalent potentials induced by hypothermia, there were two different patterns depending on the degree of hypothermia, and the borderline rectal temperature was found to be around 32 degrees C. (3) During cooling, regional differences in the changes in equivalent potentials were observed in nine patients. A decrease in slow waves was marked in the occipital head area, and a decrease in fast waves was prominent in the anterior head area. (4) Arterial hypotension caused transient EEG abnormalities. Of them, bilaterally synchronous rhythmic high voltage slow waves were remarkable and exhibited bifrontal or bicentral dominance. (5) The EEG changes induced by hypothermia were influenced not only by the rectal temperature itself, but also by the rate of change in rectal temperature, and we speculated that this phenomenon was a result of adaptation. In intraoperative EEG monitoring, these findings constitute the basis for early detection of a cerebral hypoxic-ischemic state during pediatric cardiovascular surgery.

Objective: We report on a patient who showed an unusual transition from complex partial seizures to a combination of myoclonic seizures and partial seizures, and then to isolated myoclonic seizures. The pathophysiological mechanism of the myoclonic seizures in this uncommon condition was studied., Methods: The interhemispheric small time differences were estimated in the ictal EEG discharges of myoclonic seizures for differentiation between primary and secondary bilateral synchrony. The estimation was performed by coherence and phase analysis based on the two-dimensional autoregressive model., Results: The estimated interhemispheric time differences were at most 27.4 ms. The ictal activity of the myoclonic seizures was suggested to originate from a cortical focus in the right hemisphere, which was also the origin of the partial seizures., Conclusion: The patient was considered to have an unusual type of myoclonic seizures with a probable pathophysiological mechanism of secondary bilateral synchrony.

We report on a patient with early-onset spasms in series and partial seizures associated with focal cortical dysplasia whose EEGs showed suppression-burst patterns during early infancy. These electroclinical characteristics suggested a diagnosis of Ohtahara syndrome, but the EEG findings were atypical because of the lack of suppression-burst patterns during wakefulness. In addition, the patient did not have severe psychomotor retardation. With high-dose pyridoxal phosphate therapy, seizures were suppressed and suppression-burst patterns disappeared at 2 months of age. Focal motor seizures recurred later and they often evolved into epilepsia partialis continua. Patients with early-onset intractable seizures associated with suppression-burst patterns on EEGs have several different etiologies, and these patients should be categorized according to their etiology in addition to their syndromic diagnosis.

In order to evaluate the effectiveness of presurgical dipole analysis of interictal spikes as a non-invasive technique for the determination of epileptogenic area, we compared the results of this method with those of electrocorticography (ECoG) localization in the diagnosis of a patient with tumor-related epilepsy. A preoperative MRI revealed a temporal lobe tumor on the right side. The individual dipoles estimated from the interictal spikes were located mainly in the anterolateral region of the right temporal lobe, although some were located in the mesial side. The ECoG recorded frequent spikes in the anterolateral region of the right temporal lobe consistent with the location estimated by dipole analysis. After surgery, the patient suffered from residual seizures. Therefore, the residual epileptogenic area was examined by dipole analysis using a four-layered head model instead of the previous three-layered head model. As a result, the dipole analysis was able to pinpoint the epileptic focus in the area directly adjacent to the resected area, and in the mesial temporal lobe. In conclusion, EEG dipole analysis appears to hold promise as a non-invasive presurgical evaluation technique for locating epileptogenic areas as well as for postsurgical evaluation of residual epileptic focus.

Estimation of interhemispheric small time differences (TDs) during spike-wave bursts in the EEG by coherence and phase analysis is useful for differentiation between primary bilateral synchrony (PBS) and secondary bilateral synchrony (SBS) in epilepsy. Because the previous method via Fast Fourier Transform needed long bursts for reliable analysis, a method using a 2-dimensional autoregressive model was newly developed to enable estimation of TDs even in 1.2 sec bursts, and applied to 19 epileptic patients with apparently bilaterally synchronous spike-wave bursts. At the onsets of bursts, estimated maximal TDs were 5.8 msec or less and inconsistent in leading hemispheres in 10 patients with a clinical diagnosis of idiopathic, cryptogenic or symptomatic generalized epilepsy indicating PBS, while the maximal TDs were 9.3-41.5 msec and consistent in leading in 7 patients with clinically symptomatic partial epilepsy and also in two with idiopathic and symptomatic generalized epilepsy suggesting SBS. Among 8 patients with bursts which suggested SBS and long enough for evaluation of intra-burst TD variation, TDs tended to disappear in the middle to end parts of the bursts in 5 cases, but not in the other 3, suggesting 2 different pathophysiological mechanisms in SBS.

A simple and rapid preconcentration technique, based on collecting trace elements on a membrane filter and dissolving the membrane filter in an organic solvent, has been applied to the spectrophotometric determination of phosphorus in water. Phosphorus, 0.5-7 mug in 50-500 ml of water sample, is collected as phosphomolybdenum blue on a nitrocellulose or acetylcellulose membrane in the presence of n-dodecyltrimethylammonium bromide, the membrane is dissolved in 5 ml of dimethyl-sulphoxide (DMSO), and the absorbance of the DMSO solution is measured at 710 nm against a reagent blank. Moderate concentrations of silicate, anionic and non-ionic surfactants and high concentrations of sodium chloride do not interfere. Interference from arsenate can be eliminated by reducing the arsenate to arsenite. Condensed and organic phosphates can be determined if they are first converted into orthophosphoric acid by digestion with persulphate. The limit of determination is 0.002 mug of phosphorus in 100 ml of sample.

In 45 cases of Lennox syndrome treated with ACTH, the immediate and long-term effects and the various factors affecting them were investigated by a follow-up study. 1) Regarding the immediate effect, 23 (51.1%) of the 45 cases became "seizure free" for over 10 days. 2) As to the long-term prognosis of these 23 cases, 10 cases relapsed into Lennox syndrome within 6 months and in the remaining 13 cases, seizures were suppressed for over 6 months; out of these 13, seizure relapse was observed in eight cases from 9 months to 7 years later, and the other five cases followed a very favorable course without relapse. 3) The favorable factors related to the effect of ACTH for Lennox syndrome are: a) age at ACTH treatment: up to 4 years old, b) time lag between onset of Lennox syndrome and initiation of ACTH treatment: the shorter the better; at least within 1 year, preferably within 3 months, c) presumptive causes and underlying diseases: idiopathic cases are best, d) mental defects before treatment: the slighter the better, e) seizure patterns: without tonic seizures, and f) EEG findings: disorganized diffuse slow spike-waves without asymmetry. 4) It is desirable to continue the ACTH treatment as long as possible, with the goal of the disappearance of seizure discharges, or at least the disappearance of diffuse seizure discharges.

A clinico-electroencephalographic study on 14 cases of the early-infantile epileptic encephalopathy with suppression-burst (EIEE) including long-term follow-up studies for one year 8 months to 12 years 2 months disclosed the specificity of EIEE in its developmental aspects. With age, clinical evolution from EIEE to the West syndrome was observed in as many as 10 cases, among which two cases showed further transition to the Lennox-Gastaut syndrome. Electroencephalographically, suppression-burst pattern gradually began to disappear from age of 3 months and disappeared by 6 months in all the cases, transforming to hypsarhythmia in 10 cases from 2 to 6 months of age, showing further transition to diffuse slow spike-and-waves in 2 cases at one year and one month and at 3 years and one month of age, respectively. Changing pattern of EEG were classifiable into two types which strongly related to the prognosis. These findings indicated EIEE to be an independent epileptic syndrome as the earliest form of the age-dependent epileptic encephalopathy.