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Magnetoencephalographic analysis of bilaterally synchronous discharges in benign rolandic epilepsy of childhood
Abstract
The purpose of this study was to examine the spatial and temporal relationship between bilateral foci of bilaterally synchronous discharges in benign rolandic epilepsy of childhood (BREC) using a whole-scalp neuromagnetometer. We simultaneously recorded interictal magnetoencephalographic (MEG) and electroencephalographic (EEG) signals in six children with BREC. Interictal spikes were classified into three groups: bilaterally synchronous discharges (BSDs), unilateral discharges on right side (UD-R), and unilateral discharges on left side (UD-L). We used equivalent current dipole (ECD) modelling to analyse the cortical sources of interictal spikes. Both BSDs and UDs were found in Patients 1-4, whereas only UDs were identified in Patients 5 and 6. The ECDs of interictal spikes were located in rolandic regions, 10-20mm anterior and lateral to hand somatosensory cortices. Multi-dipole analysis of BSDs showed two ECDs in homotopic motor areas of the hemispheres. During BSDs, the right-sided activation preceded the left-sided activation by 15-21 milliseconds in Patients 1 and 2. In Patients 3 and 4, the activation occurred 17-20 milliseconds earlier in the left than the right hemisphere. Within the same hemisphere, the sources of BSDs and UDs were located in similar areas. In conclusion, our results imply the cortical epileptogenicity in bilateral perirolandic areas in BREC. The sequential activation during BSDs in both hemispheres suggest the existence of synaptic connections, possibly via the corpus callosum, between bilateral irritative foci.
... Combining EEG/MEG source localisation and fMRI of tongue movements localised IEDs to the lower somatosensory cortex with co-located tongue movement fMRI activation (van der Meij et al., 2001). Later studies using whole head MEG localised IEDs 10- 20 mm anterior and lateral to the hand somatosensory cortex (with concurrent median nerve stimulation) (Lin et al., 2003a). Dipole analysis of bilateral discharges showed two ECD sources in homotopic motor areas (Lin et al., 2003b). ...
... A single ECD accounted for most of the unilateral spikes in a pre-central location and over 98% of spikes were seen simultaneously on EEG and MEG, suggesting a stable tangential dipole source. For bilateral IED, the temporal difference between bilateral foci was 15-21 ms (Lin et al., 2003a). The same group correlated the location of IED sources with sensory responses (Lin et al., 2003b), finding IED sources closer to S2 than S1. ...
The term idiopathic focal epilepsies of childhood (IFE) is not formally recognised by the ILAE in its 2010 revision (Berg et al., 2010), nor are its members and boundaries precisely delineated. The IFEs are amongst the most commonly encountered epilepsy syndromes affecting children. They are fascinating disorders that hold many "treats" for both clinicians and researchers. For example, the IFEs pose many of the most interesting questions central to epileptology: how are functional brain networks involved in the manifestation of epilepsy? What are the shared mechanisms of comorbidity between epilepsy and neurodevelopmental disorders? How do focal EEG discharges impact cognitive functioning? What explains the age-related expression of these syndromes? Why are EEG discharges and seizures so tightly locked to slow-wave sleep? In the last few decades, the clinical symptomatology and the respective courses of many IFEs have been described, although they are still not widely appreciated beyond the specialist community. Most neurologists would recognise the core syndromes of IFE to comprise: benign epilepsy of childhood with centro-temporal spikes or Rolandic epilepsy (BECTS/RE); Panayiotopoulos syndrome; and the idiopathic occipital epilepsies (Gastaut and photosensitive types). The Landau-Kleffner syndrome and the related (idiopathic) epilepsy with continuous spikes and waves in sleep (CSWS or ESES) are also often included, both as a consequence of the shared morphology of the interictal discharges and their potential evolution from core syndromes, for example, CSWS from BECTS. Atypical benign focal epilepsy of childhood also has shared electro-clinical features warranting inclusion. In addition, a number of less well-defined syndromes of IFE have been proposed, including benign childhood seizures with affective symptoms, benign childhood epilepsy with parietal spikes, benign childhood seizures with frontal or midline spikes, and benign focal seizures of adolescence. The term "benign" is often used in connection with the IFEs and is increasingly being challenged. Certainly most of these disorders are not associated with the devastating cognitive and behavioural problems seen with early childhood epileptic encephalopathies, such as West or Dravet syndromes. However, it is clear that specific, and sometimes persistent, neuropsychological deficits in attention, language and literacy accompany many of the IFEs that, when multiplied by the large numbers affected, make up a significant public health problem. Understanding the nature, distribution, evolution, risk and management of these is an important area of current research. A corollary to such questions regarding comorbidities is the role of focal interictal spikes and their enduring impact on cognitive functioning. What explains the paradox that epilepsies characterised by abundant interictal epileptiform abnormalities are often associated with very few clinical seizures? This is an exciting area in both clinical and experimental arenas and will eventually have important implications for clinical management of the whole child, taking into account not just seizures, but also adaptive functioning and quality of life. For several decades, we have accepted an evidence-free approach to using or not using antiepileptic drugs in IFEs. There is huge international variation and only a handful of studies examining neurocognitive outcomes. Clearly, this is a situation ready for an overhaul in practice. Fundamental to understanding treatment is knowledge of aetiology. In recent years, there have been several significant discoveries in IFEs from studies of copy number variation, exome sequencing, and linkage that prompt reconsideration of the "unknown cause" classification and strongly suggest a genetic aetiology. The IFE are strongly age-related, both with regards to age of seizure onset and remission. Does this time window solely relate to a similar age-related gene expression, or are there epigenetic factors involved that might also explain low observed twin concordance? The genetic (and epigenetic) models for different IFEs, their comorbidities, and their similarities to other neurodevelopmental disorders deserve investigation in the coming years. In so doing, we will probably learn much about normal brain functioning. This is because these disorders, perhaps more than any other human brain disease, are disorders of functional brain systems (even though these functional networks may not yet be fully defined). In June 2012, an international group of clinical and basic science researchers met in London under the auspices of the Waterloo Foundation to discuss and debate these issues in relation to IFEs. This Waterloo Foundation Symposium on the Idiopathic Focal Epilepsies: Phenotype to Genotype witnessed presentations that explored the clinical phenomenology, phenotypes and endophenotypes, and genetic approaches to investigation of these disorders. In parallel, the impact of these epilepsies on children and their families was reviewed. The papers in this supplement are based upon these presentations. They represent an updated state-of-the-art thinking on the topics explored. The symposium led to the formation of international working groups under the umbrella of "Luke's Idiopathic Focal Epilepsy Project" to investigate various aspects of the idiopathic focal epilepsies including: semiology and classification, genetics, cognition, sleep, high-frequency oscillations, and parental resources (see www.childhood-epilepsy.org). The next sponsored international workshop, in June 2014, was on randomised controlled trials in IFEs and overnight learning outcome measures.
... Interictal spikes were visually checked on both EEG and MEG channels. Identified spikes were collected and classified into 3 groups: unilateral rolandic discharges (RD) in the left hemisphere (RD_L), RD in the right hemisphere (RD_R), and bilaterally synchronous rolandic discharges (BSRD) (Lin et al., 2003). BSRDs were defined as those bilaterally simultaneous spikes with side-to-side time lag of main peaks less than 50 ms. ...
... If signals of some brain region were left inadequately explained by the model, the data were reevaluated for more accurate estimation of the generators. This approach, explained previously in detail (Hämäläinen et al., 1993), has been successfully applied in previous MEG studies (Hari et al., 1984 Hämäläinen et al., 1993; Forss et al., 1994, Huttunen et al., 1996; Lin et al., 2000 Lin et al., , 2003 Lin and Forss, 2002). ...
The purpose of this study was to study the relationship between interictal spike sources and somatosensory cortices in benign rolandic epilepsy of childhood (BREC) using a whole-scalp neuromagnetometer. We recorded spontaneous magnetoencephalography (MEG) and EEG signals and cortical somatosensory-evoked magnetic fields (SEFs) to electric stimulation of the median nerve in 9 children with BREC. Interictal rolandic discharges (RDs) and SEFs were analyzed by equivalent current dipole (ECD) modeling. Based on the orientation and locations of corresponding ECDs, we compared generators of RDs with primary (SI) and second somatosensory cortices (SII). Our results showed that RDs and SII responses had similar ECD orientation on the magnetic field maps. The ECDs of RDs were localized 15.3 +/- 1.9 and 12.2 +/- 2.8 mm anterior to SI and SII, respectively. The spatial distance on average from the location of RDs to SII (21.9 +/- 1.6 mm) cortex was significantly shorter than to SI cortex (29.7 +/- 1.7 mm) (P<0.01, Wilcoxon signed-rank test). In conclusion, the cortical generators for RDs in patients with BREC are localized in the precentral motor cortex, closer to hand SII than to SI cortex.
... Interictal spikes, typically localized around the central sulcus, may be observed in one or both hemispheres (Lerman and Kivity, 1975; Lin et al., 2003a,b ). Recent studies show evidence of inter-hemispheric source shifting (Kellaway, 2000; Lin et al., 2003a; Huiskamp et al., 2004; Ishitobi et al., 2005 ). However, the exact neuronal mechanisms underlying the cortical excitability remain not clear. ...
... In contrast to the conventional view of focal epileptogenicity , our present data suggest that this developmental disorder may actually cause bilateral cortical hyperexcitability even for unilateral spikes in time-domain presentations. This idea may agree with earlier observations of bilateral independent spikes (Lombroso, 1967; Kellaway, 2000; Lin et al., 2003a) or even generalized spike-wave complexes in BRE (Lerman and Kivity, 1975). Moreover, we suppose a possible involvement of thalamo-cortical circuits in the concomitant increase in alpha oscillation over both hemispheres. ...
To elucidate the oscillatory dynamics with respect to interictal spike occurrence in benign rolandic epilepsy (BRE).
Using a whole-scalp magnetoencephalography (MEG), we recorded scalp EEG and MEG signals in 10 BRE patients (age 8-12 years) and visually identified unilateral interictal spikes that were simultaneously present on both EEG and MEG channels. We obtained the peak timing of individual spike complex based on MEG single-dipole modeling, and then applied wavelet transform to analyze the time-frequency components of corresponding MEG signals with respect to spike occurrence.
In the hemisphere with time-domain spike waveforms, we identified a clear increase of 0.5-40 Hz activity around the spike peak, most prominent at alpha band (8-13 Hz). Notably, at the approximate timing we also observed an increase in 0.5-25 Hz oscillations over the homotopic area in the other hemisphere where no spike signals were found.
Our results indicate bilateral increases in 0.5-25 Hz oscillations during unilateral spike formation in BRE patients. By using wavelet transform analysis, one could be able to detect some irritative feature that would in visual analysis remain undetected.
... Magnetoencephalography (MEG) is a totally noninvasive tool for localization of epileptic activity (Barth et al., 1982, 1984; Modena et al., 1982; Sato and Smith, 1985; Ricci et al., 1987; Rose et al., 1987a, 1987b; Sutherling et al., 1987, 1988; Sutherling and Barth, 1989; Stefan et al., 1990, 1992, 1994, 2000; Tiihonen et al., 1990; Eisenberg et al., 1991; Ogashiwa et al., 1991; Yotsumoto et al., 1991; Paetau et al., 1992, 1994, 1999; Hari et al., 1993; Nakasato et al., 1994; Smith et al., 1995; Ebersole, 1997b; Knowlton et al., 1997; Merlet et al., 1997; Mikuni et al., 1997; Ko et al., 1998; Minassian et al., 1999; Wheless et al., 1999; Baumgartner et al., 2000; Iwasaki et al., 2002; Oishi et al., 2002; Lin et al., 2003a,b). MEG is less affected by conductivity properties than EEG; thus MEG may localize the spike sources more accurately (Cuffin and Cohen, 1979; Nakasato et al., 1994; Wheless et al., 1999). ...
... MEG recordings were conducted in a magnetically shielded room with a whole-scalp 306-channel neuromagnetometer (Vectorview, 4-D Neuroimaging, San Diego, CA) comprising 102 identical triple sensor elements (Lin et al., 2003a,b). Each sensor element consists of two orthogonal planar gradiometers and one magnetometer coupled to 3 SQUIDs (superconducting quantum interference devices) and thus provides three independent measures of the magnetic fields. ...
To compare magnetoencephalography (MEG) with scalp electroencephalography (EEG) in the detection of interictal spikes in temporal lobe epilepsy (TLE), we simultaneously recorded MEG and scalp EEG with a whole-scalp neuromagnetometer in 46 TLE patients. We visually searched interictal spikes on MEG and EEG channels and classified them into three types according to their presentation on MEG alone (M-spikes), EEG alone (E-spikes), or concomitantly on both modalities (M/E-spikes). The M-spikes and M/E-spikes were localized with MEG equivalent current dipole modeling. We analyzed the relative contribution of MEG and EEG in the overall yield of spike detection and also compared M-spikes with M/E-spikes in terms of dipole locations and strengths. During the 30- to 40-min MEG recordings, interictal spikes were obtained in 36 (78.3%) of the 46 patients. Among the 36 patients, most spikes were M/E-spikes (68.3%), some were M-spikes (22.1%), and some were E-spikes (9.7%). In comparison with EEG, MEG gave better spike yield in patients with lateral TLE. Sources of M/E- and M-spikes were situated in the same anatomical regions, whereas the average dipole strength was larger for M/E- than M-spikes. In conclusion, some interictal spikes appeared selectively on either MEG or EEG channels in TLE patients although more spikes were simultaneously identified on both modalities. Thus, simultaneous MEG and EEG recordings help to enhance spike detection. Identification of M-spikes would offer important localization of irritative foci, especially in patients with lateral TLE.
... In some patients, it is possible to follow the spread of epileptic activity from one hemisphere to another ( Figure 12-1), or within a hemisphere. The identifi cation of the earliest source of epileptic activity naturally makes the localization of the epileptogenic zone more reliable (Hari et al., 1993 ;Paetau et al., 1999 ;Lin et al., 2003 ;Yu et al., 2004 ;Hara et al., 2007 ). The analysis of epileptiform MEG by using multidipole models is more demanding and time-consuming than applying a single dipole model into each spike and calculating the clusters of sources-but should be attempted, as the obtained additional data may signifi cantly aid in the clinical decision-making. ...
This chapter discusses the application of MEG in clinical settings. It argues that although MEG is an exciting tool to use in clinical settings, it is only a part of multifaceted clinical evaluation deriving information from all available sources for the benefit of the patient. The relative weight of MEG in this evaluation depends on individual clinical details of each patient. The emerging applications are highly exciting and will provide new opportunities for MEG studies in clinical settings.
... We can often follow the spread of epileptic activity from one hemisphere to another (Fig. 8) or within a hemisphere (Fig. 9). The identification of the earliest source of epileptic activity adds reliability to localization of the epileptogenic zone (39,72,93,135). ...
Objective:
To present applications of magnetoencephalography (MEG) in studies of neurosurgical patients.
Methods:
MEG maps magnetic fields generated by electric currents in the brain, and allows the localization of brain areas producing evoked sensory responses and spontaneous electromagnetic activity. The identified sources can be integrated with other imaging modalities, e.g., with magnetic resonance imaging scans of individual patients with brain tumors or intractable epilepsy, or with other types of brain imaging data.
Results:
MEG measurements using modern whole-scalp instruments assist in tailoring individual therapies for neurosurgical patients by producing maps of functionally irretrievable cortical areas and by identifying cortical sources of interictal and ictal epileptiform activity. The excellent time resolution of MEG enables tracking of complex spaciotemporal source patterns, helping, for example, with the separation of the epileptic pacemaker from propagated activity. The combination of noninvasive mapping of subcortical pathways by magnetic resonance imaging diffusion tensor imaging with MEG source localization will, in the near future, provide even more accurate navigational tools for preoperative planning. Other possible future applications of MEG include the noninvasive estimation of language lateralization and the follow-up of brain plasticity elicited by central or peripheral neural lesions or during the treatment of chronic pain.
Conclusion:
MEG is a mature technique suitable for producing preoperative "road maps" of eloquent cortical areas and for localizing epileptiform activity.
... Benign Rolandic epilepsy of childhood (BREC) is a common primary partial epilepsy syndrome, which usually appears to children under age of 15 [21]. Interictal spike waveform of a child whose spike can be viewed as bilaterally synchronous discharge (BSD) was measured using a 45-channel scalp EEG system. ...
In this paper, a new hybrid approach to reconstruct more accurate brain functional source images from electroencephalography is proposed. The proposed approach combines extended source model and focal underdetermined system solution algorithm. Feasibility studies with realistic simulation data and the epilepsy patient's data demonstrate that continuous, as well as focalized, brain electrical source images can be reconstructed utilizing the proposed approach
Epilepsy and sleep are characterized by spontaneously occurring large graphoelements in electroencephalography (EEG) and magnetoencephalography (MEG) recordings, such as ictal and interictal epileptiform discharges in epilepsy and K-complexes (KC) in sleep. Localization of the neural sources of these graphoelements, which is of immense clinical and research importance, requires application of electromagnetic source analysis methods. A number of such methods are available; however their ability to localize widespread synchronous cortical sources, such as the sources of KCs and widespread epileptiform discharges, is contested. Here, we used KC as an exemplar of large graphoelements with such sources to test the performance of a diverse set of commonly employed source analysis methods. We analyzed segments of sleep MEG data with clear KCs using equivalent current dipole models, beamformer methods, linear distributed source methods, and a non-linear distributed source method—magnetic field tomography (MFT). MFT provided the most robust and steady localization across KCs, which was also highly consistent with the intracranial findings: strong and widespread activations were reliably found in superior aspects of bilateral frontal cortex. Conversely, the localizations provided by the other methods were very variable across KCs and were all inconsistent with the intracranial findings: in many cases, the KCs were incorrectly localized in deep medial brain structures. Our current and earlier results showing the excellent localization accuracy of MFT for focal as well as extended brain sources and the smart uses of MEG and EEG in epilepsy, demonstrate that the MFT analysis of MEG signals may be a powerful tool for the studies of epilepsy, epilepsy monitoring and in pre-surgical evaluation of patients.
To present applications of magnetoencephalography (MEG) in studies of neurosurgical patients.
MEG maps magnetic fields generated by electric currents in the brain, and allows the localization of brain areas producing evoked sensory responses and spontaneous electromagnetic activity. The identified sources can be integrated with other imaging modalities, e.g., with magnetic resonance imaging scans of individual patients with brain tumors or intractable epilepsy, or with other types of brain imaging data.
MEG measurements using modern whole-scalp instruments assist in tailoring individual therapies for neurosurgical patients by producing maps of functionally irretrievable cortical areas and by identifying cortical sources of interictal and ictal epileptiform activity. The excellent time resolution of MEG enables tracking of complex spaciotemporal source patterns, helping, for example, with the separation of the epileptic pacemaker from propagated activity. The combination of noninvasive mapping of subcortical pathways by magnetic resonance imaging diffusion tensor imaging with MEG source localization will, in the near future, provide even more accurate navigational tools for preoperative planning. Other possible future applications of MEG include the noninvasive estimation of language lateralization and the follow-up of brain plasticity elicited by central or peripheral neural lesions or during the treatment of chronic pain.
MEG is a mature technique suitable for producing preoperative "road maps" of eloquent cortical areas and for localizing epileptiform activity.
This paper proposes an alternative approach to enhance localization accuracy of MEG and EEG focal sources. The proposed approach assumes anatomically constrained spatio-temporal dipoles, initial positions of which are estimated from local peak positions of distributed sources obtained from a pre-execution of distributed source reconstruction. The positions of the dipoles are then adjusted on the cortical surface using a novel updating scheme named cortical surface scanning. The proposed approach has many advantages over the conventional ones: (1) as the cortical surface scanning algorithm uses spatio-temporal dipoles, it is robust with respect to noise; (2) it requires no a priori information on the numbers and initial locations of the activations; (3) as the locations of dipoles are restricted only on a tessellated cortical surface, it is physiologically more plausible than the conventional ECD model. To verify the proposed approach, it was applied to several realistic MEG/EEG simulations and practical experiments. From the several case studies, it is concluded that the anatomically constrained dipole adjustment (ANACONDA) approach will be a very promising technique to enhance accuracy of focal source localization which is essential in many clinical and neurological applications of MEG and EEG.
Magnetoencephalography (MEG) is a functional modality to register magnetic brain activity with high spatiotemporal resolution. Since distortion of magnetic fields by the skin, skull and cerebrospinal fluids is negligible, the technique offers an almost undistorted view on brain activity. While MEG systems are still expensive and complex, the technique's characteristics offer promising possibilities for the investigation of epilepsy patients, for example, for focus localization and presurgical functional mapping. This review gives an overview of the method and discusses advantages and limitations in the clinical context of presurgical epilepsy diagnosis.
To report benign epileptiform discharges (BEDs) in the Rolandic region, coexisting in a pediatric patient with intractable localization-related epilepsy, secondary to hippocampal sclerosis.
We describe the clinical features, MRI, scalp video EEG, magnetoencephalography (MEG) and intracranial video EEG findings, and surgical outcome in a 9-year-old boy with BEDs and intractable complex partial seizures.
MRI showed left hippocampal sclerosis. Scalp video EEG interictally demonstrated left temporal spike and sharply contoured slow waves, and right fronto-centro-temporal spike and waves. Ictal scalp video EEG showed left temporal rhythmic sharp waves after the clinical onset of epigastric aura, followed by staring. MEG showed interictal dipoles in the bilateral Rolandic regions with a uniform orientation and right hemispheric predominance. Intracranial video EEG, with bilateral mesial temporal depth and fronto-temporo-parietal strip electrodes, interictally showed polyspikes and slow waves with superimposed low-amplitude fast waves in the left mesial and posterior lateral temporal regions, and spike and waves in the bilateral fronto-parietal regions. Ictal onset was marked by low-amplitude fast waves in the left mesial and posterior lateral temporal regions. He underwent left anterior temporal lobectomy with hippocampectomy. Pathology was hippocampal sclerosis. Predominant right fronto-centro-temporal spike and waves and MEG right Rolandic dipoles persisted after surgery. He was seizure-free 14 months after surgery.
This is the first report on MEG and intracranial video EEG features of BEDs in the Rolandic region, coexisting with hippocampal sclerosis. Persistence of contralateral benign MEG Rolandic dipoles after surgery indicates that BEDs are coincidental in mesial temporal lobe epilepsy. MEG identified Rolandic dipoles, although was unable to localize the deep and focal epileptogenic dipoles from the hippocampal sclerosis.
The neurogenesis and functional organization of the interictal spikes in benign rolandic epilepsy of childhood (BREC) still remains controversial.
We performed a combined neuroelectric and neuromagnetic study in 24 consecutive patients with BREC using a 143-channel whole-head magnetoencephalography (MEG) system simultaneously with electroencephalography (EEG) recorded from 40 closely spaced scalp-EEG electrodes. Isopotential and isofield maps were calculated over the time window from 250ms before to 250ms after the maximum of the negative peak of the spike. We then performed principal component analysis (PCA) and spatio-temporal dipole modeling in order to estimate the number, location and temporal activity of sources.
EEG and MEG spikes were characterized by a stereotypical appearance both within and across patients showing a stable dipolar field distribution over the entire time window. The spikes were generated by a single tangential dipolar source located in the precentral gyrus with the positive pole directed frontally and the negative pole directed centro-temporally.
One source located in the precentral gyrus can adequately explain the spike complex in BREC.
Simultaneous EEG and MEG provide comprehensive information on functional organization of spikes in BREC.
Magnetoencephalography (MEG) is a noninvasive technique for investigating neuronal activity in the living human brain. The time resolution of the method is better than 1 ms and the spatial discrimination is, under favorable circumstances, 2-3 mm for sources in the cerebral cortex. In MEG studies, the weak 10 fT-1 pT magnetic fields produced by electric currents flowing in neurons are measured with multichannel SQUID (superconducting quantum interference device) gradiometers. The sites in the cerebral cortex that are activated by a stimulus can be found from the detected magnetic-field distribution, provided that appropriate assumptions about the source render the solution of the inverse problem unique. Many interesting properties of the working human brain can be studied, including spontaneous activity and signal processing following external stimuli. For clinical purposes, determination of the locations of epileptic foci is of interest. The authors begin with a general introduction and a short discussion of the neural basis of MEG. The mathematical theory of the method is then explained in detail, followed by a thorough description of MEG instrumentation, data analysis, and practical construction of multi-SQUID devices. Finally, several MEG experiments performed in the authors' laboratory are described, covering studies of evoked responses and of spontaneous activity in both healthy and diseased brains. Many MEG studies by other groups are discussed briefly as well.
In discussing the terminology used to identify this electro-clinical syndrome it is convenient to deal independently with (a) terms used to describe the characteristic location of the EEG sharp waves and (b) terms used to identify the electroclinical syndrome itself.
THE PRECISE and constant location of origin of the bilateral, symmetrical patterns of electrical discharge as they occur in man with "idiopathic" or "essential epilepsy" ("petit mal" and "grand mal") has not yet been completely defined. The characteristic electroencephalographic patterns which accompany the "absence" seizure of petit mal have not yet been exactly reproduced in animals.
The most distinctive electroencephalographic pattern of idiopathic epilepsy in childhood is the 2.5 to 3.5 cycle-per-second (cps) spike wave associated with the "absence" seizure. This discharge is abrupt in onset, bilateral, nearly synchronous, and of nearly equal amplitude in the two hemisphere. It is often precipitated by hyperventilation and photic stimulation.
Two distinct categories of hypotheses of the location of the lesion responsible for originating the bilateral grouped discharges of idiopathic epilepsy, especially in petit mal, have emerged: (1) The "centrencephalic" hypothesis of exclusive origin of the process giving rise to the spike
Benign focal epilepsy of childhood is an entity that includes characteristic clinical and electroencephalographic manifestations. Clinically, it consists of typical brief, hemifacial seizures that tend to become generalized when they occur nocturnally. The EEG findings include slow, diphasic, high-voltage, centro-temporal spikes, often followed by slow waves. Retrospective and prospective studies were carried out on 100 such patients, all of whom recovered before reaching adulthood, with the disappearance of both the clinical manifestations and the EEG findings.
Sequential topographic mapping was performed to differentiate "epileptic" from "non-epileptic" rolandic spikes. Twenty-four children without any indication of organic brain lesion were divided into a group with epilepsy and a group without epilepsy. The group with epilepsy was subdivided into "classical BECT" (benign focal epilepsy of childhood with centro-temporal spikes) and "non-classical BECT." Sequential mapping of the rolandic spikes revealed two different topographic patterns: a pattern of stationary potential fields and a pattern of non-stationary potential fields. The topographic pattern of stationary potential fields was morphologically represented by a single spike-and-wave complex whereas that of non-stationary potential fields was morphologically represented by a "double" spike-and-wave complex. Among the non-stationary topographic patterns represented by a "double" spike, one specific sequence of changes of potential fields was found. This sequence started with a dipolar field, with the negative pole in the frontal region and the positive pole in the centro-temporal region, morphologically represented by the small first spike of the "double" spike-and-wave complex. This dipolar field, changes to a unipolar or dipolar field, with a negative potential field in the centro-temporal region and, sometimes, a simultaneous positive potential field in the frontal region, morphologically represented by the prominent rolandic spike. This characteristic pattern was found to be significantly related to classical BECT.
Topographic EEG investigation with instant voltage mapping showed maximal negativity of 'rolandic' spikes over central or midtemporal electrodes with spread to parietal or upper frontal areas, and a dipole distribution (centrotemporal negativity, frontal positivity). There was no correlation of spike amplitude or duration with spread to adjacent areas. No other focal abnormalities, such as focal slowing, occurred. Spike activity was pronounced during light sleep and was often associated with generalized spike-wave activity, and thus was a sign of functional disturbance rather than the sequelae of brain damage. A review of the literature indicates that this pattern is helpful in differentiating this from focal abnormalities due to brain lesions.
In 41 patients with EEG features of benign epilepsy of childhood with centrotemporal spikes (BECCT), we noted associated generalized spike-wave discharges (GSWD) in 14.6% and multiple independent sharp wave foci in 9.8%. The presence or absence of these EEG features was not predictive of the clinical course. The high incidence of GSWD in children with BECCT suggests a possible relation in the expression of these two EEG traits.
In rolandic epilepsy, consideration of the stereotyped ictal symptomatology suggests that the epileptic zone is likely to be in the same cortical structure in different patients. Routine EEG tracings of the interictal spike activity suggests a deep Sylvian fissure location. On the basis of the predominantly tangential potential field at the peak spike negativity seen in this group of patients, the inferior bank of the Sylvian fissure appears to be a good candidate. Without invasive studies, little refinement to this rather imprecise localization can be made as there is neither neurologic deficit nor lesion to provide a marker on radiological imaging. However, the application of source modelling technique using a simple single-dipole spherical head model has resulted in improved understanding of the generator behaviour, and facilitated the generation of new ways of analyzing spikes (e.g., stability index). Review of newer quantitative approaches including matrix and singular value decomposition of the dataset, spatial-temporal constrained source estimates etc. suggest other fruitful approaches. At least in some patients with partial epilepsy, the source characteristics of interictal scalp spikes appear to contain information of the ictal generator. Under certain circumstances, such derived information which is not otherwise available from routine electrophysiology may influence clinical management and prognosis. This is an additional bonus to the primary objectives of quantification and data reduction.
The clinical literature has suggested that while the clinical features and presentation of benign rolandic epilepsy in children (BREC) are known, the neuronal mechanism of the epileptic focus is poorly understood. Classification of clinical subtypes is usually made by determining whether there are supplementary clinical signs of brain damage, in which case the epilepsy is classified as non-benign or "atypical". Studies of EEG findings in BREC have suggested that the source of the epilepsy is in the Rolandic fissure. We investigated dipole source modelling in 24 children, comparing the results of one and two dipole models. The results indicate that atypical BREC patients have a more complex distribution of dipoles and that single dipole fits may be more predictive of typical BREC than multiple dipole fits. The implications of these results are discussed.
We studied the effect of corpus callosum section on secondary bilaterally synchronous interictal EEG discharges in 13 patients with partial and secondarily generalized seizures before and after partial or complete section of the corpus callosum. Bilaterally synchronous discharges were completely eliminated in one patient. In 12 patients, there was a distinct reduction in frequency. Our clinical experience agrees with experimental data to suggest that epileptic discharges follow pathways, both across the corpus callosum and/or down to diencephalic/mesencephalic structures, before there is bilateral spread.
A 10 year material of patients with centro-temporal EEG foci and seizures was studied retrospectively. 94 patients were found, all children. Estimates of the prevalence in the geographical area under study showed that this type of epilepsy with the accompanying EEG changes is about seven times more common than petit mal.
A positive family history of seizures was found in 18 % of the cases, which suggests an hereditary predisposition of the same type as that proposed for petit mal and the 3/sec spike and wave trait. 55 % of the patients had had nocturnal seizures only.
40 patients were more than 15 years old and were further studied with respect to long-term prognosis. At the follow-up, 38 patients had been seizure-free (with or without therapy) for between 4 and 13 (mean: 8.1) years. The patients nevertheless had met with some social difficulties on account of their seizures. Most EEGs (35 of 40) were normal or border-line at the follow-up. In no case did the Rolandic paroxysms persist.
It is concluded that this is a benign form of convulsive disorder found exclusively in childhood. The typical case is described and the term “benign epilepsy in children with centro-temporal EEG foci” is proposed.
Un lot de patients, présentant un foyer EEG centro-temporal et des crises, a étéétudié rétrospectivement pendant 10 ans.
On a trouvé 94 sujets quiétaient tous des enfants. L'évaluation de la prévalence dans la région étudiée a montré que ce type d'épilepsie avec ses modifications EEG est environ 7 fois plus commun que le Petit Mal.
Dans 17 % des cas, on a trouvé une histoire familiale de crises, ce qui suggère une prédisposition héréditaire du même type que celle proposée pour le Petit Mal et les pointe-ondes à 3 c/s. 55 % des patients avaient présenté seulement des crises nocturnes. 40 patients avaient plus de 15 ans et ils ont été suivis par la suite pour avoir un prognostic à long terme.
Dans leur évolution, 38 sujets n'avaient pas présenté de crises (avec ou sans traitement) pendant 4 à 13 ans (moyenne: 8.1ans).
Néanmoins, certains patients avaient rencontré quelques difficultés sociales à cause de leurs crises. La plupart des EEG (35 sur 40) avaient été normaux ou à la limite de la normale, dans l'évolution. Dans aucun cas, il n'avait persisté de paroxysme rolandique.
On-en conclut qu'il s'agit d'une forme d'épilepsie bénigne qu'on trouve seulement dans l'enfance.
Le tableau clinique typique est décrit et le terme de ←crises sylviennes bénignes de l'enfant avec foyer EEG, centro-temporal→ est proposé.
This discussion has examined 2 central questions regarding the pathophysiology of petit mal epilepsy. First, what is the locus of the lesion responsible for the bilateral synchronous and symmetrical spike‐slow wave discharges and the associated behavioral absence of petit mal epilepsy? We have demonstrated that it is possible to produce an experimental model of petit mal epilepsy in the otherwise intact cat or monkey without the necessity of lesions in the brain stem or diencephalic structures. The essential lesion in this model is solely cortical and bilateral in location. In particular our experiments have involved the production of acute relatively large bilateral and symmetrical cortical epileptogenic foci. The interaction of these foci resulted in the development of synchronous and symmetrical patterns of bilateral discharge resembling the various forms of human primary bilateral synchrony including the 2½‐4 c/s spike‐slow wave complex. In the monkey, regional variations in capacity for bilateral discharge were noted, related to regional differences in callosal projection. Particularly well regulated bilaterally synchronous and symmetrical bursts of 2½‐4 c/s spike‐slow wave complexes occurred with bilateral foci in the premotor area of monkey frontal lobe. Studies of behavior and simultaneously recorded electroencephalogram indicated that bilateral synchronous discharges of 3 c/s spike‐slow wave complex resulting from bilateral foci in anterior premotor area were closely correlated with short staring spells resembling petit mal (absence) seizures.
Second, irrespective of where the responsible lesion(s) may be located, are the brain stem and diencephalic structures essential for the development of these bilateral symmetrical and synchronous discharges of 2½‐3 c/s spike‐slow wave complexes which are the hallmark of petit mal epilepsy? From the standpoint of the present model, it is demonstrated that section of the corpus callosum in the cat or of all major commissures in the monkey markedly disrupted the synchrony of discharge of bilateral foci. Alternate pathways for coarse synchrony at low rates of discharge were demonstrated. These results should be compared to the high degree of synchrony of bilateral discharge obtained in the cat or monkey preparation in which large blocks of cerebral cortex in each hemisphere were isolated from subcortical structures but remained connected via the corpus callosum. The spike discharges of bilateral foci in this preparation were synchronized within 10–20 msec, well within the limits noted in the intact animal and in the patient with petit mal epilepsy. The patterns of bilateral discharge in this cortical‐callosal preparation included bilateral synchronous bursts of 2½‐3 c/s spike‐slow wave complexes.
RÉSUMÉ
Ce travail envisage deux questions essentielles concernant la physiopathologie de l'épilepsie petit mal. Première question: Quel est le siège de la lésion responsable des décharges bilatérales, synchrones et symétriques de pointes‐ondes qui accompagnent les absences petit mal? Nous avons démontréà ce propos qu'il est possible de reproduire une épilepsie du type petit mal chez un chat ou un singe d'autre part normal indépendamment de toutes lésions du tronc cérébral ou du diencéphale. II suffit de réaliser chez ces animaux des lésions corticales bilatérales, notamment des foyeis épileptogènes corticaux aigus, bilatéraux et symétriques, assez étendus. L'interaction de ces foyers aboutit à la production de décharges bilatérales synchrones et symétriques ressemblant aux différents types de synchronic bilatérale primaire observée chez FHomme, y compris la pointe‐onde à 2½‐4 c/s. Chez le singe on observe des variations régionales dans la capacityé de produire des décharges bilatérales qui dépendent des différences régionales dans les projections commissurales calleuses; c'est ainsi que les bouffées de pointes‐ondes bilatérales synchrones et symétriques à 2½‐4 c/s particulièrement régulierès, accompagnees de troubles du comportement evoquant une absence, surviennent sous l'effet de foyers bilatéraux dans l'aire prémotrice des lobes frontaux.
Deuxième question: Quel que soit le siège des lésions responsables, le tronc cérébral et le diencéphale sont‐ils indispensables pour le développement des décharges bilatérales synchrones et symétriques de pointes‐ondes à 2½‐4 c/s qui sont caracté‐ristiques des épilepsies petit mal?
En ce qui concerne nos propres expériences, il apparaît que la section du corps calleux du chat ou celle de toutes les grandes commissures chez le singe altère considérablement la synchronic des décharges de foyers bilatéraux. Ces résultats contrasted avec le haut degré de synchronic des décharges bilatérales obtenues dans les larges étendues de cortex cérébral qui, dans chaque hémisphère, sont isolées des structures sous‐corticales mais demeurent interconnectées à travers le corps calleux. Dans de telles préparations cortico‐callosales, les décharges de pointes des complexes pointes‐ondes recueillies dans les foyers bilatéraux sont synchronisés dans des limites de 10–20 msec qui correspondent à celles observées chez l'animal intact ou chez le sujet humain présentant une épilepsie petit mal.
"S ylvian SEIZURES" is a term proposed for one of the partial epilepsies of childhood, with a relatively elementary symptomatology, yet one that may be confused within the protean group of temporal lobe epilepsy.
Their age incidence, the peripheral manifestations, the clinical and electrographic correlates, the mode of propagation, prognosis are all sufficiently homogenous to justify a special subgrouping.
The most characteristic peripheral features can be summarized as follows. First, there is almost always some somatosensory involvement, most often of the tongue, but occasionally of inner cheeks, lips or gums, or even of a single tooth, while typical visceral aurae are rare. The sensory involvement is usually contralateral to the electroencephalographic focus but may be ipsilateral. More rarely a vertiginous component may be present. Second, speech arrest, not due to dysphasia but to motor interference, or anarthria. Third, preservation of consciousness, in most cases. Fourth, excessive pooling of saliva. Fifth
The onset, distribution, and spread of the average of 20 centrotemporal discharges for each of 10 patients with typical benign rolandic epilepsy of childhood (BREC) were examined using a computerized topographical mapping technique. A stereotypic dipole field was present along the rolandic region in all discharges. During its most prominent phase, the negative pole of the dipole was maximum at the centrotemporal region, with the positive pole involving the bifrontal region. A hypothesis is proposed that all discharges arise from a single generator which is oriented tangential to the surface. The generator is most likely situated in the lower rolandic region where the zero potential zone exists, between the frontal positivity and the centrotemporal negativity. Identification of this dipole configuration may be useful for differentiating BREC from focal epilepsy of other etiologies.
RÉSUMÉ
Le début, la distribution, et la propagation de la moyenne de 20 décharges centrotemporales pour chacun de dix patients ayant une épilepsie rolandique bénigne de l'enfant (EPR), ont étéétudiés, en utilisant une technique d'analyse topographique computorisée. Un champ dipole stéréotypéétait présenté sur la région rolandique dans toutes les décharges. Pendant sa phase la plus importante, le pôle négatif du dipole était maximum dans la région centrotemporale, et le pôle positif occupant la région bifrontale. Il est proposé l'hypothèse que toutes les décharges proviennent d'un seul générateur qui est orienté tangentiellement á la surface. Le générateur est le plus probablement situé dans la région rolandique basse ou existe la zone de potentiel zéro, entre la positivité frontale et la négativité centro‐temporale. L'identification de la configuration de ce dipole peut être utile pour différencier l'EPR des epilepsies focales d'autres etiologies.
ZUSAMMENFASSUNG
Der Beginn, die Verteilung und die Ausbreitung des Mittel‐werts 20 centrotemporaler Entladungen bei jedem der 10 Pa‐tienten mit typischer benigner Rolandischer Epilepsie des Kin‐desalters (B.R.E.C.) wurden mit Hilfe einer komputerisierten topographischen Landkartentechnik untersucht. Ein stereotyp‐isches Dipol‐Feld konnte bei alien Entladungen entlang der Ro‐landischen Region beobachtet werden. Auf seinem Höhepunkt zeigte der negative Pol zur Zentro‐Temporal‐Region, der positive Pol zu beiden Frontalregionen. Als Hypothese wird vorge‐schlagen, daβ alle Entladungen von einem einzigen Generator ihren Ausgang nehmen, der tangential zur Oberfläche orientiert ist. Dieser Generator sitzt am wahrscheinlichsten in der unteren Rolandischen Gegend, in der das Nullpotential zu denken ist zwischen der frontalen Positivität und der zentro‐temporalen Negativität. Die Identifizierung dieser Dipol‐Konfiguration mag nützlich sein für Differenzierung von B.R.E.C. und fokalen Epi‐lepsien anderer Ätiologie.
Post-natal development of the cerebello-cerebral response was investigated in 126 kittens from birth to 142 days of age by analysis of laminar field potentials in the cerebral cortex; the thalamocortical projection mediating the cerebello-cerebral response was examined on four new-born and three one-month-old kittens by means of anterograde axonal transport of horseradish peroxidase. A marked response was evoked in the frontal motor cortex from birth and an appreciable response could be evoked in the parietal association cortex at 2 days after birth. The latency of response in the frontal cortex decreased sharply from birth till 3 weeks of age whereas that in the parietal cortex remained almost unchanged until 2 weeks of age. Maturation of the cerebello-cerebral projection, in every respect, proceeds earlier in the frontal cortex than in the parietal cortex. The cerebello-cerebral response in kittens at any age, like in adult cats, consisted of two types of elementary responses: one which is characterized by a surface positive-depth negative (s.p.-d.n.) wave and the other which is characterized by a surface negative-depth positive (s.n.-d.p.) wave. The response in the frontal cortex was a sequential occurrence of the two waves while the responses in the parietal cortex was a pure form of the s.n.-d.p. wave. Two types of thalamocortical projections corresponding to the two types of elementary responses were revealed: one is the projection mainly onto layer I which appears to mediate the s.n.-d.p. wave and the other is the projection mainly onto layer III which appears to mediate the s.p.-d.n. wave. Development of the cerebello-cerebral response and changes in the terminal distribution of the thalamocortical projection during maturation are consistent with the principle of ontogenesis of the mammalian neocortical organization, i.e. ascending sequential maturation.
In this study on interhemispheric synchrony of spike and wave discharges in feline generalized penicillin epilepsy, four groups of cats were treated in the following manner: Group A underwent complete section of the corpus callosum and anterior commissure; group B underwent division of the massa intermedia alone; group C underwent partial section of the corpus callosum; and in group D, a slab of the cortex on one side, comprising the middle parts of the lateral and suprasylvian gyri, was severed from all its subcortical inputs, without disturbing its connections with the opposite hemisphere through the corpus callosum. Two weeks after surgery or later the cats received an i.m. injection of penicillin. Bilateral synchrony of the epileptic discharges was abolished in group A, but not in group B. In group C, bilateral synchrony of the epileptic bursts was impaired, but not abolished. In group D, epileptic bursts synchronous with those occurring in the intact hemisphere continued to occur in the slab, but at lower amplitude. It is concluded that the corpus callosum is the main, if not the exclusive, pathway ensuring bilateral synchrony of the epileptic discharges of feline generalized penicillin epilepsy.
RÉSUMÉ
Sur des préparations chroniques la section du corps calleux et de la commissure antérieure abolit la synchronic bilatérale des décharges généralisdes de Ľépilepsie généralisée pénicillinique du chat. Cette bisynchronie ne réapparaît pas, même au bout de 3 mois. La section de la massa intérmedia du thalamus n'abolit pas cette synchronie bilatérale. La section partielle du corps calleux gêne cette synchronie bilatérale sans toutefois la supprimer. Sur un lambeau cortical unilatéral déconnecté de ses afférences ďorigine sous corticale mais connectéàĽhémisphère opposé par Ľintermédiaire du corps calleux, on observe toujours des bouffées synchrones avec celles qui surviennent sur Ľhémisphère intact, mais elles sont moins amples. De ces données on tire la conclusion que le corps calleux est la voie principale, sinon exclusive, qui assure la synchronie bilatérale des décharges de Ľépilepsie généralisée pénicillinique du chat. On ignore toutefois si le même mécanisme est responsable de la synchronie bilatérale de Ľépilepsie généralisée cortico‐réticulaire de Ľhomme.
RESUMEN
La sección del cuerpo calloso y de la comisura anterior en preparaciones crónicas suprime la sincronía bilateral de las descargas generalizadas en la epilepsía generalizada por penicilina en felinos. La sincronía bilateral no reaparece, incluso 3 meses después. La sección de la masa intermedia del tálamo no abole la sincronía bilateral de las descargas epilépticas en este modelo. La sección parcial del cuerpo calloso afecta parcialmente la sincronía bilateral de los paroxismos epilépticos, sin suprimirlos del todo. En una rodaja unilateral de corteza, desconectada de estímulos subcorticales pero conectada al hemisferio contralateral a través del cuerpo calloso, descargas epilépticas síncronas con las observadas en el hemisferio intacto siguen observándose, aunque son de menor amplitud. La conclusión es que el cuerpo calloso es la vía principal, si no exclusiva, que posibilita la sincronía bilateral de las descargas epilépticas del modelo de felino con epilepsía generalizada por penicilina. Sigue sin saberse si el mismo mecanismo es responsable de la sincronía bilateral de la epilepsía córtico‐reticular en humanos.
ZUSAMMENFASSUNG
Im chronischen Versuch verhindert die Durchschneidung des Corpus callosum une der vorderen Commissur die bilaterale Synchronie der generalisier‐ten Entladungen einer generalisierten Penicillin‐Epilepsie der Katze. Selbst nach 3 Monaten ist keine bilaterale Synchronie wieder zu erkennen. Die Durchtrennung der Massa intermedia des Thalamus verhindert in diesem Modell nicht die bilaterale Synchronie epileptischer Entladungen. Die partielle Durchtrennung des Corpus callosum beeintrachtigt die bilaterale Synchronie epileptischer Entladungen ohne sie jedoch vollständig zu verhindern. Innerhalb eines einseitigen kortikalen Areals, das von subkortikalen Zuflüssen abgetrennt wurde, jedoch in Kontakt blieb mit der intakten Gegenhemisphäre durch das Corpus callosum, treten weiter epileptische Ausbrüche synchron mit solchen auf, die in der intakten Hemisphäre erscheinen; aber sie zeigen eine niedrigere Amplitude. Es ist zu folgern, daß das corpus callosum den wesentlichen aber nicht einzigen Weg darstellt, eine bilaterale Synchronie epileptischer Entladungen bei der generalisierten Penicillin‐Epilepsie der Katze zu gewährleisten. Es bleibt unbekannt, ob die gleichen Mechanismen verantwortlich sind für die bilaterale Synchronie bei der generalisierten kortikoretikulären Epilepsie des Menschen.
Whole-head magnetoencephalographic recordings revealed two parietal epileptic foci in homotopic areas of the hemispheres. The discharges occurred 17-20 ms later on the left than on the right hemisphere, implying the existence of a left-sided mirror focus. The foci were about 1 cm posterior to the hand primary somatosensory area, identified by evoked response measurements, and thus suggested epileptic activity at the parietal association cortex, in agreement with the observed callosal conduction time.
Until relatively recently, genetic influences in partial seizures were thought to be of minimal importance. However, with further identification of childhood benign partial seizures it is becoming clear that inheritance plays a major role in the pathogenesis of these seizures. Diagnostic criteria proposed for benign partial seizures include absence of neurologic or intellectual deficits, family history of epilepsy, onset of seizures after age 2 years, stereotyped brief seizures, frequent nocturnal occurrence, spontaneous remission in adolescence, and electroencephalograms (EEGs) demonstrating spikes with a distinctive morphology and localization superimposed on normal background activity. The two most commonly described benign partial epilepsies of childhood are benign Rolandic epilepsy (BRE) and benign occipital epilepsy (BOE). Both disorders begin in childhood, are associated with characteristic EEG patterns, have seizures that are easily controlled with medication, often are familial, and have an excellent prognosis. The other benign partial seizure disorders in children that have been described are not as well studied as BOE and BRE, and the role of inheritance pattern, if any, is less clear.
"Centrotemporal" (rolandic) spikes are elemental to the diagnosis of benign rolandic epilepsy (BRE) and may reveal a characteristic dipole distribution. Yet, not all children with rolandic spikes present with clinical seizures. Using additional scalp coverage according to the 10-10 electrode system, we attempted to correlate 2 specific spike features: (a) dipole fields, and (b) exact location of maximum negativity, with the presence or absence of clinical seizures in 42 neurodevelopmentally normal children with rolandic (central) spikes. Thirty-three (79%) presented with seizures. Seventeen of 21 children revealing dipoles (81%) and 16 of 21 patients without dipoles (74%) had seizures. Children with high central (C3/C4) foci were just as likely to present with seizures (10 of 15, 67%) as were those with low central (C5/C6) foci (23 of 27, 85%) (P > 0.10). The majority of our study subjects (27 of 42, 64%) revealed maximum negativity in the low central region (C5/C6), and the dipole feature was as likely to be associated with high central foci (7 of 15, 47%) as with low central foci (14 of 27, 52%). Although rolandic spikes are a reliable indicator of potential epileptogenicity, neither their exact location nor dipolar distribution help to further define the population with clinical seizures.
We report the detailed analysis of the generator and propagation of rolandic discharges in benign childhood epilepsy with centrotemporal spikes by means of 37-channel magnetoencephalography with neuromagnetic three-dimensional dipole localization. Equivalent current dipoles of prominent negative sharp waves of rolandic discharges appeared as tangential dipoles in the rolandic region, positive poles being situated anteriorly. These equivalent current dipoles showed a relatively limited localization and regular directions compared with other components. Equivalent current dipoles of preceding small positive waves, positive waves following negative sharp waves, and negative slow waves appeared in the vicinity of negative sharp waves. Equivalent current dipoles of rolandic discharges were located around the generator of somatosensory evoked magnetic fields stimulated at the lower lip. These findings suggest that rolandic discharges are generated through basically a mechanism similar to that for the middle-latency components of somatosensory evoked responses.
We studied the functional organization of the interictal epileptic spike complex in patients with benign rolandic epilepsy of childhood (BREC).
We recorded interictal epileptiform spikes and somatosensory evoked potentials after median nerve stimulation, providing a biologic marker for the location of the central sulcus in 12 patients with BREC. We used multiple dipole modeling to assess the number, the three-dimensional intracerebral location, and the time activity of the underlying neuronal sources.
Although the interictal spike complex could be modeled by a single tangential dipolar source in seven patients (group 1), in the remaining five patients, two sources-a radial and a tangential dipole-were necessary adequately to explain the interictal spikes (group 2). The tangential source was located deeper than the radial source and was characterized by a frontal positivity and a centroparietal negativity with a phase reversal across the central sulcus, suggesting that the interictal spikes originated in the anterior wall of the central sulcus. The radial source showed a single electronegativity over the ipsilateral central region, which would be compatible with involvement of the top of either the pre- or postcentral gyrus. Both sources showed biphasic time patterns with an average latency difference of 30 ms.
Our results indicate that in some patients with typical BREC, the interictal epileptiform spike complex is generated by multiple, simultaneously active neuronal populations within the central region and that epileptiform activity is propagated between these two adjacent cortical areas.
Benign epilepsy of childhood with rolandic spikes (BECRS) is an electroclinical syndrome characterized by partial sensorimotor seizures with centrotemporal spikes. We report a detailed localization analysis of spontaneous magnetic brain activities in seven BECRS patients using magnetoencephalography (MEG). All patients had BECRS diagnosis with typical seizures and electroencephalographic findings and five patients had minor psychomotor deficits. MEG was recorded over both parieto-temporal regions using a 2x37-channel biomagnetic system. The collected data were digitally bandpass-filtered (2-6, 14-30, or 1-70 Hz) to analyze slow- and fast-wave magnetic activities and rolandic spikes. Slow-wave activity was increased in four hemispheres of three patients. Increased fast-wave activity was found in all five patients with minor neuropsychological deficits. The presence of increased fast-wave magnetic brain activity appeared to cause functional anomalies in the higher brain function processes. In the spike analysis, the dipoles of rolandic spikes which constantly manifested anterior positivity in direction were concentrated in the superior rolandic region in four cases and the inferior rolandic region in three cases. The localizations of increased slow- and fast-wave activities were identical with those of the spikes. The seizure profiles were frequently characterized by the spike locations. Source localizations of the focal brain activities and rolandic spikes by MEG will contribute to the different diagnosis and pathophysiological elucidation of BECRS.
We studied eight healthy subjects with a whole-scalp 306-channel neuromagnetometer to explore the effect of motor activity from different body parts on somatosensory responses to left median nerve stimulation. The stimuli produced clear tactile sensation without any motor movement. In the rest condition, the subject had no task. During contraction conditions, the subject had to maintain submaximal isometric contraction in masseter, left deltoid, left thenar, or left tibialis muscles. Short-latency responses from the primary somatosensory cortex did not change during contraction. Responses from both the right (contralateral) and left second somatosensory cortices (SII) were significantly enhanced during contraction of the left thenar muscles. Responses from the left SII were significantly enhanced also during contraction of the left deltoid muscles, but they were decreased during contraction of the masseter and left tibialis anterior muscles. This study implies that SII activation is modulated by motor activity and that the effect depends on the topographical proximity of the stimulated and contracted body parts.
We report five patients with rolandic epilepsy associated with giant somatosensory responses to median nerve stimulation, in whom we analyzed the pathophysiologic relationship between rolandic discharges and the somatosensory responses using magnetoencephalography. Four of the five patients showed giant P30m, the current source of which was localized in the primary somatosensory cortex, while the first cortical response, N20m, was not enhanced, except in one patient. The current source of the giant middle-latency component, N70m, was localized posterior to that of N20m, possibly in the posterior parietal cortex, in all patients. The initial positive peak and large negative peak of rolandic discharges were identical to P30m and N70m with respect to the current source localization, wave form, topographic pattern, and time relationship in the electroencephalogram and magnetoencephalogram, and somatosensory evoked magnetic field and somatosensory evoked potential records, respectively. In addition, the secondary sensory cortex was considered to be the generator of the middle-latency component in one patient. In one patient, the current intensity of the N70m was normalized along with clinical improvement and the disappearance of rolandic discharges, whereas those of other somatosensory evoked magnetic field components remained unchanged. Our data suggest that the rolandic discharge generator mechanism in these patients could be closely related to the developmental alteration of excitability in the primary somatosensory cortex, posterior parietal cortex, and secondary somatosensory cortex, which decreased with age, and it could share a common neuronal pathway, at least in part, with the giant P30m-N70m (N90m) in the somatosensory evoked magnetic field through the sequential and parallel processing of somatosensory information.
To evaluate the source location and clinical significance of rhythmic mid-temporal theta discharges (RMTD) by MEG in non-epileptic and epileptic patients, we conducted simultaneous MEG and EEG recordings with a whole-scalp 306-channel neuromagnetometer in three patients: one with right temporal lobe epilepsy (TLE), one with right frontal lobe epilepsy (FLE), and one with tension headache. We visually detected the RMTD activity and interictal spikes, and then localised their generators by MEG source modelling. We repeated MEG measurement 3 months after right anterior temporal lobectomy (ATL) in the TLE patient; 3 months after anticonvulsant medication in the FLE patient. In epileptic patients, RMTD activities were found during drowsiness over the left temporal channels of both MEG and EEG recordings, and their generators were localised to the left posterior inferior temporal region. In the patient with tension headache, RMTD was localised in the right inferior temporal area. When the epileptic patients became seizure free with disappearance of epileptic spikes, RMTD was still found over the left temporal channels. Besides, some bursts of RMTD appeared also in the right temporal channels in our TLE patient after ATL. Our results indicate that the source of RMTD activity is located in the fissural cortex of the posterior inferior temporal region. As a physiologic rhythm related to dampened vigilance, RMTD has no direct relation to epileptogenic activity.
THE EFFECT of section of the corpus callosum on human epilepsy remains a controversial issue. Van Wagenen and Herren1 found that in patients with generalized convulsions section of commissural pathways contained in the corpus callosum limited the spread in a unilateral convulsion with no loss of consciousness. Erickson,2 using electrical stimuli, showed that in the monkey section of the corpus callosum played a definite role in the spread of a discharge from one hemisphere to the other. Curtis3 concluded that the typical response to the application of a convulsant drug in monkeys and cats was mediated by the corpus callosum and abolished by its section. Obrador Alcalde,4 studying convulsive attacks produced by electrical stimulation of the cortex in cats, reported that section of the corpus callosum did not change the fundamental character of the convulsions and concluded that the corpus callosum was not an association system
The electroencephalogram in parasagittal lesions
- K Tukel
- H Jasper
Tukel, K. and Jasper, H. The electroencephalogram in
parasagittal lesions. Electroencephalography and Clinical
Neurophysiology 1952; 4: 481–494.