146 research outputs found

    Evidence for the role of magnetic source imaging in the presurgical evaluation of refractory epilepsy patients

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    Magnetoencephalography (MEG) in the field of epilepsy has multiple advantages; just like electroencephalography (EEG), MEG is able to measure the epilepsy specific information (i.e., the brain activity reflecting seizures and/or interictal epileptiform discharges) directly, non-invasively and with a very high temporal resolution (millisecond-range). In addition MEG has a unique sensitivity for tangential sources, resulting in a full picture of the brain activity when combined with EEG. It accurately allows to perform source imaging of focal epileptic activity and functional cortex and shows a specific high sensitivity for a source in the neocortex. In this paper the current evidence and practice for using magnetic source imaging of focal interictal and ictal epileptic activity during the presurgical evaluation of drug resistant patients is being reviewed

    The ictal wavefront is the spatiotemporal source of discharges during spontaneous human seizures

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    abstract: The extensive distribution and simultaneous termination of seizures across cortical areas has led to the hypothesis that seizures are caused by large-scale coordinated networks spanning these areas. This view, however, is difficult to reconcile with most proposed mechanisms of seizure spread and termination, which operate on a cellular scale. We hypothesize that seizures evolve into self-organized structures wherein a small seizing territory projects high-intensity electrical signals over a broad cortical area. Here we investigate human seizures on both small and large electrophysiological scales. We show that the migrating edge of the seizing territory is the source of travelling waves of synaptic activity into adjacent cortical areas. As the seizure progresses, slow dynamics in induced activity from these waves indicate a weakening and eventual failure of their source. These observations support a parsimonious theory for how large-scale evolution and termination of seizures are driven from a small, migrating cortical area.The final version of this article, as published in Nature Communications, can be viewed online at: https://www.nature.com/articles/ncomms1109

    Imaging of epileptic activity using EEG-correlated functional MRI.

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    This thesis describes the method of EEG-correlated fMRI and its application to patients with epilepsy. First, an introduction on MRI and functional imaging methods in the field of epilepsy is provided. Then, the present and future role of EEG-correlated fMRI in the investigation of the epilepsies is discussed. The fourth chapter reviews the important practicalities of EEG-correlated fMRI that were addressed in this project. These included patient safety, EEG quality and MRI artifacts during EEG-correlated fMRI. Technical solutions to enable safe, good quality EEG recordings inside the MR scanner are presented, including optimisation of the EEG recording techniques and algorithms for the on-line subtraction of pulse and image artifact. In chapter five, a study applying spike-triggered fMRI to patients with focal epilepsy (n = 24) is presented. Using statistical parametric mapping (SPM), cortical Blood Oxygen Level-Dependent (BOLD) activations corresponding to the presumed generators of the interictal epileptiform discharges (IED) were identified in twelve patients. The results were reproducible in repeated experiments in eight patients. In the remaining patients no significant activation (n = 10) was present or the activation did not correspond to the presumed epileptic focus (n = 2). The clinical implications of this finding are discussed. In a second study it was demonstrated that in selected patients, individual (as opposed to averaged) IED could also be associated with hemodynamic changes detectable with fMRI. Chapter six gives examples of combination of EEG-correlated fMRI with other modalities to obtain complementary information on interictal epileptiform activity and epileptic foci. One study compared spike-triggered fMRI activation maps with EEG source analysis based on 64-channel scalp EEG recordings of interictal spikes using co-registration of both modalities. In all but one patient, source analysis solutions were anatomically concordant with the BOLD activation. Further, the combination of spike- triggered fMRI with diffusion tensor and chemical shift imaging is demonstrated in a patient with localisation-related epilepsy. In chapter seven, applications of EEG-correlated fMRI in different areas of neuroscience are discussed. Finally, the initial imaging findings with the novel technique for the simultaneous and continuous acquisition of fMRI and EEG data are presented as an outlook to future applications of EEG-correlated fMRI. In conclusion, the technical problems of both EEG-triggered fMRI and simultaneous EEG-correlated fMRI are now largely solved. The method has proved useful to provide new insights into the generation of epileptiform activity and other pathological and physiological brain activity. Currently, its utility in clinical epileptology remains unknown

    Methodological and clinical aspects of ictal and interictal MEG

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    During the last years magnetoencephalography (MEG), has become an important part of the pre-surgical epilepsy workup. Interictal activity is usually recorded. Nevertheless, the technological advances now enable ictal MEG recordings as well. The records of 26 pharmaco-resistant focal epilepsy patients, who underwent ictal MEG and epilepsy surgery, were reviewed. In 12 patients prediction of ictal onset zone (IOZ) localization by ictal and interictal MEG was compared with ictal intracranial EEG (icEEG). On the lobar surface level the sensitivity of ictal MEG in IOZ location was 0.71 and the specificity 0.73. The sensitivity of the interictal MEG was 0.40 and specificity 0.77. The records of 34 operated epilepsy patients with focal cortical dysplasia (FCD) were retrospectively evaluated. The resected proportion of the source cluster related to interictal MEG was evaluated in respect to postoperative seizure outcome. 17 out of 34 patients with FCD (50%) achieved seizure freedom. The seizure outcome was similar in patients with MR-invisible and MR-visible FCD. With MEG source clusters and favorable seizure outcome (Engel class I and II) the proportion of the cluster volume resection was 49% - significantly higher (p=0.02) than with MEG clusters but unfavorable outcome (5.5% of cluster volume resection). Median nerve somatosensory evoked MEG responses were processed by movement compensation based on signal space separation (MC-SSS) and on spatio-temporal signal space separation (MC-tSSS). MEG was recorded in standard and deviant head positions. With up to 5 cm head displacement, MC-SSS decreased the mean localization error from 3.97 to 2.13 cm, but increased noise of planar gradiometers from 3.4 to 5.3 fT/cm. MC-tSSS reduced noise from 3.4 to 2.8 fT/cm and reduced the mean localization error from 3.91 to 0.89 cm. The MEG data containing speech-related artifacts and data containing alpha rhythm were processed by tSSS with different correlation limits. The speech artifact was progressively suppressed with the decreasing tSSS correlation limit. The optimal artifact suppression was achieved at correlation of 0.8. The randomly distributed source current (RDCS), and auditory and somatosensory evoked fields (AEFs and SEFs) were simulated. The information was calculated employing Shannon's theory of communication for a standard 306-sensor MEG device and for a virtual MEG helmet (VMH), which was constructed based on simulated MEG measurements in different head positions. With the simulation of 360 recorded events using RDCS model the maximum Shannon's number was 989 for single head position in standard MEG array and 1272 in VMH (28.6% additional information). With AEFs the additional contribution of VMH was 12.6% and with SEFs only 1.1%. To conclude, ictal MEG predicts IOZ location with higher sensitivity than interictal MEG. Resection of larger proportion of the MEG source cluster in patients with FCD is associated with a better seizure outcome, however, complete resection of MEG source cluster is often not required for achievement of favorable seizure outcome. The seizure outcome is similar in patients having MR-positive and MR-negative FCD. MC-tSSS decreases the source localization error to less than 1 cm, when the head is displaced up to 5 cm; however, it is reasonable to limit use of movement compensation for no more than 3-cm head displacement to keep the head inside sensor helmet. The optimization of the tSSS correlation limit to about 0.8 can improve the artifact suppression in MEG without substantial change of brain signals. MEG recording of the same brain activity in different head positions with subsequent construction of VMH can improve the information content of the data.Magnetoenkefalografia (MEG) on menetelmä, jolla mitataan aivojen tuottamia heikkoja magneettikenttiä. Yksi menetelmän tärkeimmistä kliinisistä käyttö-tarkoituksista on paikantaa epilepsiapesäkkeitä aivoissa. Tämä on tärkeää epilepsiakirurgian suunnittelussa. Potilaan liikkeet mittauksen aikana ovat aiheuttaneet epätarkkuutta pesäkkeiden paikannukseen ja häiriösignaaleja mittauksiin. Ongelma on ollut erityisen korostunut lasten mittauksissa ja epileptisten kohtausten rekisteröinneissä. Useimmissa potilaissa MEG-paikannus onkin perustunut kohtausten välisten epileptiformisten aivosähköilmiöiden paikannukseen. Pitkät MEG-rekisteröinnit ovat myös olleet haastavia koska yhteistyökykyisten potilaidenkin on vaikea olla liikkumatta pitkiä aikoja. Viime vuosien tekninen kehitys on mahdollistanut MEG-mittaukset myös pään liikkeiden aikana. Myös aivosignaalien ja kehossa olevien magneettisten materiaalien (esim hammaspaikat, sydämen tahdistimet tai aivostimulaattorit) aiheuttamien magneettisten häiriöiden erottaminen on nykyisin toteutettavissa. Tämä kehitys on mahdollistanut MEG-mittaukset potilailla, joilla aiemmin ei ollut mahdollisuutta hyötyä MEG-paikannuksista ja myös MEG-mittaukset epileptisten kohtausten aikana. Tärkeä osa väitöskirjaa on epilepsiakohtausten aikaisten MEG-mittausten kliinisen hyödyn arviointi. Tulokset osoittavat, että kohtauksenaikaiset MEG-mittaukset paikantavat herkemmin epilepsiakohtauksen lähdealueen aivoissa kuin kohtausten välisten epilepsiailmiöiden lähdepaikannus. Lähdealueiden paikannus on yhtä tarkka sekä aivokuoren pinnalla että 4 cm syvyydessä aivouurteissa. Pää ei kuitenkaan saisi liikkua 3 cm enempää MEG-mittauksen aikana, ja menetelmän herkkyys paranee oilennaisesti magneettikenttien matemaattiseen mallinnukseen perustuvalla magneettisten liikehäiriöiden poistolla. Väitöskirja tutkii lisäksi aivokuoren rakennemuutosten (paikallinen aivokuoridysplasia) aiheuttaman epilepsian kohtausten välisiä MEG-mittauksia. Päinvastoin kuin aiemmin on väitetty, ei aina ole tarpeen poistaa koko epileptisia lähdealueita sisältävää aivojen aluetta hyvän leikkaustuloksen saamiseksi. Väitöskirja esittelee myös laskennallisen MEG-anturiston määritysmenetelmän , joka lisää MEG-mittausten informaatiosisältöä huomioimalla pään liikkeet tulosten analyysissä

    Biomarkers to Localize Seizure from Electrocorticography to Neurons Level

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    Influence of time-series normalization, number of nodes, connectivity and graph measure selection on seizure-onset zone localization from intracranial EEG

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    We investigated the influence of processing steps in the estimation of multivariate directed functional connectivity during seizures recorded with intracranial EEG (iEEG) on seizure-onset zone (SOZ) localization. We studied the effect of (i) the number of nodes, (ii) time-series normalization, (iii) the choice of multivariate time-varying connectivity measure: Adaptive Directed Transfer Function (ADTF) or Adaptive Partial Directed Coherence (APDC) and (iv) graph theory measure: outdegree or shortest path length. First, simulations were performed to quantify the influence of the various processing steps on the accuracy to localize the SOZ. Afterwards, the SOZ was estimated from a 113-electrodes iEEG seizure recording and compared with the resection that rendered the patient seizure-free. The simulations revealed that ADTF is preferred over APDC to localize the SOZ from ictal iEEG recordings. Normalizing the time series before analysis resulted in an increase of 25-35% of correctly localized SOZ, while adding more nodes to the connectivity analysis led to a moderate decrease of 10%, when comparing 128 with 32 input nodes. The real-seizure connectivity estimates localized the SOZ inside the resection area using the ADTF coupled to outdegree or shortest path length. Our study showed that normalizing the time-series is an important pre-processing step, while adding nodes to the analysis did only marginally affect the SOZ localization. The study shows that directed multivariate Granger-based connectivity analysis is feasible with many input nodes (> 100) and that normalization of the time-series before connectivity analysis is preferred

    Passive and active markers of cortical excitability in epilepsy

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    Electroencephalography (EEG) has been the primary diagnostic tool in clinical epilepsy for nearly a century. Its review is performed using qualitative clinical methods that have changed little over time. However, the intersection of higher resolution digital EEG and analytical tools developed in the past decade invites a re-exploration of relevant methodology. In addition to the established spatial and temporal markers of spikes and high-frequency oscillations, novel markers involving advanced postprocessing and active probing of the interictal EEG are gaining ground. This review provides an overview of the EEG-based passive and active markers of cortical excitability in epilepsy and of the techniques developed to facilitate their identification. Several different emerging tools are discussed in the context of specific EEG applications and the barriers we must overcome to translate these tools into clinical practice

    Cortical Stimulation Mapping of Heschl’s Gyrus in the Auditory Cortex for Tinnitus Treatment

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    Tinnitus is the perception of sound in the absence of an actual sound stimulus. Recent developments have shifted the focus to the central nervous system and the neural correlate of tinnitus. Broadly, tinnitus involves cortical map rearrangement, pathological neural synchrony, and increased spontaneous firing rates. Various cortical regions, such as Heschl’s gyrus in the auditory cortex, have been found to be associated with different aspects of tinnitus, such as perception and loudness. I propose a cortical stimulation mapping study of Heschl’s gyrus using a depth and subdural electrode montage to conduct electrocorticography. This study would provide high-resolution data on abnormal frequency band oscillations characteristic of tinnitus and pinpoint regions where they occur. The validity of the neural synchrony model would also be tested in this study

    Mapping Functional Architecture in Neocortical Epileptic Networks

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    Epilepsy is a debilitating brain disorder that causes recurring seizures in approximately 60 million people worldwide. For the one-third of epilepsy patients whose seizures are refractory to medication, effective therapy relies on reliably localizing where seizures originate and spread. This clinical practice amounts to delineating the epileptic network through neural sensors recording the electrocorticogram. Mapping functional architecture in the epileptic network is promising for objectively localizing cortical targets for therapy in cases of neocortical refractory epilepsy, where post-surgical seizure freedom is unfavorable when cortical structures responsible for generating seizures are difficult to delineate. In this work, we develop and apply network models for analyzing and interrogating the role of fine-grain functional architecture during epileptic events in human neocortical networks. We first develop and validate a model for objectively identifying regions of the epileptic network that drive seizure dynamics. We then develop and validate a model for disentangling network pathways traversed during ``normal\u27\u27 function from pathways that drive seizures. Lastly, we devise and apply a novel platform for predicting network response to targeted lesioning of neocortical structures, revealing key control areas that influence the spread of seizures to broader network regions. The outcomes of this work demonstrate network models can objectively identify and predict targets for treating neocortical epilepsy, blueprint potential control strategies to limit seizure spread, and are poised for further validation prior to near-term clinical translation
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