Search

Introduction: Seizures occur rarely during EEG-fMRI acquisitions of epilepsy patients, but can potentially offer a better estimation of the epileptogenic zone than interictal activity. Independent component analysis (ICA) is a data-driven method that imposes minimal constraints on the hemodynamic response function (HRF). In particular, the investigation of HRFs with clear peaks, but varying latency, may be used to differentiate the ictal focus from propagated activity., Methods: ICA was applied on ictal EEG-fMRI data from 15 patients. Components related to seizures were identified by fitting an HRF to the component time courses at the time of the ictal EEG events. HRFs with a clear peak were used to derive maps of significant BOLD responses and their associated peak delay. The results were then compared with those obtained from a general linear model (GLM) method. Concordance with the presumed epileptogenic focus was also assessed., Results: The ICA maps were significantly correlated with the GLM maps for each patient (Spearman's test, p<0.05). The ictal BOLD responses identified by ICA always included the presumed epileptogenic zone, but were also more widespread, accounting for 20.3% of the brain volume on average. The method provided a classification of the components as a function of peak delay. BOLD response clusters associated with early HRF peaks were concordant with the suspected epileptogenic focus, while subsequent HRF peaks may correspond to ictal propagation., Conclusion: ICA applied to EEG-fMRI can detect areas of significant BOLD response to ictal events without having to predefine an HRF. By estimating the HRF peak time in each identified region, the method could also potentially provide a dynamic analysis of ictal BOLD responses, distinguishing onset from propagated activity.

Photoparoxysmal response (PPR) is an electroencephalographic (EEG) trait characterized by the occurrence of epileptiform discharges in response to visual stimulation. Studying this trait helps to learn about mechanisms of epileptogenicity. While simultaneous recordings of EEG and functional MRI (EEG-fMRI) in patients with spontaneous generalised spike-wave discharges (GSW) have revealed activation of the thalamus and deactivation in frontoparietal areas, EEG-fMRI studies on evoked GSW such as PPR are lacking. In this EEG-fMRI study, 30 subjects with reported generalised PPR underwent intermittent photic stimulation (IPS) in a 3 T MR scanner. PPR was elicited in 6 subjects, four diagnosed with idiopathic generalised epilepsy and two with tension-type headache. Because PPR is preceded by synchronization of cortical gamma oscillations, blood oxygenation level-dependent (BOLD) signal changes were analysed at the onset of the PPR (standard regressor) and 3 s before the onset of PPR (early regressor) in one model. In all subjects, IPS led to a significant activation of the visual cortex. Based on the early regressor, PPR associated activation was found in the parietal cortex adjacent to the intraparietal sulcus in five and in the premotor cortex in all 6 subjects. The standard regressor revealed deactivation in early activated areas in all subjects and thalamic activation in one subject. In contrast to spontaneous GSW, these results suggest that PPR is a cortical phenomenon with an involvement of the parietal and frontal cortices. Pronounced haemodynamic changes seen with the early regressor could mirror gamma activity that is known to precede PPR.

Simultaneous recording of EEG and functional MRI (EEG-fMRI) is a promising tool that may be applied in patients with epilepsy to investigate haemodynamic changes associated with interictal epileptiform discharges (IED). As the yield of the EEG-fMRI technique in children with epilepsy is still unclear, the aim of this study was to evaluate whether the combination of EEG-fMRI and EEG source analysis could improve localization of epileptogenic foci in children. Six children with an unambiguous focus localization were selected based on the criterion of the consistency of ictal EEG, PET and ictal SPECT. IEDs were taken as time series for fMRI analysis and as averaged sweeps for the EEG source analysis based on the distributed linear local autoregressive average (LAURA) solution. In four patients, the brain area with haemodymanic changes corresponded to the epileptogenic zone. However, additional distant regions with haemodynamic response were observed. Source analysis located the source of the initial epileptic activity in all cases in the presumed epileptogenic zone and revealed propagation in five cases. In three cases there was a good correspondence between haemodynamic changes and source localization at both the beginning and the propagation of IED. In the remaining three cases, at least one area of haemodynamic changes corresponded to either the beginning or the propagation. In most children analysed, EEG-fMRI revealed extended haemodynamic response, which were difficult to interpret without an appropriate reference, i.e. a priori hypothesis about epileptogenic zone. EEG source analysis may help to differentiate brain areas with haemodynamic response.

EEG-fMRI is a non-invasive technique that allows the investigation of epileptogenic networks in patients with epilepsy. Lately, BOLD changes occurring before the spike were found in patients with generalized epilepsy. The study of metabolic changes preceding spikes might improve our knowledge of spike generation. We tested this hypothesis in patients with idiopathic and symptomatic focal epilepsy. Eleven consecutive patients were recorded at 3 T: five with idiopathic focal and 6 with symptomatic focal epilepsy. Thirteen spike types were analyzed separately. Statistical analysis was performed using the timing of spikes as events, modeled with HRFs peaking between -9 s and +9 s around the spike. HRFs were calculated the most focal BOLD response. Eleven of the thirteen studies showed prespike BOLD responses. Prespike responses were more focal than postspike responses. Three studies showed early positive followed by later negative BOLD responses in the spike field. Three had early positive BOLD responses in the spike field, which remained visible in the later maps. Three others had positive BOLD responses in the spike field, later propagating to surrounding areas. HRFs peaked between -5 and +6 s around the spike timing. No significant EEG changes could be identified prior to the spike. BOLD changes prior to the spike frequently occur in focal epilepsies. They are more focal than later BOLD changes and strongly related to the spike field. Early changes may result from increased neuronal activity in the spike field prior to the EEG spike and reflect an event more localized than the spike itself.

The pathophysiology of generalized spike wave discharges (GSW) is not completely understood. Thalamus, basal ganglia and neocortex have been implicated in the generation of GSW, yet the specific role of each structure remains to be clarified. In six children with idiopathic generalized epilepsy (IGE), we performed combined EEG-fMRI to identify GSW-related changes in blood oxygen level-dependent (BOLD) signal in the striato-thalamo-cortical network. In all patients, within-subject analysis demonstrated BOLD signal changes that preceded the GSW. An increase in BOLD signal in the medial thalamus started 6 s before the onset of the GSW. Decreases in cortical BOLD signal were mainly found in frontoparietal areas and precuneus starting 6 to 3 s before the GSW. All patients showed a decrease in BOLD signal in the head of the caudate nucleus with a variable onset. The temporospatial pattern of BOLD signal changes suggests that GSW on the cortical surface is preceded by a sequence of neuronal events in the thalamo-cortical-striatal network. Approximately 6 s before the GSW, the thalamus shows an increase in neuronal activity along with regional decreases in cortical activity. These changes in thalamo-cortical activity are followed by a deactivation of the caudate nucleus. These early changes in BOLD signal may reflect changes in neuronal activity that contribute to the generation of GSW and may contribute to the transition from a normal to a generalized hypersynchronous pattern of neuronal activity. Our preliminary findings warrant further studies on a larger number of patients to explore the influence of age, medication and type of epileptic syndrome.

The ballistocardiogram (BCG) represents one of the most prominent sources of artifacts that contaminate the electroencephalogram (EEG) during functional MRI. The BCG artifacts may affect the detection of interictal epileptiform discharges (IED) in patients with epilepsy, reducing the sensitivity of the combined EEG-fMRI method. In this study we improved the BCG artifact correction using a multiple source correction (MSC) approach. On the one hand, a source analysis of the IEDs was applied to the EEG data obtained outside the MRI scanner to prevent the distortion of EEG signals of interest during the correction of BCG artifacts. On the other hand, the topographies of the BCG artifacts were defined based on the EEG recorded inside the scanner. The topographies of the BCG artifacts were then added to the surrogate model of IED sources and a combined source model was applied to the data obtained inside the scanner. The artifact signal was then subtracted without considerable distortion of the IED topography. The MSC approach was compared with the traditional averaged artifact subtraction (AAS) method. Both methods reduced the spectral power of BCG-related harmonics and enabled better detection of IEDs. Compared with the conventional AAS method, the MSC approach increased the sensitivity of IED detection because the IED signal was less attenuated when subtracting the BCG artifacts. The proposed MSC method is particularly useful in situations in which the BCG artifact is spatially correlated and time-locked with the EEG signal produced by the focal brain activity of interest.