EEG spectral changes underlying BOLD responses contralateral to spikes in patients with focal epilepsy

Montreal Neurological Institute and Department of Neurology and Neurosurgery, McGill University, Montreal, Canada.
Epilepsia (Impact Factor: 4.57). 05/2009; 50(7):1804-9. DOI: 10.1111/j.1528-1167.2009.02080.x
Source: PubMed


Simultaneous electroencephalogram and functional magnetic resonance imaging (EEG-fMRI) in patients with focal epilepsy and unilateral spikes often shows positive blood oxygenation level-dependent (BOLD) responses (activations), not only ipsilateral but also contralateral to the spikes. We aimed to investigate whether minimal EEG changes could underlie these contralateral BOLD responses by using EEG spectral analysis.
We studied 19 patients with focal epilepsy and unilateral spikes. According to the pattern of BOLD activation, patients were divided into Group 1 (ipsi- and contralateral to the spikes) or Group 2 (only ipsilateral). EEG from outside the scanner was used to mark spikes similar to those recorded in the scanner. Epochs of 640 ms before and after the peak of the spikes were chosen as baseline and spike epochs. Spectral analysis was performed in referential montage (FCz reference), and differences between baselines and spikes were analyzed by paired t-test.
Significant EEG changes in electrodes contralateral to the spikes were seen in 9 of 10 patients in Group 1 and in only 2 of 10 patients in Group 2 (one patient had two types of spikes that were analyzed separately). Spectral changes were seen in delta and/or theta bands in all patients except one (in Group 1) who had changes in all bands.
Significant contralateral EEG changes occurred in 90% of contralateral BOLD activations and in only 20% of patients without contralateral BOLD responses. The reason why these changes predominate in lower frequencies rather than in higher frequencies is unclear. These spectral changes in areas corresponding to contralateral activations might reflect poorly synchronized but possibly intense neuronal activity.

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Available from: Louise Tyvaert, Oct 22, 2014
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    • "Another explanation is that the more extensive inter-hemispheric synaptic connections between extra-temporal lobe regions facilitate the spread or propagation of epileptic activity between these hemispheres when the focus is in these regions. This is supported by evidence from EEG-fMRI studies (Yu et al., 2009; Kobayashi et al., 2006) (Tyvaert et al., 2008) as well as human and animal data (Keller and Roberts, 2008; Blumenfeld et al., 2007); (Holmes et al., 1999; Zilles et al., 1998; Silva-Barrat et al., 1986) which show regional as well as distant cortical and subcortical changes associated with focal interictal spikes, being more so in patients with extra-temporal foci. It also would correlate well with the described increased incidence of bilateral features in extra-temporal lobe seizure semiologies (Luders et al., 1998; Gastaut, 1970) and of bilateral interictal and ictal discharges seen in patients with extra-TLE (Bautista et al., 1998; Taylor et al., 2003; Gibbs and Gibbs, 1955) as opposed to TLE where most reports show that even if bilateral interictal discharges are recorded, they are predominant over the side with seizure onset in 60–70% of patients (Hirsch et al., 1991; Williamson et al., 1993). "
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    ABSTRACT: Objective To investigate whether cortical excitability measures on transcranial magnetic stimulation (TMS) differed between groups of patients with different focal epilepsy syndromes. Methods 85 patients with focal epilepsy syndromes divided into temporal and extra-temporal lobe epilepsy were studied. The cohorts were further divided into drug naïve- new onset, refractory and seizure free groups. Motor threshold (MT) and paired pulse TMS at short (2, 5, 10, 15 ms) and long (100 - 300 ms) interstimulus intervals (ISIs) were measured. Results were compared to those of 20 controls. Results Cortical excitability was higher at 2 & 5 ms and 250, 300 ms ISIs (p< 0.01) in focal epilepsy syndromes compared to controls however significant inter-hemispheric differences in MT and the same ISIs were only seen in the drug naïve state early at onset and were much more prominent in temporal lobe epilepsy. Conclusion Disturbances in cortical excitability are more confined to the affected hemisphere in temporal lobe epilepsy but only early at onset in the drug naïve state. Significance Group TMS studies show that cortical excitability measures are different in temporal lobe epilepsy and can be distinguished from other focal epilepsies early at onset in the drug naïve state. Further studies are needed to determine whether these results can be applied clinically as the utility of TMS in distinguishing between epilepsy syndromes at an individual level remains to be determined.
    Clinical Neurophysiology 06/2014; 126(2). DOI:10.1016/j.clinph.2014.05.029 · 3.10 Impact Factor
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    • "In animal and human EEG-fMRI studies, widespread and distant (both positive and negative) BOLD signal changes are seen with focal interictal epileptic spikes or brief seizures (Kobayashi et al., 2006a; Englot et al., 2008; Truccolo et al., 2011). Using EEG spectral analysis, Yu et al. (2009) revealed significant contralateral EEG changes (predominating in lower frequencies ) in 90% of contralateral BOLD activations triggered by spikes. These authors suggested that these spectral changes in areas corresponding to contralateral activations possibly reflected poorly synchronized but intense neuronal activity. "
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    ABSTRACT: Purpose: To investigate spatial and metabolic changes associated with frontal lobe seizures. Methods: Functional near-infrared spectroscopy combined with electroencephalography (EEG-fNIRS) recordings of patients with confirmed nonlesional refractory frontal lobe epilepsy (FLE). Key findings: Eighteen seizures from nine patients (seven male, mean age 27 years, range 13-46 years) with drug-refractory FLE were captured during EEG-fNIRS recordings. All seizures were coupled with significant hemodynamic variations that were greater with electroclinical than with electrical seizures. fNIRS helped in the identification of seizures in three patients with more subtle ictal EEG abnormalities. Hemodynamic changes consisted of local increases in oxygenated (HbO) and total hemoglobin (HbT) but heterogeneous deoxygenated hemoglobin (HbR) behavior. Furthermore, rapid hemodynamic alterations were observed in the homologous contralateral region, even in the absence of obvious propagated epileptic activity. The extent of HbO activation adequately lateralized the epileptogenic side in the majority of patients. Significance: EEG-fNIRS reveals complex spatial and metabolic changes during focal frontal lobe seizures. Further characterization of these changes could improve seizure detection, localization, and understanding of the impact of focal seizures.
    Epilepsia 11/2012; 54(2). DOI:10.1111/epi.12011 · 4.57 Impact Factor
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    ABSTRACT: Precise seizure focus localization and unraveling different structures involved in the genesis of the epileptic process is a major challenge that faces epilepsy research. The combination of electroencephalography (EEG) and functional magnetic resonance imaging (fMRI) is a well-established method that offers the unique advantage of measuring noninvasively specific hemodynamic changes related to epileptic discharges, providing unique localizing information on seizure foci and different cortical and subcortical structures that may be involved in this process. In addition, functional connectivity studies are emerging as a promising tool that can be used to interrogate epileptic networks and possible changes within physiological networks in epileptic brain. fMRI is thus an excellent tool that provides novel and unique insights into the genesis of epileptiform activity and how this differs in various epileptic syndromes. With the improved sensitivity as more sophisticated data analysis and EEG event localization and artifact elimination paradigms evolve, there is no doubt that fMRI will continue to help our understanding of the genesis of epilepsy and contribute to clinical evaluation.
    Handbook of Clinical Neurology 09/2012; 107:369-85. DOI:10.1016/B978-0-444-52898-8.00023-9
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