LP31: EEG and MEG source localization of the epileptogenic foci in tuberous sclerosis complex: a pediatric case report

2014 
P796 – Figure 1 LP31 EEG and MEG source localization of the epileptogenic foci in tuberous sclerosis complex: a pediatric case report A. Hunold1, J. Haueisen1, B. Ahtam2,3, C. Doshi2,4, C. Harini4, S. Camposano4, S.K. Warfield5,6, P.E. Grant2,3,6, Y. Okada2,4, C. Papadelis2,4 1Technische Universitaet Ilmenau, Institute of Biomedical Engineering and Informatics, Ilmenau, Germany; 2Boston Children’s Hospital, Harvard Medical School, Fetal-Neonatal Neuroimaging & Developmental Science Center, Boston, MA, United States; 3Boston Children’s Hospital, Harvard Medical School, Department of Newborn Medicine, Boston, MA, United States; 4Boston Children’s Hospital, Harvard Medical School, Department of Neurology, Boston, MA, United States; 5Boston Children’s Hospital, Harvard Medical School, Department of Radiology, Boston, MA, United States; 6Boston Children’s Hospital, Harvard Medical School, Computational Radiology Laboratory, Boston, MA, United States Question: Tuberous sclerosis complex (TSC) is a disorder of tissue growth and differentiation, characterized by benign hamartomas in the brain triggering epilepsy in up to 90% of TSC patients. There is an ongoing debate on whether or not the epileptogenic zone is within the tuber itself or in abnormally developed surrounding tissue. Methods: We examined a four-year old patient with TSC-related refractory epilepsy undergoing magnetoencephalography (MEG) and electroencephalography (EEG) recordings. For MEG, we used a prototype system that offers higher spatial resolution and sensitivity compared to the conventional adult systems. EEG was simultaneously recorded from 32-leads according to the 10-20 international system. The source analysis of interictal activity was performed using both EEG and MEG data. Equivalent current dipoles (ECD) were fitted to the peak of individual interictal spikes. For averaged interictal spike signals, we performed ECD localizations to the spike upslope. Further, we estimated the minimum norm estimates (MNEs) to averaged interictal spike signals. Results: Multiple cortical tubers were identified in patient’s MRI including one prominent calcified tuber in the right parietal-occipital lobe. The simultaneously recorded spikes in EEG and MEG data provided a time shift of 20 ms between peak latencies. ECDs localized to individual and averaged interictal activity in EEG and MEG consistently clustered in the millimeter Abstracts of Poster Presentations / Clinical Neurophysiology 125, Supplement 1 (2014) S1–S339 S175s of Poster Presentations / Clinical Neurophysiology 125, Supplement 1 (2014) S1–S339 S175 vicinity of the large calcified cortical tuber. The ECD trace localized to the averaged EEG data located on the posterior side ∼5 mm superior to the tuber. The ECD trace localized to the averaged MEG spike located ∼4 mm anterior to the tuber. MNE and ECDs indicated epileptiform activity in the same areas. Conclusion: Our source analysis indicated generators of epileptiform activity in the millimeter vicinity of the tuber margin outside the tuber volume. Separate EEG and MEG source analysis provided distinct source characteristics. LP32 Scalp EEG in malformations of cortical development (MDC). Analysis by localization S. Cieza, A. Gomez, F. Escobar, N. Pereira, C. Viteri, J. Artieda, E. Urrestarazu Clinica Universidad de Navarra, Neurophysiology, Pamplona, Spain Objectives: The aim of our study was to describe the EEG findings of the MDC according to the localisation in the MRI. Patients and methods: We analyze the scalpEEGs of the patients diagnosed of MDC by RM in the Clinica Universidad de Navarra, and we considerate: the background activity, the presence and regional localisation of focal slow waves, interictal epileptiform discharges and focal fast frequencies. Results: We identified 51 patients with MDC (31 women and 20 men). In 21 patients the MDC was located in the temporal lobe, 12 showed focal slow waves and 13 showed epileptiform discharges. These EEG abnormalities had a high topographic correlation with MRI findings (>80% for slow waves and>90% for epileptiform discharges). In 19 patients the lesion was located in the frontal lobe, and the EEG showed focal slow waves in 12 of these patients, and epileptiform discharges in 9; however, these abnormalities coincide with the location in the MRI in less than 50% of the cases. In 8 patients the lesion was located in the parietal lobe, and just in only one case the EEG abnormalities correctly identified the location showed by MRI. Finally in 3 patients the lesion was located in the occipital lobe, and EEG showed slow waves in one case and epileptiform discharges in 2 cases. Only 2 patients had theta-alpha rhythm and were well correlated with the MRI findings (frontal and temporal MDC). One patient with temporal lobe MDC had a no localising continuos beta rhythm. Conclusions: Most of the MDC were located in the temporal and frontal lobes. The slow waves and the epileptiform discharges were highly well localising when the lesion was located in the temporal lobe, but failed in more than 50% of the cases when it was extra temporal. Focal rhythms were rare but have a good correlation with dysplasia. Therefore the presence and locator value of the EEG abnormalities are highly dependent on the location of the focus. Poster session 27. ICU monitoring P472 Epileptiform activity in patients treated with therapeutic hypothermia after cardiac arrest C. Santos-Sanchez1, M. Agundez Sarasola2, X. Mancisidor Solaberrie3, A. Martin Lopez3, P. Goiriena Seijo3, T. Perez Concha2, I. Yurrebaso Santamaria1 1Cruces University Hospital, Clinical Neurophysiology, Barakaldo, Spain; 2Cruces University Hospital, Neurology, Barakaldo, Spain; 3Cruces University Hospital, Cardiology, Barakaldo, Spain Question: Since the implementation of therapeutic hypothermia (TH) after cardiac arrest (CA), some researchers have been trying to redefine the value of the parameters traditionally used as predictors of neurologic outcome. In this context, the EEG represents an important tool to improve prognostication in postanoxic coma. Methods: We retrospectively reviewed the electronic medical records of all patients undergoing TH after CA from January 2011 until October 2013. We identified the patients with any type of epileptiform activity and reviewed their EEGs. Results: Forty patients were included. Sixteen died (40%). Epileptiform activity was found in 11 patients (27.5%), from whom only 2 (18.2%) had a favorable outcome (CPC 1 or 2). This epileptiform activity appeared in the following patterns; 2 patients had isolated interictal discharges, 2 had 2-2.5 Hz generalized periodic epileptiform discharges (GPEDs) over a continuous, diffusely slowed background, 2 had 2-2.5 Hz GPEDs over a suppressed background and 6 fulfilled non convulsive status epilepticus (NCSE) criteria. In one of the patients with NCSE, the EEG evolved into the pattern of GPEDs at 2-2.5 Hz over a suppressed background. When treating these 3 patients with benzodiazepine trials, even though they remained comatose, the epileptiform discharges stopped, and a continuous theta background appeared. Two of these patients died eventually, and the other one remains in a persistent vegetative state. Conclusions: Epileptiform activity is common in comatose patients treated with TH after CA. The presence of epileptiform discharges during the TH or shortly after was associated with a poor outcome. P473 Defining EEG reactivity in patients treated with therapeutic hypothermia after cardiac arrest C. Santos-Sanchez1, M. Agundez Sarasola2, X. Mancisidor Solaberrie3, P. Goiriena Seijo3, A. Martin Lopez3, T. Perez Concha2, I. Yurrebaso Santamaria1 1Cruces University Hospital, Clinical Neurophysiology, Barakaldo, Spain; 2Cruces University Hospital, Neurology, Barakaldo, Spain; 3Cruces University Hospital, Cardiology, Barakaldo, Spain Question: In patients treated with therapeutic hypothermia (TH) after cardiac arrest (CA), the EEG reactivity in the first 24 hours has an important prognostic value. However, it has not been reported yet whether or not there are differences between the type of stimuli required or the reactivity patterns obtained. Methods: We prospectively assessed EEG background continuity and reactivity in 16 consecutive patients undergoing TH after CA from August 2012 to October 2013. EEG background reactivity was tested to auditory, tactile and painful stimuli. We analyzed the relation between the continuity of the background, the EEG reactivity patterns, and the neurologic outcome. Results: All of our patients had the first EEG done within 24 hours after the CA. We established 4 backgrounds categories; continuous, discontinuous, burst-suppression and low voltage, and 2 reactivity patterns; increase of faster frequencies and background attenuation. All survivors (11/16) had different degrees of background reactivity in the first EEG (<24h), and the majority of them (10/11) had a favorable outcome (CPC 1 or 2). When the EEG was reactive, the response to auditory stimulus was always positive and attenuation of the background was the pattern most frequently seen. All of the non-survivors (5/16) had a low voltage background. Four of the survivors had a discontinuous background. Conclusions: Background reactivity in the first 24 hours after CA is strongly associated with neurologic outcome. In patients with a marked response to stimulus, brief periods of attenuation may represent reactivity to environmental auditory stimuli instead of a discontinuous background. P474 Quantitative EEG reactivity in comatose neurosurgical patients K. Noehr, A. Fuglsang-Frederiksen, B. Johnsen Aarhus University Hospital, Departement of Clinical Neurophysiology, Aarhus,
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