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P87. Expressive and receptive language mapping using ECoG and ECS
e146
Society Proceedings / Clinical Neurophysiology 126 (2015) e63–e170
neuromyelitis optica, were detected before any evidence of NMO and may be interpreted along with Hashimoto-thyroiditis as a propensity to autoimmune diseases. It is possible that aquporin-4-abs are presentyears before the NMO onset. Cooccurrence of these two rare abs with focus on central nervous system has not yet been described. Reports of coexistence of NMO and autoimmune diseases, which affect the peripheral nervous system (e.g. Myasthenia gravis) or diseases of rheumatic origin (e.g. Sjögren-Syndrome) were already published.
receptive/expressive language area. A next-neighbor approach that took into account the activation of surrounding electrodes showed a sensitivity of 100.0%/82.5% and a specificity of 85.0%/75.0% for receptive/expressive language mapping. The modalities show a good overlap, which is even more convincing due to the high number of tested sites in the area of interest. The passive ECoG mapping is a powerful supportive tool, as it allows reducing the number of tested sites during ECS.
References
References
Balint B et al. Progressive encephalomyelitis with rigidity and myoclonus: a new variant with DPPX antibodies. Neurology 2014;82:1521–8. Boronat A et al. Encephalitis and antibodies to DPPX, a subunit of Kv4.2 potassium channels. Ann Neurol 2013;73(1):120–8. Suchecki S et al. A rare autoimmune encephalitis – due to dipeptidyl-peptidase-like protein-6 (dppx) autoantibody: a case report. Neurology 2014;82(Supplement P5):169.
Prueckl R, Kapeller C, Potes C, Korostenskaja M, Schalk G, Lee KH, et al. cortiQ-Clinical software for electrocorticographic real-time functional mapping of the eloquent cortex. In: Eng. in Medicine and Biology Society (EMBC), 2013 35th Annual Int. Conf. of the IEEE. IEEE; 2013. p. 6365–8. Sinai A, Bowers CW, Crainiceanu CM, Boatman D, Gordon B, Lesser RP, et al. Electrocorticographic high gamma activity versus electrical cortical stimulation mapping of naming. Brain 2005;128(7):1556–70. Towle VL, Yoon HA, Castelle M, Edgar JC, Biassou NM, Frim DM, et al. ECoG gamma activity during a language task: differentiating expressive and receptive speech areas. Brain 2008;131(8):2013–27.
doi:10.1016/j.clinph.2015.04.236
P87. Expressive and receptive language mapping using ECoG and ECS—C. Kapeller a, K. Kamada b, H. Ogawa b, R. Prückl a, N. Kunii c, A. Schnürer d, C. Guger a (a Guger Technologies OG, Schiedlberg, Austria, b Asahikawa Medical University, Department of Neurosurgery, Asahikawa, Japan, c University of Tokyo, Department of Neurosurgery, Tokyo, Japan, d g.tec Medical Engineering, Sales and Marketing, Schiedlberg, Austria) Patients suffering from intractable epilepsy, who are candidates for surgical treatment, have to undergo several functional mapping procedures to make precisely diagnose for epileptogenic foci and eloquent brain regions. Since electrocorticography (ECoG) detects electric currents directly from the brain surface, it is expected to be the most reliable way to identify brain activity by focusing on changes of gamma-band oscillations. Previous studies identified the expressive and receptive language areas based on recordings with clinical standard ECoG grids (Sinai et al., 2005; Towle et al., 2008). In this study we investigated the sensitivity and specificity of passive ECoG mapping and the clinical standard electrical cortical stimulation (ECS) mapping using high-density electrode grids. The study included ECS and ECoG mapping with an epileptic patient having 236 subdural electrodes who underwent neuro-monitoring. The receptive and expressive language areas were each covered by a high-density subdural electrode grid with inter-electrode distance of 5 mm and conductive area of 1.5}mm. The ECoG mapping was performed with the real-time mapping system cortiQ (g.tec, Austria), which detects task related changes of gamma-band oscillations (Prueckl et al., 2013). In order to activate the expressive language area, a picture naming task was performed during both mapping procedures. Additionally, a listening task was performed during the cortiQ mapping, to activate the receptive language area. The cortiQ mapping was repeated two times to ensure stable mapping results. The specificity and the sensitivity were computed for expressive and receptive language areas separately. Therefore, only the stimulated electrodes on the corresponding grid were used for comparison. During the ECS mapping the receptive language area was identified based on 24 tested sites over the left superior and middle temporal gyri. For expressive language mapping, 34 sites over the left inferior frontal gyrus were stimulated. The cortiQ mapping consistently showed activation patterns for both runs leading to a sensitivity of 50.0%/57.5% and a specificity of 85.0%/75.0% for the
doi:10.1016/j.clinph.2015.04.237
P88. Identification of genome-based biomarkers for response to specific antiepileptic drugs in focal and idiopathic generalized epilepsies—S. Wolking a, F. Becker a, S. Rau a, Y. Weber a, C. Depondt b, S. Sisodiya c, H. Lerche a (a University Hospital Tübingen, Department of Neurology and Epileptology, Tübingen, Germany, b Hôpital Erasme, Université Libre de Bruxelles, Department of Neurology, Brussels, Belgium, c UCL Institute of Neurology, Queen Square, Department of Clinical and Experimental Epilepsy, London, United Kingdom) Pharmacoresistance is a major burden in the treatment of epilepsy. The search for an effective and well-tolerated antiepileptic drug (AED) is overall achieved by trial and error. This process often turns out to be challenging and irksome for both, the patient and the clinician. Genetic biomarkers can help in the choice of AEDs in order to individualize the treatment. In the framework of the EpiPGX consortium, a European research project on epilepsy pharmacogenomics, 5000 patients were recruited and meticulously phenotyped. Patient samples were supplied by 10 specialized epilepsy centers. More than 500 phenotype items were assessed. Detailed definitions for pharmacogenomics phenotypes such as multiresistance or late response – i.e. response to a second or later given AED, see below – were created. The consistency of the supplied phenotypes across the participating centers was guaranteed by repeated phenotyping workshops and two rounds of validation exercises on a set of 10 anonymized medical records. Mean inter-rater agreement was 82% for AED outcome classification. True misclassifications accounted for only 5–9% of all cases. We identified and phenotyped patients with focal epilepsies that were late responders to specific AEDs. Late response was defined as 12 months of seizure freedom after failure of at least one well-tolerated AED. We identified 338 late responders to levetiracetam, lamotrigine, or lacosamide. Those are currently being analyzed in the setting of a genome wide association study (GWAS) against a much larger group of non-reponders to the same drugs and to a group of normal controls. For idiopathic generalized epilepsies, we are comparing responders and non-responders to lamotrigine and valproate (VPA). For VPA we identified 487 responders and 164
Society Proceedings / Clinical Neurophysiology 126 (2015) e63–e170
neuromyelitis optica, were detected before any evidence of NMO and may be interpreted along with Hashimoto-thyroiditis as a propensity to autoimmune diseases. It is possible that aquporin-4-abs are presentyears before the NMO onset. Cooccurrence of these two rare abs with focus on central nervous system has not yet been described. Reports of coexistence of NMO and autoimmune diseases, which affect the peripheral nervous system (e.g. Myasthenia gravis) or diseases of rheumatic origin (e.g. Sjögren-Syndrome) were already published.
receptive/expressive language area. A next-neighbor approach that took into account the activation of surrounding electrodes showed a sensitivity of 100.0%/82.5% and a specificity of 85.0%/75.0% for receptive/expressive language mapping. The modalities show a good overlap, which is even more convincing due to the high number of tested sites in the area of interest. The passive ECoG mapping is a powerful supportive tool, as it allows reducing the number of tested sites during ECS.
References
References
Balint B et al. Progressive encephalomyelitis with rigidity and myoclonus: a new variant with DPPX antibodies. Neurology 2014;82:1521–8. Boronat A et al. Encephalitis and antibodies to DPPX, a subunit of Kv4.2 potassium channels. Ann Neurol 2013;73(1):120–8. Suchecki S et al. A rare autoimmune encephalitis – due to dipeptidyl-peptidase-like protein-6 (dppx) autoantibody: a case report. Neurology 2014;82(Supplement P5):169.
Prueckl R, Kapeller C, Potes C, Korostenskaja M, Schalk G, Lee KH, et al. cortiQ-Clinical software for electrocorticographic real-time functional mapping of the eloquent cortex. In: Eng. in Medicine and Biology Society (EMBC), 2013 35th Annual Int. Conf. of the IEEE. IEEE; 2013. p. 6365–8. Sinai A, Bowers CW, Crainiceanu CM, Boatman D, Gordon B, Lesser RP, et al. Electrocorticographic high gamma activity versus electrical cortical stimulation mapping of naming. Brain 2005;128(7):1556–70. Towle VL, Yoon HA, Castelle M, Edgar JC, Biassou NM, Frim DM, et al. ECoG gamma activity during a language task: differentiating expressive and receptive speech areas. Brain 2008;131(8):2013–27.
doi:10.1016/j.clinph.2015.04.236
P87. Expressive and receptive language mapping using ECoG and ECS—C. Kapeller a, K. Kamada b, H. Ogawa b, R. Prückl a, N. Kunii c, A. Schnürer d, C. Guger a (a Guger Technologies OG, Schiedlberg, Austria, b Asahikawa Medical University, Department of Neurosurgery, Asahikawa, Japan, c University of Tokyo, Department of Neurosurgery, Tokyo, Japan, d g.tec Medical Engineering, Sales and Marketing, Schiedlberg, Austria) Patients suffering from intractable epilepsy, who are candidates for surgical treatment, have to undergo several functional mapping procedures to make precisely diagnose for epileptogenic foci and eloquent brain regions. Since electrocorticography (ECoG) detects electric currents directly from the brain surface, it is expected to be the most reliable way to identify brain activity by focusing on changes of gamma-band oscillations. Previous studies identified the expressive and receptive language areas based on recordings with clinical standard ECoG grids (Sinai et al., 2005; Towle et al., 2008). In this study we investigated the sensitivity and specificity of passive ECoG mapping and the clinical standard electrical cortical stimulation (ECS) mapping using high-density electrode grids. The study included ECS and ECoG mapping with an epileptic patient having 236 subdural electrodes who underwent neuro-monitoring. The receptive and expressive language areas were each covered by a high-density subdural electrode grid with inter-electrode distance of 5 mm and conductive area of 1.5}mm. The ECoG mapping was performed with the real-time mapping system cortiQ (g.tec, Austria), which detects task related changes of gamma-band oscillations (Prueckl et al., 2013). In order to activate the expressive language area, a picture naming task was performed during both mapping procedures. Additionally, a listening task was performed during the cortiQ mapping, to activate the receptive language area. The cortiQ mapping was repeated two times to ensure stable mapping results. The specificity and the sensitivity were computed for expressive and receptive language areas separately. Therefore, only the stimulated electrodes on the corresponding grid were used for comparison. During the ECS mapping the receptive language area was identified based on 24 tested sites over the left superior and middle temporal gyri. For expressive language mapping, 34 sites over the left inferior frontal gyrus were stimulated. The cortiQ mapping consistently showed activation patterns for both runs leading to a sensitivity of 50.0%/57.5% and a specificity of 85.0%/75.0% for the
doi:10.1016/j.clinph.2015.04.237
P88. Identification of genome-based biomarkers for response to specific antiepileptic drugs in focal and idiopathic generalized epilepsies—S. Wolking a, F. Becker a, S. Rau a, Y. Weber a, C. Depondt b, S. Sisodiya c, H. Lerche a (a University Hospital Tübingen, Department of Neurology and Epileptology, Tübingen, Germany, b Hôpital Erasme, Université Libre de Bruxelles, Department of Neurology, Brussels, Belgium, c UCL Institute of Neurology, Queen Square, Department of Clinical and Experimental Epilepsy, London, United Kingdom) Pharmacoresistance is a major burden in the treatment of epilepsy. The search for an effective and well-tolerated antiepileptic drug (AED) is overall achieved by trial and error. This process often turns out to be challenging and irksome for both, the patient and the clinician. Genetic biomarkers can help in the choice of AEDs in order to individualize the treatment. In the framework of the EpiPGX consortium, a European research project on epilepsy pharmacogenomics, 5000 patients were recruited and meticulously phenotyped. Patient samples were supplied by 10 specialized epilepsy centers. More than 500 phenotype items were assessed. Detailed definitions for pharmacogenomics phenotypes such as multiresistance or late response – i.e. response to a second or later given AED, see below – were created. The consistency of the supplied phenotypes across the participating centers was guaranteed by repeated phenotyping workshops and two rounds of validation exercises on a set of 10 anonymized medical records. Mean inter-rater agreement was 82% for AED outcome classification. True misclassifications accounted for only 5–9% of all cases. We identified and phenotyped patients with focal epilepsies that were late responders to specific AEDs. Late response was defined as 12 months of seizure freedom after failure of at least one well-tolerated AED. We identified 338 late responders to levetiracetam, lamotrigine, or lacosamide. Those are currently being analyzed in the setting of a genome wide association study (GWAS) against a much larger group of non-reponders to the same drugs and to a group of normal controls. For idiopathic generalized epilepsies, we are comparing responders and non-responders to lamotrigine and valproate (VPA). For VPA we identified 487 responders and 164