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F135. Ictal connectivity in childhood absence epilepsy: Associations with outcome
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Abstracts / Clinical Neurophysiology 129 (2018) e66–e141
F135. Ictal connectivity in childhood absence epilepsy: Associations with outcome—Jeffrey Tenney *, Darren Kadis, Leonid Rozhkov, Mekibib Altaye, Jing Xiang, MD, Jennifer Vannest, Tracy Glauser (USA) ⇑
Presenting author.
Introduction: The understanding of Childhood Absence Epilepsy (CAE) has been revolutionized over the past decade but the biological mechanisms responsible for variable treatment outcomes are unknown. Our purpose was to determine how pre-treatment ictal network pathways, defined using a combined EEG-functional magnetic resonance imaging (EEG-fMRI) and magnetoencephalography (MEG) effective connectivity analysis, were related to treatment response. Methods: Sixteen children with newly diagnosed and drug naïve CAE had 31 typical absence seizures during EEG-fMRI and 74 during MEG. The spatial extent of the pre-treatment ictal network was defined using fMRI hemodynamic response with an event related independent component analysis (eICA). This spatially defined pretreatment ictal network supplied prior information for MEG effective connectivity analysis calculated using phase slope index (PSI). Treatment outcome was assessed 2 years following diagnosis and dichotomized to ethosuximide (ETX) treatment responders (N = 11) or non-responders (N = 5). Effective connectivity of the pretreatment ictal network was compared to the treatment response. Results: Patterns of pre-treatment connectivity demonstrated strongest connections in the thalamus and posterior brain regions (parietal, posterior cingulate, angular gyrus, precuneus, and occipital) at delta frequencies and the frontal cortices at gamma frequencies (p < 0.05). ETX treatment non-responders had pre-treatment connectivity which was decreased in the precuneus region and increased in the frontal cortex compared to ETX responders (p < 0.05). Conclusion: Pre-treatment ictal connectivity differences in children with CAE were associated with response to anti-epileptic treatment. This is a possible mechanism for the variable treatment response seen in patients sharing the same epilepsy syndrome. doi:10.1016/j.clinph.2018.04.298
F136. Quantitative EEG offers potential utility of biomarkers for non-dopaminergic disease severity in Parkinson’s disease—Victor Geraedts, J. Marinus, Alida Gouw, Arne Mosch, Cornelis Stam, Bob van Hilten, M.F. Contarino, Martijn Tannemaat * (Netherlands) ⇑
Presenting author.
Introduction: Parkinson’s Disease (PD) patients are eligible for Deep Brain Stimulation (DBS) when oral medication offers insufficient benefit; however, accurate assessment of disease severity is crucial as non-dopaminergic features may deteriorate postoperatively. There is currently no reliable biomarker for nondopaminergic disease severity. We therefore aimed to investigate whether quantitative EEG reflects non-dopaminergic disease severity. Methods: Sixty-three consecutive PD patients screened for DBS between September 2015 and July 2017 were included (mean age 62.4 ± 7.2 years, 32% females). Relative spectral powers and the Phase-Lag-Index (PLI) reflecting functional connectivity were analysed.. The SENS-PD score and its subdomains quantified nondopaminergic disease severity, whereas the MDS-UPDRS III quantified motor-severity.
Results: The SENS-PD composite score correlated with a spectral ratio (d + h/ a1 + a1 + b powers) (global spectral ratio Pearson r = 0.4, 95% Confidence Interval (95%CI) 0.1 to 0.6), as well as PLI in the a2 band (10–13 Hz) (r = 0.3, 95%CI 0.5 to 0.1). These correlations seem driven by cognition (global spectral ratio: r = 0.4, 95%CI 0.2 to 0.6; global a2 PLI r = 0.3, 95%CI 0.5 to 0.2) and psychotic symptoms (global spectral ratio: r = 0.5, 95%CI 0.2 to 0.8; global a2 PLI: r = 0.2, 95%CI 0.3 to 0.0). MDS-UPDRS III was not significantly correlated with EEG parameters. Conclusion: Both EEG slowing and reduced functional connectivity in the a2 band were associated with advanced non-dopaminergic disease severity in PD. Further study is needed to evaluate the complementary utility of EEG parameters as a predictive tool of nondopaminergic involvement in PD. doi:10.1016/j.clinph.2018.04.299
F137. Effects of repetitive transcranial magnetic stimulation on short-latency afferent inhibition: A study in treatment-resistant depression—Elisa Kallioniemi 1,*, Sara Määttä 2, Mervi Könönen 2, Esa Mervaala 2, Heimo Viinamäki 2, Minna Valkonen-Korhonen 2 (1 USA, 2 Finland) ⇑
Presenting author.
Introduction: Short-latency afferent inhibition (SAI) is a phenomenon in which transcranial magnetic stimulation (TMS) induced motor evoked potentials (MEPs) are decreased in amplitude due to preceding electrical stimulation of the peripheral nerve, such as the median nerve at the wrist. If the nerve is stimulated around 21 ms before giving the TMS pulse to the cortical representation area of a muscle innervated by the same nerve, the resulting MEP amplitude is smaller than without electrical stimulation. On the contrary, if the nerve is stimulated 30 ms before giving the TMS pulse, there is no effect in MEP amplitude in healthy humans. In some movement disorders, such as in writer’s cramp, the 30 ms stimulation may, however, result in facilitation of the MEP amplitude. SAI is thought to reflect the sensorimotor interaction and cholinergic activity of the cerebral cortex and is likely mediated by the GABAA receptor subtype bearing the a1-subunit. In this study, we evaluated the effects of repetitive TMS (rTMS) therapy on SAI in treatmentresistant depression (TRD). Methods: Two patient groups received either active (12 patients) or sham (12 patients) rTMS daily for 27 days. During treatment, excitatory 10 Hz stimulation was applied on the left and inhibitory 1 Hz on the right dorsolateral prefrontal cortex. Before and after the treatment, SAI was measured from right abductor pollicis brevis muscle by using time-intervals of 21 ms and 30 ms between the electric stimulation of the right median nerve at the wrist and TMS of the left motor cortex. Furthermore, baseline MEPs were recorded before and after the treatment. Results: Before the treatment, the 21 ms SAI was inhibitory (p = 0.001) whereas the 30 ms SAI was facilitatory (p = 0.023) in TRD patients. After treatment in the active group, the baseline MEPs decreased in amplitude (p = 0.030), the 21 ms SAI MEPs stayed the same (p = 0.299) and the 30 ms SAI MEPs decreased (p = 0.047) compared to pre-treatment amplitudes. In the sham group, treatment did not induce any changes (p P 0.188). Conclusion: rTMS treatment modulates the sensorimotor interaction of TRD patients. doi:10.1016/j.clinph.2018.04.300
Abstracts / Clinical Neurophysiology 129 (2018) e66–e141
F135. Ictal connectivity in childhood absence epilepsy: Associations with outcome—Jeffrey Tenney *, Darren Kadis, Leonid Rozhkov, Mekibib Altaye, Jing Xiang, MD, Jennifer Vannest, Tracy Glauser (USA) ⇑
Presenting author.
Introduction: The understanding of Childhood Absence Epilepsy (CAE) has been revolutionized over the past decade but the biological mechanisms responsible for variable treatment outcomes are unknown. Our purpose was to determine how pre-treatment ictal network pathways, defined using a combined EEG-functional magnetic resonance imaging (EEG-fMRI) and magnetoencephalography (MEG) effective connectivity analysis, were related to treatment response. Methods: Sixteen children with newly diagnosed and drug naïve CAE had 31 typical absence seizures during EEG-fMRI and 74 during MEG. The spatial extent of the pre-treatment ictal network was defined using fMRI hemodynamic response with an event related independent component analysis (eICA). This spatially defined pretreatment ictal network supplied prior information for MEG effective connectivity analysis calculated using phase slope index (PSI). Treatment outcome was assessed 2 years following diagnosis and dichotomized to ethosuximide (ETX) treatment responders (N = 11) or non-responders (N = 5). Effective connectivity of the pretreatment ictal network was compared to the treatment response. Results: Patterns of pre-treatment connectivity demonstrated strongest connections in the thalamus and posterior brain regions (parietal, posterior cingulate, angular gyrus, precuneus, and occipital) at delta frequencies and the frontal cortices at gamma frequencies (p < 0.05). ETX treatment non-responders had pre-treatment connectivity which was decreased in the precuneus region and increased in the frontal cortex compared to ETX responders (p < 0.05). Conclusion: Pre-treatment ictal connectivity differences in children with CAE were associated with response to anti-epileptic treatment. This is a possible mechanism for the variable treatment response seen in patients sharing the same epilepsy syndrome. doi:10.1016/j.clinph.2018.04.298
F136. Quantitative EEG offers potential utility of biomarkers for non-dopaminergic disease severity in Parkinson’s disease—Victor Geraedts, J. Marinus, Alida Gouw, Arne Mosch, Cornelis Stam, Bob van Hilten, M.F. Contarino, Martijn Tannemaat * (Netherlands) ⇑
Presenting author.
Introduction: Parkinson’s Disease (PD) patients are eligible for Deep Brain Stimulation (DBS) when oral medication offers insufficient benefit; however, accurate assessment of disease severity is crucial as non-dopaminergic features may deteriorate postoperatively. There is currently no reliable biomarker for nondopaminergic disease severity. We therefore aimed to investigate whether quantitative EEG reflects non-dopaminergic disease severity. Methods: Sixty-three consecutive PD patients screened for DBS between September 2015 and July 2017 were included (mean age 62.4 ± 7.2 years, 32% females). Relative spectral powers and the Phase-Lag-Index (PLI) reflecting functional connectivity were analysed.. The SENS-PD score and its subdomains quantified nondopaminergic disease severity, whereas the MDS-UPDRS III quantified motor-severity.
Results: The SENS-PD composite score correlated with a spectral ratio (d + h/ a1 + a1 + b powers) (global spectral ratio Pearson r = 0.4, 95% Confidence Interval (95%CI) 0.1 to 0.6), as well as PLI in the a2 band (10–13 Hz) (r = 0.3, 95%CI 0.5 to 0.1). These correlations seem driven by cognition (global spectral ratio: r = 0.4, 95%CI 0.2 to 0.6; global a2 PLI r = 0.3, 95%CI 0.5 to 0.2) and psychotic symptoms (global spectral ratio: r = 0.5, 95%CI 0.2 to 0.8; global a2 PLI: r = 0.2, 95%CI 0.3 to 0.0). MDS-UPDRS III was not significantly correlated with EEG parameters. Conclusion: Both EEG slowing and reduced functional connectivity in the a2 band were associated with advanced non-dopaminergic disease severity in PD. Further study is needed to evaluate the complementary utility of EEG parameters as a predictive tool of nondopaminergic involvement in PD. doi:10.1016/j.clinph.2018.04.299
F137. Effects of repetitive transcranial magnetic stimulation on short-latency afferent inhibition: A study in treatment-resistant depression—Elisa Kallioniemi 1,*, Sara Määttä 2, Mervi Könönen 2, Esa Mervaala 2, Heimo Viinamäki 2, Minna Valkonen-Korhonen 2 (1 USA, 2 Finland) ⇑
Presenting author.
Introduction: Short-latency afferent inhibition (SAI) is a phenomenon in which transcranial magnetic stimulation (TMS) induced motor evoked potentials (MEPs) are decreased in amplitude due to preceding electrical stimulation of the peripheral nerve, such as the median nerve at the wrist. If the nerve is stimulated around 21 ms before giving the TMS pulse to the cortical representation area of a muscle innervated by the same nerve, the resulting MEP amplitude is smaller than without electrical stimulation. On the contrary, if the nerve is stimulated 30 ms before giving the TMS pulse, there is no effect in MEP amplitude in healthy humans. In some movement disorders, such as in writer’s cramp, the 30 ms stimulation may, however, result in facilitation of the MEP amplitude. SAI is thought to reflect the sensorimotor interaction and cholinergic activity of the cerebral cortex and is likely mediated by the GABAA receptor subtype bearing the a1-subunit. In this study, we evaluated the effects of repetitive TMS (rTMS) therapy on SAI in treatmentresistant depression (TRD). Methods: Two patient groups received either active (12 patients) or sham (12 patients) rTMS daily for 27 days. During treatment, excitatory 10 Hz stimulation was applied on the left and inhibitory 1 Hz on the right dorsolateral prefrontal cortex. Before and after the treatment, SAI was measured from right abductor pollicis brevis muscle by using time-intervals of 21 ms and 30 ms between the electric stimulation of the right median nerve at the wrist and TMS of the left motor cortex. Furthermore, baseline MEPs were recorded before and after the treatment. Results: Before the treatment, the 21 ms SAI was inhibitory (p = 0.001) whereas the 30 ms SAI was facilitatory (p = 0.023) in TRD patients. After treatment in the active group, the baseline MEPs decreased in amplitude (p = 0.030), the 21 ms SAI MEPs stayed the same (p = 0.299) and the 30 ms SAI MEPs decreased (p = 0.047) compared to pre-treatment amplitudes. In the sham group, treatment did not induce any changes (p P 0.188). Conclusion: rTMS treatment modulates the sensorimotor interaction of TRD patients. doi:10.1016/j.clinph.2018.04.300