OBJECTIVESudden unexpected death in epilepsy (SUDEP) is the leading cause of death for patients with refractory epilepsy, and there is increasing evidence for a centrally mediated respiratory depression as a pathophysiological mechanism. The brain regions responsible for a seizure’s inducing respiratory depression are unclear—the respiratory nuclei in the brainstem are thought to be involved, but involvement of forebrain structures is not yet understood. The aim of this study was to analyze intracranial EEGs in combination with the results of respiratory monitoring to investigate the relationship between seizure spread to specific mesial temporal brain regions and the onset of respiratory dysfunction and apnea.METHODSThe authors reviewed all invasive electroencephalographic studies performed at Northwestern Memorial Hospital (Chicago) since 2010 to identify those cases in which 1) multiple mesial temporal electrodes (amygdala and hippocampal) were placed, 2) seizures were captured, and 3) patients’ respiration was monitored. They identified 8 investigations meeting these criteria in patients with temporal lobe epilepsy, and these investigations yielded data on a total of 22 seizures for analysis.RESULTSThe onset of ictal apnea associated with each seizure was highly correlated with seizure spread to the amygdala. Onset of apnea occurred 2.7 ± 0.4 (mean ± SEM) seconds after the spread of the seizure to the amygdala, which was significantly earlier than after spread to the hippocampus (10.2 ± 0.7 seconds; p < 0.01).CONCLUSIONSThe findings suggest that activation of amygdalar networks is correlated with central apnea during seizures. This study builds on the authors’ prior work that demonstrates a role for the amygdala in voluntary respiratory control and suggests a further role in dysfunctional breathing states seen during seizures, with implications for SUDEP pathophysiology.
Objective: To investigate whether high-frequency oscillations (HFOs) show spatiotemporal propagation and assess the relevance of the earliest oscillations in relation to the seizure onset zone (SOZ) and postsurgical outcome. Methods: We retrospectively investigated the intracerebral electroencephalography (EEG) of patients who became seizure free after subsequent surgery. We marked HFOs during 1 hour of recordings. We calculated the time delay between pairs of channels as the median delay between their HFOs and constructed a time line of the delay of each channel with respect to the earliest channel (first source channel). A network was defined when a temporal order could be established among the channels based on the existence of statistically significant delays. Results: Fifteen patients with good surgical outcome were included. We found ripple networks in all patients, and fast ripple networks in 9. For ripples, first source channels were found in a higher proportion in the SOZ than the rest of the network channels (15 of 27 [56%] versus 93 of 262 [35%]; p = 0.04). For both ripples and fast ripples, first source channels were resected more often that the rest of the network channels (ripples: 13 of 27 [48%] versus 65 of 262 [25%]; p = 0.01; fast ripples: 8 of 9 [89%] versus 17 of 40 [43%]; p = 0.002); channels with the highest rates of ripples and fast ripples were resected in a similar proportion. Interpretation: These results demonstrate that interictal HFOs are organized in networks and indicate a possible need for the resection of first source channels. However, resecting them is not superior to resecting channels with highest rates of HFOs. ANN NEUROL 2019;85:485-494 P athological high-frequency oscillations (HFOs) are a View this article online at wileyonlinelibrary.com.
Objective: Surgical specimens from patients with mesial temporal lobe epilepsy (MTLE) show abnormalities in tissue concentrations of metabotropic glutamate receptor type 5 (mGluR5). To clarify whether these abnormalities are specific to the epileptogenic zone (EZ), we characterized in vivo whole-brain mGluR5 availability in MTLE patients using positron emission tomography (PET) and [ 11 C]ABP688, a radioligand that binds specifically to the mGluR5 allosteric site. Methods: Thirty-one unilateral MTLE patients and 30 healthy controls underwent [ 11 C]ABP688 PET. We compared partial volume corrected [ 11 C]ABP688 nondisplaceable binding potentials (BP ND ) between groups using region-of-interest and whole-brain voxelwise analyses. [ 18 F]Fluorodeoxyglucose (FDG) PET was acquired in 15 patients, for whom we calculated asymmetry indices of [ 11 C]ABP688 BP ND and [ 18 F]FDG uptake to compare lateralization and localization differences. Results: [ 11 C]ABP688 BP ND was focally reduced in the epileptogenic hippocampal head and amygdala (p < 0.001). Patients with hippocampal atrophy showed more extensive abnormalities, including the ipsilateral temporal neocortex (p = 0.006). [ 11 C]ABP688 BP ND showed interhemispheric differences of higher magnitude and discriminated the epileptogenic structures more accurately when compared to [ 18 F]FDG uptake, which showed more widespread hypometabolism. Among 23 of 25 operated patients with >1 year of follow-up, 13 were seizure-free (Engel Ia) and showed significantly lower [ 11 C]ABP688 BP ND in the ipsilateral entorhinal cortex. Interpretation: [ 11 C]ABP688 PET provides a focal biomarker for the EZ in MTLE with higher spatial accuracy compared to [ 18 F]FDG PET. Focally reduced mGluR5 availability in the EZ might reflect receptor internalization or conformational changes in response to excessive extracellular glutamate, supporting a potential role for mGluR5 as therapeutic target in human MTLE. ANN NEUROL 2019;85:218-228 M etabotropic glutamate receptor type 5 (mGluR5) is a subtype of glutamate receptor that has garnered much interest as to its role in epilepsy. 1 mGluR5 is a postsynaptic G-protein-coupled receptor expressed mostly on the periphery of postsynaptic densities of neurons and astrocytes. It is widely distributed throughout the brain, particularly in limbic regions. 2,3 Group I mGluRs (including mGluR1 and mGluR5) are involved in the postsynaptic modulation of glutamatergic neurotransmission, being able to induce either long-term depression or potentiation. 4,5 View this article online at wileyonlinelibrary.com.
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