Abstracts

Rationale: Epilepsia partialis continua (EPC) is a type of focal motor status epilepticus characterized by unremitting focal myoclonus. It is a condition that often shows no clear ictal findings on EEG or MEG. This case series explores the role of jerk-locked back averaging (JLBA) in MEG to identify the ictal changes associated with these focal motor seizures. Methods: Two cases of EPC undergoing jerk-locked back averaging during magnetoencephalography (MEG) at Texas Children’s Hospital (TCH) were reviewed. MEG data was acquired using the Elekta Neuromag Triux system, which utilizes 102 magnetometers and 204 planar gradiometers, at a total of 102 sites. EEG was recorded simultaneously using standard 10-20 electrode positions, plus subtemporal electrodes. At least one hour of spontaneous combined recording was collected in each patient. EMG leads were placed in the muscle groups affected by the EPC and the EMG leads were used as trigger time points for JLBA. Time periods of 500 msec before and after the trigger points were averaged to create averaged waveform tracings. Magnetic sources were estimated using single equivalent current dipole (ECD) models and co-registered to the patient's most recent MRI, using a combination of the Elekta proprietary software and Curry 7 software. Results: The first patient was a 6 y.o. female presenting with new onset repetitive myoclonic jerks of both hands.  She was initially felt to have a movement disorder, and initial routine EEGs were normal.  Upon presentation to the MEG, near continuous myoclonic jerks were seen most prominently in the left ECU and right abductor pollicis brevis (APB).  EMG leads were placed over both muscles, but only the left ECU provided a reliable EMG tracing.  The EEG and MEG did demonstrate epileptiform spikes at this time, and ECD modeling identified tight clusters in the left and right central sulci.  Visual inspection of the EMG activity did not demonstrate a consistent EEG or MEG change with the myoclonus, however.  Upon averaging 200 trigger time points, an identifiable waveform was identified with a peak at -10 msec.  ECD modeling of this averaged waveform placed a source in the right central sulcus.  The second case was a 4 y.o. male with history developmental delay, SARS2 variant causing mitochondrial abnormality, and known prior choreioform movement disorder, presenting initially with new movements.  The movements began during pneumonia, described as twitching movements of the right side of his body.  Initial EEG done at TCH showed 1-2.5 Hz periodic spikes in the right posterior quadrant, but no clear changes associated with his movements.  Upon presentation to the MEG facility, near continuous myoclonic jerks were noted over the left orbicularis oris, left quadriceps, and left APB.  EMG leads were placed, with only the former two providing reliable EMG tracings.  MEG and EEG demonstrated right hemispheric spikes.  ECD modeling revealed a MEG cluster in the right postcentral sulcus, as well as more scattered spike sources in the posterior perisylvian temporal and parietal lobes.  JLBA was performed using EMG leads placed over the left orbicularis oris and quadriceps, with 627 and 697 triggers, respectively.  ECD modeling of both trials placed an averaged source in the right central sulcus at -50 msec. Conclusions: The results of this study suggest JLBA may play an important role in confirming epilepsia partialis continua, as opposed to other causes of abnormal movements.  Funding: None