Freund, Brin

Summary: The responsive neurostimulator continuously monitors the electrocorticogram. It delivers short bursts of high-frequency electrical stimulation when personalized patterns are detected. Intracranial EEG recording including electrocorticography is susceptible to artifacts, albeit at a lesser frequency compared with scalp recording. The authors describe a novel case of a patient with focal epilepsy, bitemporal responsive neurostimulation, and seizures without self-awareness manifest as focal impaired awareness seizures adversely affecting memory. At follow-up evaluation, the patient reported being clinically seizure-free although a single long episode was detected using the Patient Data Management System over the course of 3 years. Initial review identified a left-sided rhythmic discharge with a bilateral spatial field of involvement. In response to detection, the responsive neurostimulation delivered a series of five electrical stimulations. On further review, the patient recalled undergoing cervical radiofrequency ablation, which coincided with the appearance of the “electrographic seizure.” Extrinsic electrical artifact involving monomorphic nonevolving waveforms confirmed electrical artifact identified and treated by responsive neurostimulation as an epileptic seizure. On rare occasion, implanted electrical devices may lead to misdiagnosis and mistreatment of patients because of intracranial artifact.

AbstractNeuromodulation in epilepsy is a proven treatment for people with drug‐resistant focal epilepsy. Dual device therapies are increasingly utilized in people with drug‐resistant epilepsy. Vagus nerve stimulation (VNS) and deep brain stimulation (DBS) target the thalamus involving the primary neurobiological network in patients with genetic generalized epilepsy (GGE). We report a novel case of combined neuromodulation in a patient with drug‐resistant GGE who achieved a partial response with seizure reduction after VNS implantation yet following VNS‐DBS polyneurostimulation gradually achieved prolonged seizure freedom. We speculate that by combining the indirect activating effects of VNS with the direct inhibitory effects of DBS, this may provide synergy to thalamic modulated networks. We hypothesize a “rational polytherapy” may exist in some patients with GGE undergoing dual neuromodulation.

Purpose: Electroencephalogram is used for prognostication and diagnosis in critically ill patients and is vital in developing clinical management algorithms. Unique waveforms on EEG may distinguish neurological disorders and define a potential for seizures. To better characterize zeta waves, we sought to define their electroclinical spectrum. Methods: We performed a systematic review using MEDLINE, Embase, Cochrane Central Register of Controlled Trials and Cochrane Database of Systematic Review [through Ovid], Scopus, Science Citation Index Expanded and Emerging Sources Citation Index [through the Web of Science], and Epistemonikos. Grey literature resources were searched. Results: Five hundred thirty-seven articles were identified. After excluding duplicates and reviewing titles, abstracts, and bodies and bibliographies of articles, four studies reported 64 cases describing data from patients with zeta waves, with a prevalence of 3 to 4%. Various and often incomplete clinical, neuroimaging, and EEG data were available. 57 patients (89.1%) had a focal cerebral lesion concordant with the location of zeta waves on EEG. 26 patients (40.6%) had clinical seizures, all but one being focal onset. Thirteen patients (20%) had epileptiform activity on EEG. Typically, zeta waves were located in the frontal head regions, often with generalized, frontal, predominant, rhythmic delta activity and associated with focal EEG suppression. Conclusions: Zeta waves frequently represent an underlying focal structural lesion. Their presence suggests a heightened risk for seizures. The small number of retrospective cases series in the literature reporting zeta waves might be an underrepresentation. We suggest a need for prospective studies of cEEG in critically ill patients to determine their clinical significance.

OBJECTIVE The authors hypothesized that the proximity of deep brain stimulator contacts to the anterior thalamic nucleus–mammillothalamic tract (ANT-MMT) junction determines responsiveness to treatment with ANT deep brain stimulation (DBS) in drug-resistant epilepsy and conducted this study to test that hypothesis. METHODS This retrospective study evaluated patients who had undergone ANT DBS electrode implantation and whose devices were programmed to stimulate nearest the ANT-MMT junction based on direct MRI visualization. The proximity of the active electrode to the ANT and the ANT-MMT junction was compared between responders (≥ 50% reduction in seizure frequency) and nonresponders. Linear regression was performed to assess the percentage of seizure reduction and distance to both the ANT and the ANT-MMT junction. RESULTS Four (57.1%) of 7 patients had ≥ 50% reduction in seizures. All 4 responders had at least one contact within 1 mm of the ANT-MMT junction, whereas the 3 patients with < 50% seizure improvement did not have a contact within 1 mm of the ANT-MMT junction. Additionally, the 4 responders demonstrated contact positioning closer to the ANT-MMT junction than the 3 nonresponders (mean distance from MMT: 0.7 mm on the left and 0.6 mm on the right in responders vs 3.0 mm on the left and 2.3 mm on the right in nonresponders). However, proximity of the electrode contact to any point in the ANT nucleus did not correlate with seizure reduction. Greater seizure improvement was correlated with a contact position closer to the ANT-MMT junction (R2 = 0.62, p = 0.04). Seizure improvement was not significantly correlated with proximity of the contact to any ANT border (R2 = 0.24, p = 0.26). CONCLUSIONS Obtained using a combination of direct visualization and targeted programming of the ANT-MMT junction, data in this study support the hypothesis that proximity to the ANT alone does not correlate with seizure reduction in ANT DBS, whereas proximity to the ANT-MMT junction does. These findings support the importance of direct targeting in ANT DBS, as well as imaging-informed programming. Additionally, the authors provide supportive evidence for future prospective trials using ANT-MMT junction for direct surgical targeting.

AbstractTemporal lobe epilepsy is the most common form of focal epilepsy and is frequently resistant to antiseizure medication. Non‐invasive biomarkers are crucial when resective epilepsy surgery is considered in order to guide diagnostic work‐up and management. Interictal epileptiform discharges, when concordant with ictal EEG recording and a focal abnormality on functional imaging or anatomic MRI in patients with temporal lobe epilepsy, portend a favorable outcome with resective or ablative surgery. An interictal nonepileptiform feature on EEG believed to have the same localizing potential as epileptiform discharges is temporal intermittent rhythmic delta activity (TIRDA). The precise localization of TIRDA has been a subject of debate, but has been associated with seizures that arise from the temporal region. We report a 64‐year‐old female who underwent unsuccessful right anterior temporal lobectomy for drug‐resistant focal epilepsy, suspected to originate from the right temporal lobe. Subsequent video‐EEG monitoring revealed right, greater than left, TIRDA and interictal epileptiform discharges arising from the temporal regions bilaterally, despite a generous temporal lobectomy demonstrated by brain MRI. Further, using EEG source localization, we identified TIRDA using scalp EEG in sensor space, localized to the ipsilateral orbitofrontal region. We discuss the proposed localization of TIRDA in this case and address the importance of characterizing TIRDA in the presurgical evaluation of patients with epilepsy.

Summary: Prognostication following cardiorespiratory arrest relies on the neurological examination, which is supported by neuroimaging and neurophysiological testing. Acute posthypoxic myoclonus (PHM) is a clinical entity that has prognostic significance and historically has been considered an indicator of poor outcome, but this is not invariably the case. “Malignant” and more “benign” forms of acute PHM have been described and differentiating them is key in understanding their meaning in prognosis. Neurophysiological tests, electroencephalogram in particular, and clinical phenotyping are crucial in defining subtypes of acute PHM. This review describes the neurophysiological and phenotypic markers of malignant and benign forms of acute PHM, a clinical approach to evaluating acute PHM following cardiorespiratory arrest in determining prognosis, and gaps in our understanding of acute PHM that require further study.

Purpose: Periodic discharges (PDs) are EEG patterns denoting brain dysfunction and ictal tendency. Their exact meaning regarding etiology and outcomes is not well known. In particular, bilateral independent PDs (BIPDs) are poorly described. Methods: We performed a retrospective, multicenter study evaluating neuroimaging, epileptic, clinical, and EEG correlates of BIPDs. Results: Twenty-five patients studied with a mean Glasgow Coma Scale 6.5 and modified Rankin scale 3.9 who underwent EEG monitoring, mean duration 287 hours (range 0.75–3,216). Most common causes of BIPDs were cardiac arrest, Central Nervous System infections, and acute/chronic ischemic/hemorrhagic stroke. Most had subcortical and cortical injuries on neuroimaging. Most of the PDs ranged from 0.5 to 2 Hz in frequency, were of multiple phase types, and localized to the frontal head regions. Eighteen of 25 patients had clinical or electrographic seizures. There was a trend toward seizures in those with BIPDs with a history of epilepsy (P = 0.08) and acute metabolic dysfunction (P = 0.08), particularly with coincident acute structural lesions (P = 0.05). Seizures were predicted by bilaterally symmetric frequencies (P = 0.02) and trended toward higher likelihood with PD frequency <2 Hz (P = 0.08). Two of 25 patients survived past discharge with modified Rankin scale <3. Cardiac arrest was associated with withdrawal of life-sustaining therapy (P < 0.001). Conclusions: BIPDs arise from acute and chronic neurologic injuries, often associated with metabolic dysfunction. Outcomes are poor in this population. Seizures are common, particularly in patients with PDs that are of a lower frequency or are symmetric in frequency. Further study is warranted to evaluate the association between BIPDs and seizures, as well as functional and longer term outcomes.