Sanchez-Boluarte, Sofia S

Abstract Emotional experiences during focal seizures are often misinterpreted as psychiatric disorders. We aimed to evaluate symptoms involving affective symptoms at seizure onset. We aimed to identify the most prevalent affective symptoms at seizure onset and characterize their localizing and lateralizing value. We performed a scoping review based on Preferred Reporting Items for Systematic reviews and Meta‐Analyses–extension for Scoping Reviews guidelines. A systematic search identified records from 4 databases: PubMed, Embase, CINAHL (via EBSCOhost), and Web of Science. Two reviewers independently screened titles/abstracts and full texts; discrepancies were resolved by consensus. This review focused on patients with focal seizures, as affective symptoms may occur in generalized epilepsies. The affective symptoms: fear, anxiety, panic, sadness, mystic, ecstatic, sexual, and mirth were identified, and semiology was evaluated in accordance with ILAE guidelines. Symptom onset, frequency, brain localization, and video‐EEG monitoring technique were evaluated to assess localization and lateralization of regional networks. Scalp EEG, invasive EEG recordings, and electrical stimulation were analyzed. A total of 1276 documents were identified, with 98 studies included for review. Fear was the most frequently reported ictal emotion, identified in 274 patients (66%), predominantly in temporal lobe epilepsy. Sadness and sexual, ecstatic symptoms were also consistently associated with temporal networks. Mirth was more frequently reported with frontal onset seizures. Evidence, primarily from Class IV studies, reported right hemispheric predominance for ecstasy, mystic, and sexual symptoms at seizure onset. Ictal affective symptoms at seizure onset yield localizing information. The limbic system, especially the temporal lobe, followed by the frontal lobe, was the most common site of origin. Fear was the most common spontaneous and electrically elicited symptom, followed by anxiety. While bi‐hemispheric lateralization occurred, right lateralization predominated. Recognizing paroxysmal affective symptoms as ictal phenomena may reduce misdiagnosis and aid presurgical evaluation in drug‐resistant focal epilepsy.

Abstract The objective of the study was to assess the frequency of interictal epileptiform discharges (IEDs) in calcified neurocysticercosis (NCC) and its relationship with calcification burden. Forty‐nine patients with calcified NCC (low‐burden, 1–2 calcifications, n = 24; high‐burden, ≥15 calcifications, n = 25) and seizure history underwent prolonged (8‐h) electroencephalography (EEG), interpreted by epileptologists who were blinded to patient history and calcification category. Clinical seizure outcomes were also assessed. We found that IEDs occurred in 7 of 49 participants (14.3%), with no difference between low‐burden (12.5%) and high‐burden (16.0%) groups ( p = 1.000). All IEDs (spikes and/or sharp waves) in the high‐burden group ( n = 4) were high‐voltage (100–150 μV), whereas those in the low‐burden group ( n = 3) were low or medium voltage (20–70 μV). Among the participants who had IEDs, 5 (71.4%) had seizures in the last year, compared with 14 (33.3%) in the group without IEDs detected ( p = 0.093). Among 19 participants with seizures in the last year, 5 were identified as having drug‐resistant epilepsy (DRE). All five cases of DRE occurred in individuals with 15 or more calcifications (5/25, 20%, vs 0/24, p = 0.023). We conclude that IEDs occur frequently in individuals with calcified NCC. Although calcification burden itself was not associated with the presence of IEDs, drug‐resistant cases and high‐voltage IEDs were concentrated in the high‐burden group, supporting the role of calcified parasites as epileptogenic foci.

AbstractBackground and purposeCerebral amyloid angiopathy (CAA) is a common cause of intracranial hemorrhage (ICH), which is a risk factor for seizures. The incidence and risk factors of seizures associated with a heterogeneous cohort of CAA patients have not been studied.MethodsWe conducted a retrospective study of patients with CAA treated at Mayo Clinic Florida between 1 January 2015 and 1 January 2021. CAA was defined using the modified Boston criteria version 2.0. We analyzed electrophysiological and clinical features, and comorbidities including lobar ICH, nontraumatic cortical/convexity subarachnoid hemorrhage (cSAH), superficial siderosis, and inflammation (CAA with inflammation [CAA‐ri]). Cognition and mortality were secondary outcomes. Univariate and multivariate analyses were performed to determine risk of seizures relative to clinical presentation.ResultsTwo hundred eighty‐four patients with CAA were identified, with median follow‐up of 35.7 months (interquartile range = 13.5–61.3 months). Fifty‐six patients (19.7%) had seizures; in 21 (37.5%) patients, seizures were the index feature leading to CAA diagnosis. Seizures were more frequent in females (p = 0.032) and patients with lobar ICH (p = 0.002), cSAH (p = 0.030), superficial siderosis (p < 0.001), and CAA‐ri (p = 0.005), and less common in patients with microhemorrhage (p = 0.006). After controlling for age and sex, lobar ICH (odds ratio [OR] = 2.1, 95% confidence interval [CI] = 1.1–4.2), CAA‐ri (OR = 3.8, 95% CI = 1.4–10.3), and superficial siderosis (OR = 3.7, 95% CI = 1.9–7.0) were independently associated with higher odds of incident seizures.ConclusionsSeizures are common in patients with CAA and are independently associated with lobar ICH, CAA‐ri, and superficial siderosis. Our results may be applied to optimize clinical monitoring and management for patients with CAA.

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.