Acute EEG Research Articles

The Surgical Method of Craniectomy Differentially Affects Acute Seizures, Brain Deformation and Behavior in a TBI Animal Model.

Traumatic brain injury (TBI) is the leading cause of morbidity and mortality worldwide. Multiple injury models have been developed to study this neurological disorder. One such model is the lateral fluid-percussion injury (LFPI) rodent model. The LFPI model can be generated with different surgical procedures that could affect the injury and be reflected in neurobehavioral dysfunction and acute EEG changes. A craniectomy was performed either with a trephine hand drill or with a trephine electric drill that was centered over the left hemisphere of adult, male Sprague Dawley rats. Sham craniectomy groups were assessed by hand-drilled (ShamHMRI) and electric-drilled (ShamEMRI) to evaluate by MRI. Then, TBI was induced in separate groups (TBIH) and (TBIE) using a fluid-percussion device. Sham-injured rats (ShamH/ShamE) underwent the same surgical procedures as the TBI rats. During the same surgery session, rats were implanted with screw and microwire electrodes positioned in the neocortex and hippocampus and the EEG activity was recorded 24 hours for the first 7 days after TBI for assessing the acute EEG seizure and Gamma Event Coupling (GEC). The electric drilling craniectomy induced greater tissue damage and sensorimotor deficits compared to the hand drill. Analysis of the EEG revealed acute seizures in at least one animal from each group after the procedure. Both TBI and Sham rats from the electric drill groups had a significant greater total number of seizures than the animals that were craniectomized manually (p<0.05). Similarly, EEG functional connectivity was lower in ShamE compared to ShamH rats. These results suggest that electrical versus hand drilling craniectomies produce cortical injury in addition to the LFPI which increases the likelihood for acute post-traumatic seizures. Differences in the surgical approach could be one reason for the variability in the injury that makes it difficult to replicate results between preclinical TBI studies.

The Surgical Method of Craniectomy Differentially Affects Acute Seizures, Brain Deformation, and Behavior in a Traumatic Brain Injury Animal Model.

Traumatic brain injury (TBI) is the leading cause of morbidity and mortality worldwide. Multiple injury models have been developed to study this neurological disorder. One such model is the lateral fluid percussion injury (LFPI) rodent model. The LFPI model can be generated with different surgical procedures that could affect the injury and be reflected in neurobehavioral dysfunction and acute electroencephalograph (EEG) changes. A craniectomy was performed either with a trephine hand drill or with a trephine electric drill that was centered over the left hemisphere of adult, male Sprague Dawley rats. Sham craniectomy groups were assessed by hand-drilled (ShamHMRI) and electric-drilled (ShamEMRI) to evaluate by magnetic resonance imaging (MRI). Then, TBI was induced in separate groups, (TBIH) and (TBIE), using a fluid-percussion device. Sham-injured rats (ShamH/ShamE) underwent the same surgical procedures as the TBI rats. During the same surgery session, rats were implanted with screw and microwire electrodes positioned in the neocortex and hippocampus and the EEG activity was recorded 24 h for the first 7 days after TBI for assessing the acute EEG seizure and gamma event coupling. The electric drilling craniectomy induced greater tissue damage and sensorimotor deficits compared with the hand drill. Analysis of the EEG revealed acute seizures in at least one animal from each group after the procedure. Both TBI and Sham rats from the electric drill groups had a significant greater total number of seizures than the animals that were craniectomized manually (p < 0.05). Similarly, EEG functional connectivity was lower in ShamE compared with ShamH rats. These results suggest that electrical versus hand-drilling craniectomies produce cortical injury in addition to the LFPI which increases the likelihood for acute post-traumatic seizures. Differences in the surgical approach could be one reason for the variability in the injury that makes it difficult to replicate results between preclinical TBI studies.

Clinical features of neurotoxicity after CD19 CAR T-cell therapy in mantle cell lymphoma

AbstractCD19 chimeric antigen receptor (CAR) T-cell therapy has proven highly effective for treating relapsed/refractory mantle cell lymphoma (MCL). However, immune effector cell–associated neurotoxicity syndrome (ICANS) remains a significant concern. This study aimed to evaluate the clinical, radiological, and laboratory correlatives associated with ICANS development after CD19 CAR T-cell therapy in patients with MCL. All patients (N = 26) who received standard-of-care brexucabtagene autoleucel until July 2022 at our institution were evaluated. Laboratory and radiographic correlatives including brain magnetic resonance imaging (MRI) and electroencephalogram (EEG) were evaluated to determine the clinical impact of ICANS. Seventeen (65%) patients experienced ICANS after treatment, with a median onset on day 6. Ten (38%) patients experienced severe (grade ≥3) ICANS. All patients with ICANS had antecedent cytokine release syndrome (CRS), but no correlation was observed between ICANS severity and CRS grade. Overall, 92% of EEGs revealed interictal changes; no patients experienced frank seizures because of ICANS. In total, 86% of patients with severe ICANS with postinfusion brain MRIs demonstrated acute neuroimaging findings not seen on pretreatment MRI. Severe ICANS was also associated with higher rates of cytopenia, coagulopathy, increased cumulative steroid exposure, and prolonged hospitalization. However, severe ICANS did not affect treatment outcomes of patients with MCL. Severe ICANS is frequently associated with a range of postinfusion brain MRI changes and abnormal EEG findings. Longer hospitalization was observed in patients with severe ICANS, especially those with abnormal acute MRI or EEG findings, but there was no discernible impact on overall treatment response and survival.

Classification System for Predicting Emergent Epilepsy Phenotype in the Intra-amygdala Kainic Acid Mouse Model of Epilepsy.

Animal models of drug-resistant epilepsy represent an important resource for discovering new drug targets and testing experimental medicines. Intra-amygdala microinjection of kainic acid in mice is one of the most widely regarded models of drug-resistant epilepsy. Mice develop acute status epilepticus, which diminishes after a few hours and then, within a few days, mice display spontaneous seizures (epilepsy). The frequency of spontaneous seizures varies between mice, with some developing low or high seizure rates. The ability to predict soon after status epilepticus, which mice will go on to develop a normal frequency of seizures, would enable a significant reduction in resources and EEG reviewing time and lead to humane early end-points for the mice with low or high seizure rates. In this study, we developed two machine learning models, a feature-based and transfer learning-based approach, for predicting the emergent spontaneous seizure rates in the intra-amygdala kainic acid model based on the acute EEGs recorded in mice during status epilepticus lasting 40 minutes. The method was trained on data from 28 mice and subsequently tested on data from 16 mice. The feature-based and transfer learning-based models achieved accuracies of 69% and 75%, respectively on the test set in classifying emergent epilepsy as normal or outlier (i.e. low-frequency or high-frequency seizure rate). A limitation of the intra-amygdala kainic acid model has been the loss of time and resources from generating mice with low or high rates of spontaneous seizures. To date, no other research has attempted to predict emergent spontaneous seizure rates. The feature-based and transfer learning-based models will assist researchers in identifying mice with a normal frequency of seizures before the onset of spontaneous seizures. We have implemented this approach as a web server, which can potentially reduce the time and resources spent analysing the EEGs of mice who develop low-frequency or high-frequency seizure rates. This will enable the early humane endpoint of outlier mice, which aligns with the principles of the responsible use of animals in research and simultaneously speeds up preclinical anti-epilepsy drug discovery.

Machine learning-based prediction of post-stroke cognitive status using electroencephalography-derived brain network attributes.

More than half of patients with acute ischemic stroke develop post-stroke cognitive impairment (PSCI), a significant barrier to future neurological recovery. Thus, predicting cognitive trajectories post-AIS is crucial. Our primary objective is to determine whether brain network properties from electroencephalography (EEG) can predict post-stroke cognitive function using machine learning approach. We enrolled consecutive stroke patients who underwent both EEG during the acute stroke phase and cognitive assessments 3 months post-stroke. We preprocessed acute stroke EEG data to eliminate low-quality epochs, then performed independent component analysis and quantified network characteristics using iSyncBrain®. Cognitive function was evaluated using the Montreal cognitive assessment (MoCA). We initially categorized participants based on the lateralization of their lesions and then developed machine learning models to predict cognitive status in the left and right hemisphere lesion groups. Eighty-seven patients were included, and the accuracy of lesion laterality prediction using EEG attributes was 97.0%. In the left hemispheric lesion group, the network attributes of the theta band were significantly correlated with MoCA scores, and higher global efficiency, clustering coefficient, and lower characteristic path length were associated with higher MoCA scores. Most features related to cognitive scores were selected from the frontal lobe. The predictive powers (R-squared) were 0.76 and 0.65 for the left and right stroke groups, respectively. Estimating EEG-based network properties in the acute phase of ischemic stroke through a machine learning model has a potential to predict cognitive outcomes after ischemic stroke.

Frontal lobe epilepsy and mild malformation with oligodendroglial hyperplasia: Further observations on electroclinical and imaging phenotypes, and surgical perspectives.

Mild malformation with oligodendroglial hyperplasia (MOGHE) is a recently described clinicopathologic entity, associated with drug-resistant epilepsy and extensive epileptogenic networks. Knowledge is accumulating about particular electroclinical phenotypes, correlations with imaging, and potential prognostic significance for surgical outcomes. The study adds relevant information by documenting the presence of a hyperkinetic frontal lobe seizure phenotype in adolescents and an epileptic encephalopathy phenotype in young children. Five cases were subjected to a structured presurgical evaluation protocol, including EEG-FMRI, chronic and acute invasive EEG, subjected to frontal lobe surgery with postoperative follow-up between 15 months and 7 years. In the two adult cases, surface EEG demonstrated lateralized widespread frontal lobe epileptogenicity and hyperkinetic semiological features. MRI demonstrated cortical white matter blurring and deeper white matter abnormalities. EEG-FMRI suggested concordant frontal lobe involvement. iEEG demonstrated a widespread frontal lobe epilepsy network. The three young children demonstrated a diffuse epileptic encephalopathy phenotype, with nonlocalizing, nonlateralizing surface EEG, and "spasms" as the main seizure type. MRI demonstrated extensive frontal lobe subcortical gray and white matter abnormalities, consistent with MOGHE literature for this age, while EEG-FMRI, in 2/3, demonstrated concordant frontal lobe involvement. They did not undergo chronic iEEG, and the resection was assisted by acute intraoperative ECoG. All cases were subjected to extensive frontal lobectomies with Engel class IA (2/5), IB (1/5), and IIB (2/5) outcomes. The study confirms the presence of frontal lobe epilepsy and epileptic encephalopathy phenotypes, in accordance with epilepsy phenotypes already described in MOGHE literature. Presurgical evaluation studies, including EEG-FMRI, can provide strong lateralizing and localizing evidence of the epileptogenic networks involved. All responded favorably to extensive frontal lobe resections, despite widespread epileptic activity recorded by surface and intracranial EEG pre- and postoperatively; an epileptic encephalopathy phenotype, in the first years of life, should not discourage such a resection.

The role of neurophysiological tools in the evaluation of ischemic stroke evolution: a narrative review.

Ischemic stroke is characterized by a complex cascade of events starting from vessel occlusion. The term "penumbra" denotes the area of severely hypo-perfused brain tissue surrounding the ischemic core that can be potentially recovered if blood flow is reestablished. From the neurophysiological perspective, there are local alterations-reflecting the loss of function of the core and the penumbra-and widespread changes in neural networks functioning, since structural and functional connectivity is disrupted. These dynamic changes are closely related to blood flow in the affected area. However, the pathological process of stroke does not end after the acute phase, but it determines a long-term cascade of events, including changes of cortical excitability, that are quite precocious and might precede clinical evolution. Neurophysiological tools-such as Transcranial Magnetic Stimulation (TMS) or Electroencephalography (EEG)-have enough time resolution to efficiently reflect the pathological changes occurring after stroke. Even if they do not have a role in acute stroke management, EEG and TMS might be helpful for monitoring ischemia evolution-also in the sub-acute and chronic stages. The present review aims to describe the changes occurring in the infarcted area after stroke from the neurophysiological perspective, starting from the acute to the chronic phase.

Effects of Sublethal Organophosphate Toxicity and Anti-cholinergics on Electroencephalogram and Respiratory Mechanics in Mice

Organophosphates are used in agriculture as insecticides but are potentially toxic to humans when exposed at high concentrations. The mechanism of toxicity is through antagonism of acetylcholinesterase, which secondarily causes excess activation of cholinergic receptors leading to seizures, tremors, respiratory depression, and other physiological consequences. Here we investigated two of the major pathophysiological effects, seizures and respiratory depression, using subcutaneous injection into mice of the organophosphate diisopropylfluorophosphate (DFP) at sublethal concentrations (2.1 mg/Kg) alone and co-injected with current therapeutics atropine (50 mg/Kg) or acetylcholinesterase reactivator HI6 (3 mg/Kg). We also tested a non-specific cholinergic antagonist dequalinium chloride (2 mg/Kg) as a novel treatment for organophosphate toxicity. Electroencephalogram (EEG) recordings revealed that DFP causes focal delta frequency (average 1.4 Hz) tonic spikes in the parietal region that occur transiently (lasting an average of 171 ± 33 min) and a more sustained generalized theta frequency depression in both parietal and frontal electrode that did not recover the following 24 h. DFP also caused behavioral tremors that partially recovered the following 24 h. Using whole body plethysmography, DFP revealed acute respiratory depression, including reduced breathing rates and tidal volumes, that partially recover the following day. Among therapeutic treatments, dequalinium chloride had the most potent effect on all physiological parameters by reducing acute EEG abnormalities and promoting a full recovery after 24 h from tremors and respiratory depression. Atropine and HI6 had distinct effects on EEGs. Co-treatment with atropine converted the acute 1.4 Hz tonic spikes to 3 Hz tonic spikes in the parietal electrode and promoted a partial recovery after 24 h from theta frequency and respiratory depression. HI6 fully removed the parietal delta spike increase and promoted a full recovery in theta frequency and respiratory depression. In summary, while all anticholinergic treatments promoted survival and moderated symptoms of DFP toxicity, the non-selective anti-cholinergic dequalinium chloride had the most potent therapeutic effects in reducing EEG abnormalities, moderating tremors and reducing respiratory depression.

Psilocin acutely alters sleep-wake architecture and cortical brain activity in laboratory mice

Serotonergic psychedelic drugs, such as psilocin (4-hydroxy-N,N-dimethyltryptamine), profoundly alter the quality of consciousness through mechanisms which are incompletely understood. Growing evidence suggests that a single psychedelic experience can positively impact long-term psychological well-being, with relevance for the treatment of psychiatric disorders, including depression. A prominent factor associated with psychiatric disorders is disturbed sleep, and the sleep-wake cycle is implicated in the homeostatic regulation of neuronal activity and synaptic plasticity. However, it remains largely unknown to what extent psychedelic agents directly affect sleep, in terms of both acute arousal and homeostatic sleep regulation. Here, chronic electrophysiological recordings were obtained in mice to track sleep-wake architecture and cortical activity after psilocin injection. Administration of psilocin led to delayed REM sleep onset and reduced NREM sleep maintenance for up to approximately 3 h after dosing, and the acute EEG response was associated primarily with an enhanced oscillation around 4 Hz. No long-term changes in sleep-wake quantity were found. When combined with sleep deprivation, psilocin did not alter the dynamics of homeostatic sleep rebound during the subsequent recovery period, as reflected in both sleep amount and EEG slow-wave activity. However, psilocin decreased the recovery rate of sleep slow-wave activity following sleep deprivation in the local field potentials of electrodes targeting the medial prefrontal and surrounding cortex. It is concluded that psilocin affects both global vigilance state control and local sleep homeostasis, an effect which may be relevant for its antidepressant efficacy.

Intracorporeal Cortical Telemetry as a Step to Automatic Closed-Loop EEG-Based CI Fitting: A Proof of Concept.

Electrically evoked auditory potentials have been used to predict auditory thresholds in patients with a cochlear implant (CI). However, with exception of electrically evoked compound action potentials (eCAP), conventional extracorporeal EEG recording devices are still needed. Until now, built-in (intracorporeal) back-telemetry options are limited to eCAPs. Intracorporeal recording of auditory responses beyond the cochlea is still lacking. This study describes the feasibility of obtaining longer latency cortical responses by concatenating interleaved short recording time windows used for eCAP recordings. Extracochlear reference electrodes were dedicated to record cortical responses, while intracochlear electrodes were used for stimulation, enabling intracorporeal telemetry (i.e., without an EEG device) to assess higher cortical processing in CI recipients. Simultaneous extra- and intra-corporeal recordings showed that it is feasible to obtain intracorporeal slow vertex potentials with a CI similar to those obtained by conventional extracorporeal EEG recordings. Our data demonstrate a proof of concept of closed-loop intracorporeal auditory cortical response telemetry (ICT) with a cochlear implant device. This research breaks new ground for next generation CI devices to assess higher cortical neural processing based on acute or continuous EEG telemetry to enable individualized automatic and/or adaptive CI fitting with only a CI.

Intrathecal Chemotherapy As a Potential Alternative Treatment for Steroid-Refractory Immune Effector Cell-Associated Neurotoxicity Syndrome

IntroductionChimeric antigen receptor (CAR) T-cell therapy has revolutionized the treatment paradigm for patients with relapsed or refractory (R/R) diffuse large B-cell lymphoma (DLBCL) and other hematologic malignancies. However, its use is associated with serious adverse effects including cytokine release syndrome (CRS) and immune effector cell-associated neurotoxicity syndrome (ICANS). Severe ICANS can present with aphasia, mutism, somnolence, seizures, signs of increased intracranial pressure and rarely cerebral edema. Corticosteroids (CS) and IL-6 inhibitors are first line treatment for CRS and ICANS. Prolonged CS use has been associated with decreased over-all survival in CAR T-cell treated patients. Data on effective treatments for CART T-cell induced neurotoxicity is limited, especially in steroid-refractory ICANS. Blood-brain barrier (BBB) disruption and infiltration of myeloid and immune effector cells into the central nervous system are implicated in the pathogenesis of ICANS. This likely explains the role of intrathecal chemotherapy, which has been described in literature for treatment of steroid-refractory ICANS. Here, we report the outcomes of two patients with refractory DLBCL who developed severe ICANS after receiving axicabtagene ciloleucel (axi cel) and treated with intrathecal (IT) chemotherapy.Case PresentationOur first case is of a 66 year old male with diagnosis of R/R DLBCL, who was treated with R-CHOP, followed by R-GemOx, with no response then received axi cel. Patient developed grade 2 CRS and grade 1 ICANS (National Cancer Institute Common Terminology Criteria for Adverse Effects v4.03) on day +2 post infusion, treated with tocilizumab and dexamethasone with good response initially. While tapering dexamethasone on day +5, he developed grade 3 CRS and grade 3 ICANS. Brain MRI did not show any intracranial abnormality and EEG showed no seizure activity. Lumbar puncture (LP) was done on day +7 and showed opening pressure of 32 cm H2O, and 12 lymphocytes. He was started on IV solumedrol and tocilizumab was resumed. CRS improved while neurotoxicity progressed to grade 4 prompting intubation and mechanical ventilation on day +8. On day +9, patient received intrathecal methotrexate 12 mg and hydrocortisone 50 mg. On day +12, neurotoxicity improved to grade 1 and patient was extubated on day +13. Steroid taper stopped on +17. Despite disease response, patient remained hospitalized at day +45 for deconditioning and vocal cord paralysis related to a lengthy hospital stay and intubation. He was eventually discharged, however passed away on day +49 from complications of prolonged hospitalization.Our second case is of a 69 year old female with a diagnosis of R/R DLBCL with CNS involvement, treated with RCHOP x6 followed by salvage chemotherapy with refractory disease, She then received axi cel. Patient developed grade 1 CRS on day +4, treated with tocilizumab and dexamethasone, and patient responded well. On day +9, she developed grade 2 CRS and grade 3 ICANS. At that time, dexamethasone was switched to pulse dose solumedrol and tocilizumab was continued. CT head showed no acute intracranial abnormality and EEG did not show any epileptiform activity. LP showed opening pressure of 21, and 84 lymphocytes. On day +11, patient's CRS resolved, however ICANS developed to grade 4 and patient received 12 mg intrathecal methotrexate and hydrocortisone 50 mg for steroid-refractory ICANS. The very next day, patient showed significant neurological improvement. Steroid taper was initiated and patient's ICANS resolved on day +16. MRI brain showed decrease in size of nodular enhancement along periventricular white matter and left occipital area corresponding to treatment response. She was discharged on day +28 and continues to do well one year out of axi cel infusionConclusionOur abstract adds to the sparse literature about the use IT chemotherapy in cases with severe ICANS. It also highlights its importance as an alternative potential therapy to high doses and prolonged courses of corticosteroids which is associated with increased morbidity and mortality. Steroid-refractory ICANS has limited treatment options and further evaluation of the use of IT chemotherapy in large scale studies is warranted. DisclosuresKahn: Abbvie: Research Funding, Speakers Bureau; Astrazeneca: Research Funding, Speakers Bureau; Beigene: Research Funding, Speakers Bureau; Epizyme: Research Funding, Speakers Bureau; Genetech: Research Funding, Speakers Bureau; GSK: Speakers Bureau; Karyopharm: Speakers Bureau; Kite: Speakers Bureau; Morphosys: Speakers Bureau; Sanofi: Speakers Bureau; SeaGen: Speakers Bureau. Fazal: Agios: Consultancy, Honoraria, Speakers Bureau; AMGEN: Consultancy, Honoraria, Speakers Bureau; Bristol Myers Squibb: Consultancy, Honoraria, Speakers Bureau; Gilead Sciences: Consultancy, Honoraria, Speakers Bureau; Glaxo Smith Kline: Consultancy, Honoraria, Speakers Bureau; Incyte: Consultancy, Honoraria, Speakers Bureau; Janssen Oncology: Consultancy, Honoraria, Speakers Bureau; Jazz Pharmaceuticals: Consultancy, Honoraria, Speakers Bureau; Karyopharm Pharmaceuticals: Consultancy, Honoraria, Speakers Bureau; Novartis: Consultancy, Honoraria, Speakers Bureau; Sanofi Genzyme: Consultancy, Honoraria, Speakers Bureau; Stemline Therapeutics: Consultancy, Honoraria, Speakers Bureau; Taiho Pharmaceuticals: Consultancy, Honoraria, Speakers Bureau; Takeda: Consultancy, Honoraria, Speakers Bureau. Lister: Oncology Analytics: Other: Academic Board.

Outcomes of patients with nonepileptic transient neurologic symptoms after subdural hematoma evacuation.

Patients undergoing a subdural hematoma (SDH) evacuation can experience transient neurological symptoms (TNS) postoperatively. Electroencephalography (EEG) is used to rule out seizures. We aim to characterize patients with TNS and negative epileptiform activity on EEG and compare them to those with positive epileptiform EEG findings. We performed a retrospective study of adult patients who underwent EEG for evaluation of TNS after undergoing SDH evacuation. Patients were stratified based on SDH type (acute and non-acute) and whether or not their EEG demonstrated positive epileptiform activity. A multivariate analysis was performed to identify predictors of negative EEG findings. One hundred twenty-nine SDH patients were included (45 (34.9%) acute; 84 (65.1%) non-acute). Overall, 45 (24 acute and 21 non-acute SDH patients) had positive epileptiform EEG findings, and 84 (21 acute and 63 non-acute SDH patients) had a negative EEG. Acute and non-acute SDH patients with positive EEG findings were more likely to suffer from greater than five episodes of TNS, impaired awareness, and motor symptoms, while the negative EEG group was more likely to suffer from negative symptoms. Non-acute SDH patients with positive EEG had longer mean ICU stays (14.6 vs. 7.2; p = 0.005). Both acute and non-acute SDH-positive EEG patients had worse disposition upon discharge (p < 0.05), worse modified Rankin score at discharge (p < 0.05), and 3-month follow-up (p < 0.05) and were more likely to be discharged on more than one antiepileptic drug (p < 0.001). Postoperative acute and non-acute SDH patients with TNS and negative EEG results are likely to have a favorable clinical picture. This distinction is therapeutically and prognostically important as these patients may not respond to typical antiepileptic drugs and they have better functional outcomes.

An Exploration of Eye Artifacts and Learning Within an Acute EEG Neurofeedback Training Session

An Exploration of Eye Artifacts and Learning Within an Acute EEG Neurofeedback Training Session

Retrospective Analysis of EEG in Patients With COVID-19: EEG Recording in Acute and Follow-up Phases.

Background. Interest in electroencephalographic (EEG) coronavirus disease 2019 (COVID-19) findings has been growing, especially in the search for a specific-features EEG of encephalopathy. Methods. We made a retrospective analysis of 29 EEGs recorded in 15 patients with COVID-19 and neurological symptoms. We classified the EEGs as “Acute EEG” and “follow-up EEG.” We did a statistical analysis between voltage and respiratory status of the patient, stay or not in the intensive care unit (ICU), days of stay in the ICU, sedative drugs, pharmacological treatment, type of symptoms predominating, and outcome. Results. We found EEG abnormalities in all patients studied. We observed the amplitude of background <20 µV at 93% of “acute EEG,” versus only 21.4% of “follow-up EEG.” The average voltage went from 12.33 ± 5.09 µV in the acute EEGs to 32.8 ± 20.13 µV in the follow-up EEGs. A total of 60% of acute EEGs showed an intermittent focal rhythmic. We have not found a statistically significant association between voltage of acute EEG and nonneurological clinical status (including respiratory) that may interfere with the EEG findings. Conclusions. Nonspecific diffuse slowing EEG pattern in COVID-19 is the most common finding reported, but we found in addition to that, as a distinctive finding, low voltage EEG, that could explain the low prevalence of epileptic activity published in these patients. A metabolic/hypoxic mechanism seems unlikely on the basis of our EEG findings. This pattern in other etiologies is reminiscent of severe encephalopathy states associated with poor prognosis. However, an unreactive low voltage pattern in COVID-19 patients is not necessarily related to poor prognosis.

Long-term electro-clinical profile of sudden cardiac arrest survivors.

ObjectiveRecent research has explored the use of continuous EEG (cEEG) monitoring for prognostication of spontaneous cardiac arrest (SCA). However, there is limited literature on the long‐term (post‐hospital discharge) electrographic findings among SCA survivors and their clinical correlates. Our study aims to fill this critical knowledge gap.MethodsWe retrospectively used our EEG database to identify adults (≥18 years) with SCA history who underwent an outpatient laboratory‐based EEG between 01/01/2011 and 12/31/2018. After electronic medical records (EMR) review, patients with epilepsy history and unclear/poorly documented SCA history were excluded. Outpatient EEGs were reviewed by authors. Acute EEG findings were extracted from the EEG database and EMR. In addition, we extracted data on acute and long‐term neuroimaging findings (CT/MRI), post‐SCA seizures, and anti‐seizure medications (ASM) status. Descriptive analysis and Fisher's exact test were performed.ResultsWe included 32 SCA survivors (50% women; mean age = 52.1 ± 13.6 years) in the study. During a median clinical follow‐up of 28.2 months, 3 patients suffered only clinical seizures, 3 only chronic post‐hypoxic myoclonus, and 5 had both [11 (34.4%) in total]. Interictal epileptiform discharges (IEDs) were noted in one‐third of the patients, which localized to vertex and frontocentral regions in all but one patient. Five (15.6%) of them did not suffer a clinical seizure despite the presence of EAs. Patients who developed epilepsy were significantly more likely to have abnormal neuroimaging findings [10/11 (90.9%)] during the follow‐up compared to the rest of the patients [OR = 25 (95% CI 2.6–>100, P = .002)]. Half of the study cohort was taking ASM at the last follow‐up.SignificanceOur small study reveals a signature location of IEDs in SCA survivors. Neuroimaging abnormalities seem to be a better indicator of epilepsy development, while EEG may reveal markers of potential epileptogenicity in the absence of clinical seizures. Future, larger studies are needed to confirm our findings.

Generalized onset seizures during COVID-19 infection: Does it mean the diagnosis Epilepsy

We present a case report of a 58-year old man who came to our Department of Neurology for a consultation 2 months after being diagnosed with COVID-19 infection. The patient had been febrile for a week and had had 2 generalized onset seizures with clonic jerks of the upper extremities in 2 consecutive days. Then he had been admitted at a department of infection diseases. COVID-19 PCR had been positive. EEG and CT scan of the brain had been absolutely normal. The patient had been treated with azithromycin for the COVID-19 infection and following a negative PCR test, he had gone home. During the hospital stay the patient had been diagnosed with Epilepsy and valproate treatment had been started. The patient did not accept the diagnosis and did not take the anticonvulsant regularly, moreover he was a truck driver and wanted to go back to work shortly. The control EEG showed no abnormalities and he had no more seizures. Therefore we did not accept the diagnosis Epilepsy and did not recommend a regular intake of antiepileptic medications. In conclusion we would like to emphasize on the need of an individual approach to every patient. Provoked seizures which are symptoms of an infection do not necessarily mean a diagnosis Epilepsy and do not require chronic treatment, especially when they are not present after the acute stage and EEG is normal.

Generalized onset seizures during COVID-19 infection: Does it mean the diagnosis Epilepsy

We present a case report of a 58-year old man who came to our Department of Neurology for a consultation 2 months after being diagnosed with COVID-19 infection. The patient had been febrile for a week and had had 2 generalized onset seizures with clonic jerks of the upper extremities in 2 consecutive days. Then he had been admitted at a department of infection diseases. COVID-19 PCR had been positive. EEG and CT scan of the brain had been absolutely normal. The patient had been treated with azithromycin for the COVID-19 infection and following a negative PCR test, he had gone home. During the hospital stay the patient had been diagnosed with Epilepsy and valproate treatment had been started. The patient did not accept the diagnosis and did not take the anticonvulsant regularly, moreover he was a truck driver and wanted to go back to work shortly. The control EEG showed no abnormalities and he had no more seizures. Therefore we did not accept the diagnosis Epilepsy and did not recommend a regular intake of antiepileptic medications. In conclusion we would like to emphasize on the need of an individual approach to every patient. Provoked seizures which are symptoms of an infection do not necessarily mean a diagnosis Epilepsy and do not require chronic treatment, especially when they are not present after the acute stage and EEG is normal.

The COVID-19 outbreak and approaches to performing EEG in Europe.

Aims The coronavirus SARS‐CoV‐2 disease (COVID‐19) pandemic affects availability and performance of neurophysiological diagnostic methods, including EEG. Our objective was to outline the current situation regarding EEG‐based investigations across Europe. Methods A web‐based survey was distributed to centres within the European Reference Network on rare and complex epilepsies (ERN EpiCARE). Responses were collected between April 9 and May 15, 2020. Results were analysed with Microsoft Excel, Python Pandas and SciPy. Results Representants from 47 EpiCARE centres from 22 countries completed the survey. At the time of completing the survey, inpatient video‐EEGs had been stopped or restricted in most centres (61.7% vs. 36.2% for adults, and 38.3% vs. 53.2% for children). Invasive investigations and epilepsy surgery were similarly affected. Acute EEGs continued to be performed, while indications for outpatient EEGs were limited and COVID‐19 triage put in place. The strictness of measures varied according to extent of the outbreak in a given country. Conclusions The results indicate a profound impact of COVID‐19 on neurophysiological diagnostics, especially inpatient video‐EEGs, invasive investigations, and epilepsy surgery. The COVID‐19 pandemic may hamper care for patients in need of EEG‐based investigations, particularly patients with seizure disorders. ERN EpiCARE will work on recommendations on how to rapidly adapt to such situations in order to alleviate consequences for our patients.

What is the Role of Post Acute EEG in Prediction of Late Neurological Outcome in Severe Disorders of Consciousness?

What is the Role of Post Acute EEG in Prediction of Late Neurological Outcome in Severe Disorders of Consciousness?

Predicting functional outcomes after stroke: an observational study of acute single-channel EEG

ABSTRACTBackground: Early and objective prediction of functional outcome after stroke is an important issue in rehabilitation. Electroencephalography (EEG) has long been utilized to describe and monitor brain function following neuro-trauma, and technological advances have improved usability in the acute setting. However, skepticism persists whether EEG can provide the same prognostic value as neurological examination.Objective: The current cohort study examined the relationship between acute single-channel EEG and functional outcomes after stroke.Methods: Resting-state EEG recorded at a single left pre-frontal EEG channel (FP1) was obtained from 16 adults within 72 h of first stroke. At 30 and 90 days, measures of disability (modified Rankin Scale; mRS) and involvement in daily activities (modified Barthel Index; mBI) were obtained. Acute EEG measures were correlated with functional outcomes and compared to an early neurological examination of stroke severity using the National Institute of Health Stroke Scale (NIHSS). Classification of good outcomes (mRS ≤1 or mBI ≥95) was also examined using Receiver Operator Curve analyses.Results: One-third to one-half of participants experienced incomplete post-stroke recovery, depending on the time point and measure. Functional outcomes correlated with acute theta values (rs 0.45–0.60), with the strength of associations equivalent to previously reported values obtained from conventional multi-channel systems. Acute theta values ≥0.25 were associated with good outcomes, with positive (67-83%) and negative predictive values (70-90%) comparable to those obtained using the NIHSS.Conclusions: Acute, single-channel EEG can provide unique, non-overlapping clinical information, which may facilitate objective prediction of functional outcome after stroke.