by
Yilun Chen;
Songlu Li;
Wendong Ge;
Jin Jing;
Hsin Yi Chen;
Daniel Doherty;
Alison Herman;
Safa Kaleem;
Kan Ding;
Gamaleldin Osman;
Christa B. Swisher;
Christine Smith;
Carolina B. Maciel;
Ayham Alkhachroum;
Jong Woo Lee;
Monica Dhakar;
Emily J. Gilmore;
Adithya Sivaraju;
Lawrence J. Hirsch;
Sacit B. Omay;
Hal Blumenfeld;
Kevin N. Sheth;
Aaron F. Struck;
Brian L. Edlow;
M. Brandon Westover;
Jennifer A. Kim
Background:
Post-traumatic epilepsy (PTE) is a severe complication of traumatic brain injury (TBI). Electroencephalography aids early post-traumatic seizure diagnosis, but its optimal utility for PTE prediction remains unknown. We aim to evaluate the contribution of quantitative electroencephalograms to predict first-year PTE (PTE1).
Methods:
We performed a multicenter, retrospective case-control study of TBI patients. 63 PTE1 patients were matched with 63 non-PTE1 patients by admission Glasgow Coma Scale score, age, and sex. We evaluated the association of quantitative electroencephalography features with PTE1 using logistic regressions and examined their predictive value relative to TBI mechanism and Computed Tomography abnormalities.
Results:
In the matched cohort (n=126), greater epileptiform burden, suppression burden and beta variability were associated with 4.6 times higher PTE1 risk based on multivariable logistic regression analysis (area under the receiver-operating-characteristic curve, AUC [95% CI], 0.69 [0.60–0.78]). Among 116 (92%) patients with available Computed Tomography reports, adding quantitative electroencephalography features to a combined mechanism and Computed Tomography model improved performance (AUC [95% CI], 0.71 [0.61–0.80] vs 0.61 [0.51–0.72]).
Conclusions:
Epileptiform and spectral characteristics enhance covariates identified on TBI admission and Computed Tomography abnormalities in PTE1 prediction. Future trials should incorporate quantitative electroencephalography features to validate this enhancement of PTE risk stratification models.
by
Aaron F. Struck;
Andres Rodriguez Ruiz;
Gamaledin Osman;
Emily J. Gilmore;
Hiba Haider;
Monica Dhakar;
Matthew Schrettner;
Jong W. Lee;
Nicolas Gaspard;
Lawrence J. Hirsch;
M. Brandon Westover
Objective: To compare machine learning methods for predicting inpatient seizures risk and determine the feasibility of 1-h screening EEG to identify low-risk patients (<5% seizures risk in 48 h). Methods: The Critical Care EEG Monitoring Research Consortium (CCEMRC) multicenter database contains 7716 continuous EEGs (cEEG). Neural networks (NN), elastic net logistic regression (EN), and sparse linear integer model (RiskSLIM) were trained to predict seizures. RiskSLIM was used previously to generate 2HELPS2B model of seizure predictions. Data were divided into training (60% for model fitting) and evaluation (40% for model evaluation) cohorts. Performance was measured using area under the receiver operating curve (AUC), mean risk calibration (CAL), and negative predictive value (NPV). A secondary analysis was performed using Monte Carlo simulation (MCS) to normalize all EEG recordings to 48 h and use only the first hour of EEG as a “screening EEG” to generate predictions. Results: RiskSLIM recreated the 2HELPS2B model. All models had comparable AUC: evaluation cohort (NN: 0.85, EN: 0.84, 2HELPS2B: 0.83) and MCS (NN: 0.82, EN; 0.82, 2HELPS2B: 0.81) and NPV (absence of seizures in the group that the models predicted to be low risk): evaluation cohort (NN: 97%, EN: 97%, 2HELPS2B: 97%) and MCS (NN: 97%, EN: 99%, 2HELPS2B: 97%). 2HELPS2B model was able to identify the largest proportion of low-risk patients. Interpretation: For seizure risk stratification of hospitalized patients, the RiskSLIM generated 2HELPS2B model compares favorably to the complex NN and EN generated models. 2HELPS2B is able to accurately and quickly identify low-risk patients with only a 1-h screening EEG.
Purpose:Autoimmune encephalitis (AE) is a cause of new-onset seizures, including new-onset refractory status epilepticus, yet there have been few studies assessing the EEG signature of AE.Methods:Multicenter retrospective review of patients diagnosed with AE who underwent continuous EEG monitoring.Results:We identified 64 patients (male, 39%; white, 49%; median age, 44 years); of whom, 43 (67%) were antibody-proven AE patients. Of the patients with confirmed antibody AE, the following were identified: N-methyl-D-aspartate receptor (n = 17, 27%), voltage-gated potassium channel (n = 16, 25%), glutamic acid decarboxylase (n = 6, 9%), and other (n = 4, 6%). The remaining patients were classified as probable antibody-negative AE (n = 11, 17%), definite limbic encephalitis (antibody-negative) (n = 2, 3%), and Hashimoto encephalopathy (n = 8, 13%). Fifty-three percent exhibited electrographic seizures. New-onset refractory status epilepticus was identified in 19% of patients. Sixty-three percent had periodic or rhythmic patterns; of which, 38% had plus modifiers. Generalized rhythmic delta activity was identified in 33% of patients. Generalized rhythmic delta activity and generalized rhythmic delta activity plus fast activity were more common in anti-N-methyl-D-aspartate AE (P = 0.0001 and 0.0003, respectively). No other periodic or rhythmic patterns exhibited AE subtype association. Forty-two percent had good outcome on discharge. Periodic or rhythmic patterns, seizures, and new-onset refractory status epilepticus conferred an increased risk of poor outcome (OR, 6.4; P = 0.0012; OR, 3; P = 0.0372; OR, 12.3; P = 0.02, respectively).Conclusion:Our study confirms a signature EEG pattern in anti-N-methyl-D-aspartate AE, termed extreme delta brush, identified as generalized rhythmic delta activity plus fast activity in our study. We found no other pattern association with other AE subtypes. We also found a high incidence of seizures among patients with AE. Finally, periodic or rhythmic patterns, seizures, and new-onset refractory status epilepticus conferred an increased risk of poor outcome regardless of AE subtype.
by
Alexis N. Simpkins;
Katharina M. Busl;
Edilberto Amorim;
Carolina Barnett-Tapia;
Mackenzie C. Cervenka;
Monica Dhakar;
Mark R. Etherton;
Celia Fung;
Robert Griggs;
Robert G. Holloway;
Adam G. Kelly;
Imad R. Khan;
Karlo J. Lizarraga;
Hannah G. Madagan;
Chidinma L. Onweni;
Humberto Mestre;
Alejandro A. Rabinstein;
Clio Rubinos;
Dawling A. Dionisio-Santos;
Teddy S. Youn;
Lisa H. Merck;
Carolina B. Maciel
Effective treatment options for patients with life-threatening neurological disorders are limited. To address this unmet need, high-impact translational research is essential for the advancement and development of novel therapeutic approaches in neurocritical care. “The Neurotherapeutics Symposium 2019—Neurological Emergencies” conference, held in Rochester, New York, in June 2019, was designed to accelerate translation of neurocritical care research via transdisciplinary team science and diversity enhancement. Diversity excellence in the neuroscience workforce brings innovative and creative perspectives, and team science broadens the scientific approach by incorporating views from multiple stakeholders. Both are essential components needed to address complex scientific questions. Under represented minorities and women were involved in the organization of the conference and accounted for 30–40% of speakers, moderators, and attendees. Participants represented a diverse group of stakeholders committed to translational research. Topics discussed at the conference included acute ischemic and hemorrhagic strokes, neurogenic respiratory dysregulation, seizures and status epilepticus, brain telemetry, neuroprognostication, disorders of consciousness, and multimodal monitoring. In these proceedings, we summarize the topics covered at the conference and suggest the groundwork for future high-yield research in neurologic emergencies.