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Objective To determine the ability of quantitative electroencephalography (QEEG) to improve the accuracy of predicting recovery of consciousness by post-cardiac arrest day 10. Methods Unconscious survivors of cardiac arrest undergoing daily clinical and EEG assessments through post-cardiac arrest day 10 were studied in a prospective observational cohort study. Power spectral density, local coherence, and permutation entropy were calculated from daily EEG clips following a painful stimulus. Recovery of consciousness was defined as following at least simple commands by day 10. We determined the impact of EEG metrics to predict recovery when analyzed with established predictors of recovery using partial least squares regression models. Explained variance analysis identified which features contributed most to the predictive model. Results 367 EEG epochs from 98 subjects were analyzed in conjunction with clinical measures. Highest prediction accuracy was achieved when adding QEEG features from post-arrest days 4–6 to established predictors (area under the receiver operating curve improved from 0.81 ± 0.04 to 0.86 ± 0.05). Prediction accuracy decreased from 0.84 ± 0.04 to 0.79 ± 0.04 when adding QEEG features from post-arrest days 1–3. Patients with recovery of command-following by day 10 showed higher coherence across the frequency spectrum and higher centro-occipital delta-frequency spectral power by days 4–6, and globally-higher theta range permutation entropy by days 7–10. Conclusions Adding quantitative EEG metrics to established predictors of recovery allows modest improvement of prediction accuracy for recovery of consciousness, when obtained within a week of cardiac arrest. Further research is needed to determine the best strategy for integration of QEEG data into prognostic models in this patient population.

BACKGROUND: Electroencephalography (EEG) findings following cardiovascular collapse in death are uncertain. We aimed to characterize EEG changes immediately preceding and following cardiac death. METHODS: We retrospectively analyzed EEGs of patients who died from cardiac arrest while undergoing standard EEG monitoring in an intensive care unit. Patients with brain death preceding cardiac death were excluded. Three events during fatal cardiovascular failure were investigated: (1) last recorded QRS complex on electrocardiogram (QRS(0)), (2) cessation of cerebral blood flow (CBF(0)) estimated as the time that blood pressure and heart rate dropped below set thresholds, and (3) electrocerebral silence on EEG (EEG(0)). We evaluated EEG spectral power, coherence, and permutation entropy at these time points. RESULTS: Among 19 patients who died while undergoing EEG monitoring, seven (37%) had a comfort-measures-only status and 18 (95%) had a do-not-resuscitate status in place at the time of death. EEG(0) occurred at the time of QRS(0) in five patients and after QRS(0) in two patients (cohort median − 2.0, interquartile range − 8.0 to 0.0), whereas EEG(0) was seen at the time of CBF(0) in six patients and following CBF(0) in 11 patients (cohort median 2.0 min, interquartile range − 1.5 to 6.0). After CBF(0), full-spectrum log power (p < 0.001) and coherence (p < 0.001) decreased on EEG, whereas delta (p = 0.007) and theta (p = 0.007) permutation entropy increased. CONCLUSIONS: Rarely may patients have transient electrocerebral activity following the last recorded QRS (less than 5 min) and estimated cessation of cerebral blood flow. These results may have implications for discussions around cardiopulmonary resuscitation and organ donation.

Background and Purpose: Delayed cerebral ischemia (DCI) after aneurysmal subarachnoid hemorrhage negatively impacts long-term recovery but is often detected too late to prevent damage. We aim to develop hourly risk scores using routinely collected clinical data to detect DCI. Methods: A DCI classification model was trained using vital sign measurements (heart rate, blood pressure, respiratory rate, and oxygen saturation) and demographics routinely collected for clinical care. Twenty-two time-varying physiological measures were computed including mean, SD, and cross-correlation of heart rate time series with each of the other vitals. Classification was achieved using an ensemble approach with L2-regularized logistic regression, random forest, and support vector machines models. Classifier performance was determined by area under the receiver operating characteristic curves and confusion matrices. Hourly DCI risk scores were generated as the posterior probability at time t using the Ensemble classifier on cohorts recruited at 2 external institutions (n=38 and 40). Results: Three hundred ten patients were included in the training model (median, 54 years old [interquartile range, 45–65]; 80.2% women, 28.4% Hunt and Hess scale 4–5, 38.7% Modified Fisher Scale 3–4); 101 (33%) developed DCI with a median onset day 6 (interquartile range, 5–8). Classification accuracy before DCI onset was 0.83 (interquartile range, 0.76–0.83) area under the receiver operating characteristic curve. Risk scores applied to external institution datasets correctly predicted 64% and 91% of DCI events as early as 12 hours before clinical detection, with 2.7 and 1.6 true alerts for every false alert. Conclusions: An hourly risk score for DCI derived from routine vital signs may have the potential to alert clinicians to DCI, which could reduce neurological injury.

To qualitatively and quantitatively summarize curricula, teaching methods, and effectiveness of educational programs for training bedside care providers (non-experts) in the performance and screening of adult electroencephalography (EEG) for nonconvulsive seizures and other patterns. PRISMA methodological standards were followed. MEDLINE, EMBASE, Cochrane, CINAHL, WOS, Scopus, and MedEdPORTAL databases were searched from inception until February 26, 2020 with no restrictions. Abstract and full-text review was completed in duplicate. Studies were included if they were original research; involved non-experts performing, troubleshooting, or screening adult EEG; and provided qualitative descriptions of curricula and teaching methods and/or quantitative assessment of non-experts (vs gold standard EEG performance by neurodiagnostic technologists or interpretation by neurophysiologists). Data were extracted in duplicate. A content analysis and a meta-narrative review were performed. Of 2430 abstracts, 35 studies were included. Sensitivity and specificity of seizure identification varied from 38 to 100% and 65 to 100% for raw EEG; 40 to 93% and 38 to 95% for quantitative EEG, and 95 to 100% and 65 to 85% for sonified EEG, respectively. Non-expert performance of EEG resulted in statistically significant reduced delay (86 min, p

Seizures are common in critically ill patients. Electroencephalogram (EEG) is a tool that enables clinicians to provide continuous brain monitoring and to guide treatment decisions—brain telemetry. EEG monitoring has particular utility in the intensive care unit as most seizures in this setting are nonconvulsive. Despite the increased use of EEG monitoring in the critical care unit, it remains underutilized. In this review, we summarize the utility of EEG and different EEG modalities to monitor patients in the critical care setting.

ObjectiveTo better understand the heterogeneous population of patients with new-onset refractory status epilepticus (NORSE), we studied the most severe cases in patients who presented with new-onset super-refractory status epilepticus (NOSRSE).MethodsWe report a retrospective case series of 26 adults admitted to the Columbia University Irving Medical Center neurologic intensive care unit (NICU) from February 2009 to February 2016 with NOSRSE. We evaluated demographics, diagnostic studies, and treatment course. Outcomes were modified Rankin Scale score (mRS) at hospital discharge and most recent follow-up visit (minimum of 2 months post discharge), NICU and hospital length of stay, and long-term antiepileptic drug use.ResultsOf the 252 patients with refractory status epilepticus, 27/252 had NORSE and 26/27 of those had NOSRSE. Age was bimodally distributed with peaks at 27 and 63 years. The majority (96%) had an infectious or psychiatric prodrome. Etiology was cryptogenic in 73%, autoimmune in 19%, and infectious in 8%. Seven patients (27%) underwent brain biopsy, autopsy, or both; 3 (12%) were diagnostic (herpes simplex encephalitis, candida encephalitis, and acute demyelinating encephalomyelitis). On discharge, 6 patients (23%) had good or fair outcome (mRS 0–3). Of the patients with long-term follow-up data (median 9 months, interquartile range 2–22 months), 12 patients (71%) had mRS 0–3.ConclusionAmong our cohort, nearly all patients with NORSE had NOSRSE. The majority were cryptogenic with few antibody-positive cases identified. Neuropathology was diagnostic in 12% of cases. Although only 23% of patients had good or fair outcome on discharge, 71% met these criteria at follow-up.

Status epilepticus (SE) is a neurologic emergency with high morbidity and mortality. The assessment of a patient’s prognosis is crucial in making treatment decisions. In this review, we discuss various markers that have been used to prognosticate SE in terms of recurrence, mortality, and functional outcome. These markers include demographic, clinical, electrophysiological, biochemical, and structural data. The heterogeneity of SE etiology and semiology renders development of prognostic markers challenging. Currently, prognostication in SE is limited to a few clinical scores. Future research should integrate clinical, genetic and epigenetic, metabolic, inflammatory, and structural biomarkers into prognostication models to approach “personalized medicine” in prognostication of outcomes after SE.

PURPOSE OF REVIEW: Status epilepticus is a neurological emergency associated with high morbidity and mortality. There is a lack of robust data to guide the management of this neurological emergency beyond the initial treatment. This review examines recent literature on treatment considerations including the choice of continuous anesthetics or adjunctive anticonvulsant, the cause of the status epilepticus, and use of nonpharmacologic therapies. RECENT FINDINGS: Status epilepticus remains undertreated and mortality persists to be unchanged over the past 30 years. New anticonvulsant choices, such as levetiracetam and lacosamide have been explored as alternative emergent therapies. Anecdotal reports on the use of other generation anticonvulsants and nonpharmacologic therapies for the treatment of refractory and super-refractory status epilepticus have been described. Finally, recent evidence has examined etiology-guided management of status epilepticus in certain patient populations, such as immune-mediated, paraneoplastic or infectious encephalitis and anoxic brain injury. SUMMARY: Randomized clinical trials are needed to determine the role for newer generation anticonvulsants and nonpharmacologic modalities for the treatment of epilepticus remains and evaluate the long-term outcomes associated with continuous anesthetics.

Refractory and super-refractory status epilepticus (RSE and SRSE) are life-threatening conditions requiring prompt initiation of appropriate treatment to avoid permanent neurological damage and reduce morbidity and mortality. RSE is defined as status epilepticus that persists despite administering at least two appropriately dosed parenteral medications, including a benzodiazepine. SRSE is status epilepticus that persists at least 24 h after adding at least one appropriately dosed continuous anesthetic (i.e., midazolam, propofol, pentobarbital, and ketamine). Other therapeutic interventions include immunotherapy, neuromodulation, ketogenic diet, or even surgical intervention in certain cases. Continuous electroencephalogram is an essential monitoring tool for diagnosis and treatment. In this review, we focus on the diagnosis and treatment of RSE and SRSE.

The association between impaired brain perfusion, cerebrovascular reactivity status and the risk of ictal events in patients with subarachnoid hemorrhage is unknown. We identified 13 subarachnoid hemorrhage (SAH) patients with seizures and 22 with ictal-interictal continuum (IIC), and compared multimodality physiological recordings to 38 similarly poor-grade SAH patients without ictal activity. We analyzed 10,179 cumulative minutes of seizure and 12,762 cumulative minutes of IIC. Cerebrovascular reactivity (PRx) was not different between subjects with seizures, IIC, or controls. Cerebral perfusion pressure (CPP) was higher in patients with seizures [99 ± 6.5, p = .005] and IIC [97 ± 8.5, p = .007] when compared to controls [89 ± 12.3]. DeltaCPP, defined as actual CPP minus optimal CPP (CPPopt), was also higher in the seizure group [8.3 ± 7.9, p = .0003] and IIC [8.1 ± 10.3, p = .0006] when compared to controls [−0.1 ± 5]. Time spent with supra-optimal CPP was higher in the seizure group [342 ± 213 min/day, p = .002] when compared to controls [154 ± 120 min/day]. In a temporal examination, a supra-optimal CPP preceded increased seizures and IIC in SAH patients, an hour before and continued to increase during the events [ p

Troponin elevations due to Type II myocardial infarction (T2MI) are associated with hemorrhagic and ischemic strokes but there is little data on stroke severity, troponin elevation and outcome. We studied 1655 patients from a tertiary medical center between 1/2013-4/2015 using multivariate regression analysis for demographics, vascular risk factors, admission stroke severity, laboratory tests, echocardiogram results and discharge disposition. Troponin levels were classified as normal0.04 ng/ml and high0.04 ng/ml (critical if0.5 ng/ml). A T2MI was diagnosed by a trending troponin elevation; patients with type I MI, patients with subdural and epidural hematoma, or hemorrhagic metastatic disease and patients younger than 18 years old were excluded. We had 818 patients with ischemic stroke, 306 with intracerebral hemorrhage (ICH) and 169 with subarachnoid hemorrhage (SAH). Troponin was elevated (0.04 ng/ml) in 24.1% of ischemic stroke patients, 27.1% in the ICH group, and in 39% of SAH patients. High initial and peak troponin levels were associated with higher National Institutes of Health Stroke Scale (NIHSS) in patients with ischemic stroke (OR 1.04; CI 95%, 1.02-1.07, p = .001) and (OR 1.05; CI 95%, 1.03-1.07, p .001). In ICH patients, higher initial and peak troponin levels were not associated with worse ICH scores (OR 1.21; CI 95%, 0.66-2.22, p = .53) and (OR 1.36; CI 95%, 0.77-2.41, p = .29). In SAH patients, higher initial and peak troponin levels was associated with higher Hunt and Hess scores (OR 4.2; CI 95%, 1.6-11.4, p = .005) and (OR 3.14; CI 95%, 1.5-6.5, p = .002). In patients with high troponin levels mortality was 14.7% in ischemic stroke patients, 31.3% in our ICH patients, and 43.8% in our SAH. After adjusting for demographics and clinical risk factors, only high troponin ischemic stroke patients were associated with higher mortality (OR 6.16; CI95%, 2.46-15.4, p .001), and worse discharge disposition (OR 2.3; CI 95%, 1.19-4.45, p = .01). High troponin levels were not associated with change of outcomes in patients with SAH and ICH after adjusting for demographics and clinical risk factors. Elevated troponin due to T2MI is common in patients with ischemic strokes, ICH, and SAH. It is significantly associated with stroke severity, poor discharge disposition, and high mortality. Troponin levels should be considered on admission for acute strokes.

Objectives Prone positioning has been shown to be a beneficial adjunctive supportive measure for patients who develop acute respiratory distress syndrome. Studies have excluded patients with reduced intracranial compliance, whereby patients with concomitant neurologic diagnoses and acute respiratory distress syndrome have no defined treatment algorithm or recommendations for management. In this study, we aim to determine the safety and feasibility of prone positioning in the neurologically ill patients. Design and setting A systematic review of the literature, performed in accordance with the Preferred Reporting Items for Systematic Review and Meta-Analyses 2009 guidelines, yielded 10 articles for analysis. Using consensus from these articles, in combination with review of multi-institutional proning protocols for patients with nonneurologic conditions, a proning protocol for patients with intracranial pathology and concomitant acute respiratory distress syndrome was developed. Measurements and main results Among 10 studies included in the final analysis, we found that prone positioning is safe and feasible in the neurologically ill patients with acute respiratory distress syndrome. Increased intracranial pressure and compromised cerebral perfusion pressure may occur with prone positioning. We propose a prone positioning protocol for the neurologically ill patients who require frequent neurologic examinations and intracranial monitoring. Conclusions Although elevations in intracranial pressure and reductions in cerebral perfusion pressure do occur during proning, they may not occur to a degree that would warrant exclusion of prone ventilation as a treatment modality for patients with acute respiratory distress syndrome and concomitant neurologic diagnoses. In cases where intracranial pressure, cerebral perfusion pressure, and brain tissue oxygenation can be monitored, prone position ventilation should be considered a safe and viable therapy.

Objective: This study aimed to examine whether changes in intracranial pressure (ICP) waveform morphologies can be used as a biomarker for early detection of ventriculitis.

Objective. Automatic detection of interictal epileptiform discharges (IEDs, short as ‘spikes’) from an epileptic brain can help predict seizure recurrence and support the diagnosis of epilepsy. Developing fast, reliable and robust detection methods for IEDs based on scalp or intracranial electroencephalogram (iEEG) may facilitate online seizure monitoring and closed-loop neurostimulation. Approach. We developed a new deep learning approach, which employs a long short-term memory network architecture (‘IEDnet’) and an auxiliary classifier generative adversarial network (AC-GAN), to train on both expert-annotated and augmented spike events from iEEG recordings of epilepsy patients. We validated our IEDnet with two real-world iEEG datasets, and compared IEDnet with the support vector machine (SVM) and random forest (RF) classifiers on their detection performances. Main results. IEDnet achieved excellent cross-validated detection performances in terms of both sensitivity and specificity, and outperformed SVM and RF. Synthetic spike samples augmented by AC-GAN further improved the detection performance. In addition, the performance of IEDnet was robust with respect to the sampling frequency and noise. Furthermore, we demonstrated the cross-institutional generalization ability of IEDnet while testing between two datasets. Significance. IEDnet achieves excellent detection performances in identifying interictal spikes. AC-GAN can produce augmented iEEG samples to improve supervised deep learning.

To survey the literature around “big data” and “artificial intelligence” use, its challenges, and examples in clinical and research domains within neurocritical care. Innovations in digital data storage and integration technology have motivated the active development of data-driven tools for neurocritical care practice. There has been progress towards harmonization of data dictionaries within the field to boost generalizability of studies. Numerous collaborative groups have cultivated datasets that will enable further study of disease detection, prediction, and management of critically ill neurologic patients. Essential to the effective analysis of big data in neurocritical care are the increasing relationships between clinicians and data scientists. There are multiple challenges related to the efficient and ethical use of big data, including data complexity, database stewardship and governance, data quality, and safe implementation of data-driven conclusions. Continued efforts towards optimally harnessing data will be crucial in neurocritical care. Critically ill neurologic patients generate an abundant amount of data in the course of routine management. Clinical research is evolving from benefiting the “average patient” to aiming to deliver more precise treatment to the individual patient. In neurocritical care, this has manifested through big data—for triage decisions, enhancing workflow, event detection, and outcome prediction.

We report a case of focal status epilepticus (SE) associated with peri-ictal water drinking (PIWD) behavior in a nine-year-old left-handed boy with epilepsy. We reviewed prior cases of epileptic peri-ictal water drinking. Only one adult patient with status epilepticus and PIWD has been reported previously. This is the first reported case of PIWD SE in a pediatric patient with frontal lobe epilepsy. We found PIWD to have no lateralizing value., Highlights • We report a case of focal status epilepticus (SE) associated with peri-ictal water drinking (PIWD). • PIWD is a rare autonomic symptom. • We found PIWD to have no lateralizing value.

ObjectiveTo test ketamine infusion efficacy in the treatment of super-refractory status epilepticus (SRSE), we studied patients with SRSE who were treated with ketamine retrospectively. We also studied the effect of high doses of ketamine on brain physiology as reflected by invasive multimodality monitoring (MMM).MethodsWe studied a consecutive series of 68 patients with SRSE who were admitted between 2009 and 2018, treated with ketamine, and monitored with scalp EEG. Eleven of these patients underwent MMM at the time of ketamine administration. We compared patients who had seizure cessation after ketamine initiation to those who did not.ResultsMean age was 53 ± 18 years and 46% of patients were female. Seizure burden decreased by at least 50% within 24 hours of starting ketamine in 55 (81%) patients, with complete cessation in 43 (63%). Average dose of ketamine infusion was 2.2 ± 1.8 mg/kg/h, with median duration of 2 (1–4) days. Average dose of midazolam was 1.0 ± 0.8 mg/kg/h at the time of ketamine initiation and was started at a median of 0.4 (0.1–1.0) days before ketamine. Using a generalized linear mixed effect model, ketamine was associated with stable mean arterial pressure (odds ratio 1.39, 95% confidence interval 1.38–1.40) and with decreased vasopressor requirements over time. We found no effect on intracranial pressure, cerebral blood flow, or cerebral perfusion pressure.ConclusionKetamine treatment was associated with a decrease in seizure burden in patients with SRSE. Our data support the notion that high-dose ketamine infusions are associated with decreased vasopressor requirements without increased intracranial pressure.Classification of evidenceThis study provides Class IV evidence that ketamine decreases seizures in patients with SRSE.

Background The clinical presentation and risk factors of nonconvulsive status epilepticus (NCSE) in the context of electroconvulsive therapy (ECT) are poorly understood, and guidance regarding diagnosis and management remains scarce. In this article, we identify case reports of ECT-induced NCSE from literature, and discuss the presentation, diagnosis, and management of these cases in the context of what is known about NCSE from the neurology literature. Methods A literature search on PubMed for case reports of NCSE after ECT. Results We identified 13 cases for this review. Diagnosis in all cases was based on clinical features and electroencephalogram (EEG) findings. Clinical presentation was altered mental status or unresponsiveness, with subtle motor phenomena in some cases. All cases had nonspecific risk factors that have been associated with prolonged seizures and convulsions, such as recent discontinuation/reduction of benzodiazepines or anticonvulsants, and concurrent use of antipsychotics and antidepressants. All patients were treated with either benzodiazepines or antiepileptic agents. Outcomes in these post-ECT NCSE cases were generally favorable. Discussion Although rare, post-ECT NCSE should be kept in mind by physicians when confusion or unresponsiveness develops and continues after ECT; multilead EEG is gold standard for diagnosis. An intravenous (IV) antiepileptic drug (AED) challenge can help clarify the diagnosis. Initial treatment is recommended with IV benzodiazepines, with a repeat dose if necessary. If seizures persist, IV AEDs are warranted. NCSE refractory to this treatment should be treated with a scheduled IV or oral AED. Serial multilead EEGs should be used to monitor resolution of symptoms. Conclusion NCSE after ECT is a rare but recognizable clinical event. A high clinical suspicion and low threshold for EEG is necessary for prompt diagnosis.

Case series Patient: Male, 52 • Female, 68 Final Diagnosis: VBD Symptoms: Ophthalmoplegia Medication: — Clinical Procedure: — Specialty: Neurology Objective: Unusual clinical course Background: Vertebrobasilar dolichoectasia (VBD) is a complex progressive arterial disease characterized by dilation, elongation, and tortuosity of the vertebral and basilar arteries, and may be congenital or acquired. VBD may lead to progressive compression of the brainstem, cranial nerve abnormalities, and intracranial hemorrhage, but may also be associated with arterial thrombosis, with ischemic stroke as the most common clinical outcome. Case Report: Two cases of VBD are presented, both with acute bilateral ophthalmoplegia and cranial nerve palsies, and vertebrobasilar arterial thrombosis that resulted in ischemic stroke. Conclusions: VBD is a complex arterial disease with a variety of clinical manifestation, with bilateral ophthalmoplegia being a rare presentation. Clinical management of VBD is a challenge as there are no current management guidelines. Therefore, clinical management of cases of VBD should be individualized to balance the risks and benefits of treatment options for each patient.

The objective of this study was to examine whether heart rate variability (HRV) measures can be used to detect neurocardiogenic injury (NCI). Three hundred and twenty-six consecutive admissions with aneurysmal subarachnoid hemorrhage (SAH) met criteria for the study. Of 326 subjects, 56 (17.2%) developed NCI which we defined by wall motion abnormality with ventricular dysfunction on transthoracic echocardiogram or cardiac troponin-I > 0.3 ng/mL without electrocardiogram evidence of coronary artery insufficiency. HRV measures (in time and frequency domains, as well as nonlinear technique of detrended fluctuation analysis) were calculated over the first 48 h. We applied longitudinal multilevel linear regression to characterize the relationship of HRV measures with NCI and examine between-group differences at baseline and over time. There was decreased vagal activity in NCI subjects with a between-group difference in low/high frequency ratio (β 3.42, SE 0.92, p = 0.0002), with sympathovagal balance in favor of sympathetic nervous activity. All time-domain measures were decreased in SAH subjects with NCI. An ensemble machine learning approach translated these measures into a classification tool that demonstrated good discrimination using the area under the receiver operating characteristic curve (AUROC 0.82), the area under precision recall curve (AUPRC 0.75), and a correct classification rate of 0.81. HRV measures are significantly associated with our label of NCI and a machine learning approach using features derived from HRV measures can classify SAH patients that develop NCI.

Introduction: Hunter syndrome (mucopolysaccharidosis II) is a rare genetic disorder. Carpal tunnel syndrome (CTS) is a common finding in these patients. Methods: We report the ultrasound findings in a 40-year-old Hunter syndrome patient with severe CTS. Results: Marked abnormalities of the median nerve were present proximal to the carpal tunnel with an unusual area of increased echogenicity between enlarged fascicles separating the area of maximal enlargement and the normal median nerve proximally. Conclusions: This case demonstrated unique ultrasound findings in a Hunter syndrome with CTS. Ultrasound also localized the median nerve lesion in the setting of end-stage median neuropathy and nonlocalizing electrophysiology. Muscle Nerve 53: 147–150, 2016

Objective Seizures can be provoked by systemic diseases associated with metabolic derangements, but the association between liver disease and seizures remains unclear. Methods We performed a retrospective cohort study using inpatient and outpatient claims between 2008 and 2015 from a nationally representative 5% sample of Medicare beneficiaries. The primary exposure variable was cirrhosis, and the secondary exposure was mild, noncirrhotic liver disease. The primary outcome was seizure, and the secondary outcome was status epilepticus. Diagnoses were ascertained using validated International Classification of Diseases, Ninth Edition, Clinical Modification codes. Survival statistics were used to calculate incidence rates, and Cox proportional hazards models were used to examine the association between exposures and outcomes while adjusting for seizure risk factors. Results Among 1 782 402 beneficiaries, we identified 10 393 (0.6%) beneficiaries with cirrhosis and 19 557 (1.1%) with mild, noncirrhotic liver disease. Individuals with liver disease were older and had more seizure risk factors than those without liver disease. Over 4.6 ± 2.2 years of follow-up, 49 843 (2.8%) individuals were diagnosed with seizures and 25 patients (0.001%) were diagnosed with status epilepticus. Cirrhosis was not associated with seizures (hazard ratio [HR] = 1.1, 95% confidence interval [CI] = 1.0-1.3), but there was an association with status epilepticus (HR = 1.9, 95% CI = 1.3-2.8). Mild liver disease was not associated with a higher risk of seizures (HR = 0.8, 95% CI = 0.6-0.9) or status epilepticus (HR = 1.1, 95% CI = 0.7-1.5). Significance In a large, population-based cohort, we found an association between cirrhosis and status epilepticus, but no overall association between liver disease and seizures.

Purpose Generalized periodic discharges (GPDs) with a triphasic morphology have been associated with nonepileptic encephalopathies. We conducted the study to assess the reliability in which electroencephalographers can differentiate triphasic from nontriphasic periodic discharges and to evaluate for the presence of electroencephalogram and clinical characteristics that are associated with a higher risk of seizures. Methods We studied prospectively 92 patients between May 2016 and February 2017. Each pattern was analyzed by two readers, who were blinded to clinical data. Results The interrater agreement was "substantial" (Kappa 0.67). The following features significantly increased the risk of developing seizures: the absence of triphasic morphology, focality on electroencephalogram, interburst suppression, a history of epilepsy, and an abnormal scan. The "GPD score" includes a history of epilepsy, focality on electroencephalogram, and the absence of triphasic morphology. A GPD score of 0 has 13% risk of seizures, whereas a score of 5 to 6 has a 94% risk. Conclusions Triphasic morphology GPDs confer less risk of seizures when compared with patients with GPDs without triphasic morphology. Features with a higher risk of seizures include focality on electroencephalogram, interburst suppression, a history of epilepsy, and an abnormal scan. The GPD score can be used to assess the risk of developing seizures in patients with GPDs.

The goal of our study is to determine optimal criteria which can be used to avoid admission to neuroscience intensive care units for patients with intracerebral hemorrhage (ICH).This is a retrospective cohort study of 431 patients with primary ICH from January 2013 to the end of December 2015 and reviewed multiple admitting characteristics. Based on these needs, we tested the following step-down unit admission criteria: Supratentorial ICH, ICH volume20 cc, no Intraventricular hemorrhage (IVH), systolic BP200mmHg, no respiratory failure, GCS≥12. We classified 431 patients into two groups; 1-Patients who met step-down unit admission Criteria (71 patients). 2-Patients who didn't meet the criteria (360 patients).In our patients, 16.5% fulfilled the criteria. Length of stay in the ICU was 1.43days in step-down unit admission criteria patients. None of the patients who fulfilled the criteria were readmitted to the ICU, compared to 3 readmissions among the group of patients who did not fulfill the criteria (P=0.82). None of these patients required a neurosurgical procedure vs 47 patients (10.9%) in the other group (P=0.04). Among patients who met the criteria, 83.1% were discharged home or rehab RR 0.33 CI (0.19-0.55), (P0.0001).We propose that patients who fulfill step-down unit admission criteria can be safely monitored in stroke unit and they have no need for ICU admission. Further studies are needed to validate these criteria in a prospective manner.

We report a case of spinal cord infarct as a result of suspected fibrocartilaginous embolism (FCE). A 23-year-old man presented with sudden onset cervical and upper back pain followed by progressive weakness in his extremities after throwing a baseball. History, neurologic examination and spinal cord imaging were consistent with spinal cord infarct. We believe the cause was from FCE. Though rare, physicians should be familiar with this diagnosis and the proposed mechanisms. There is no specific treatment for FCE-related spinal cord infarct and long-term prognosis is largely dependent on the degree of spinal cord injury.

An 81-year-old right-handed woman with hypertension developed mild left hemiparesis over 1 week. Computed tomography of the head showed a right acute on chronic subdural hematoma (SDH). She underwent burr hole evacuation, her weakness resolved, and she was discharged to home after 4 days. One week later, she experienced transient left hemiplegia and confusion lasting a few hours. On arrival to the emergency department, her symptoms had resolved. Blood pressure was 140/90 mm Hg. Repeat head computed tomography showed a small residual SDH and mild right hemispheric edema; both hematoma volume and edema were stable compared with those of previous imaging. Magnetic resonance imaging showed no diffusion restriction underlying the SDH, and magnetic resonance angiography showed normal intra- and extracranial vasculature. Electroencephalography (EEG) showed no epileptiform activity; however, there was mild slowing in the right hemisphere. Quantitative EEG (qEEG) analysis showed reduced alpha/delta ratio within the right hemisphere (Figure 1). Levetiracetam was empirically started, and she was admitted for close observation. Figure 1. Soon after a syncopal event, electroencephalography (EEG) shows right hemispheric slowing ( A ). An hour of quantitative EEG ( B ) before and after syncope (arrow) demonstrates reduced alpha/delta ratio on the right hemisphere (red) compared with the left (blue) after the event. The asymmetry spectrogram ( C ) represents frequency of the EEG (1–18 Hz) averaged over the hemispheres, in which red represents the right hemisphere and blue represents the left. This is consistent with more slowing of the right hemisphere. The asymmetry index ( D ) shows the degree of total absolute asymmetry (yellow) with increased asymmetry after the event and relative asymmetry (green) with increased downward signal representing increased slowing on the right after the syncope. On day 2 of admission, she developed left face, arm, and leg weakness, right gaze deviation, and left-sided neglect. Blood pressure at the time was 110/78 mm Hg. EEG …

Meticulous critical care is key to achieve the best possible outcome after stroke. This includes both general critical care and neurocritical care. General critical care focuses on hemodynamics and respiratory care to ensure optimal cerebral blood flow and oxygen delivery in addition to providing adequate nutritional support and prevention of complications such as fever, hyperglycemia, deep venous thrombosis (DVT), stress ulcers, and decubitus pressure ulcers. Neurocritical care focuses on the management of cerebral edema and increased intracranial pressure (ICP). Current guidelines recommend maintaining an ICP < 20 mm Hg and a cerebral perfusion pressure (CPP) between 50 and 70 mm Hg. Decompressive craniectomy has been shown to significantly reduce the mortality and improve the functional outcome in patients with malignant hemispheric strokes. Clinicians are cautioned about the early use of do-not-attempt-resuscitation orders, as studies have shown them to be independent predictors of outcome possibly because such orders may lead to less aggressive care and the creation of a self-fulfilling prophecy.

OBJECTIVE Intracranial pressure (ICP) is an important and established clinical measurement that is used in the management of severe acute brain injury. ICP waveforms are usually triphasic and are susceptible to artifact because of transient catheter malfunction or routine patient care. Existing methods for artifact detection include threshold-based, stability-based, or template matching, and result in higher false positives (when there is variability in the ICP waveforms) or higher false negatives (when the ICP waveforms lack complete triphasic components but are valid). APPROACH We hypothesized that artifact labeling of ICP waveforms can be optimized by an active learning approach which includes interactive querying of domain experts to identify a manageable number of informative training examples. MAIN RESULTS The resulting active learning based framework identified non-artifactual ICP pulses with a superior AUC of 0.96 + 0.012, compared to existing methods: template matching (AUC: 0.71 + 0.04), ICP stability (AUC: 0.51 + 0.036) and threshold-based (AUC: 0.5 + 0.02). SIGNIFICANCE The proposed active learning framework will support real-time ICP-derived analytics by improving precision of artifact-labelling.

Objectives To review the current practice in the diagnosis, monitoring and management of TCM in SAH patients at our tertiary referral institution and the relevant literature, and to evaluate the effect of certain treatment modalities on the outcome of those patients. Patients and methods A retrospective institutional chart review of 800 patients with aneurysmal SAH from 2007 to 2014. Eighteen patients were identified to have both aneurysmal SAH and TCM based on echocardiogram. Demographic data, clinical parameters, radiographic findings, treatment modalities, and laboratory results were analyzed. Results The incidence of typical TCM in our patients was 2.2%. Mortality rate of TCM in SAH was 22% compared to the total mortality rate of all non-traumatic SAH patients of 15% in our institution over the same time period. Use of beta blockers prior to or after the diagnosis of TCM did not seem to affect their outcome. Majority of patients (61%) were on vasopressors prior to the diagnosis of TCM. Of those, 73% had good outcomes. Even after the diagnosis of TCM, good outcomes were observed in 6 of 7 patients who remained on vasopressors. Conclusion Despite the general agreement on the importance of the avoidance of vasopressors in TCM, our experience showed that the use of vasopressors is safe in these patients. The use of beta blockers in our patients was not associated with significantly better outcomes despite multiple previous reports on beta blocker usage in TCM.