Postanoxic Encephalopathy Research Articles

Perampanel as an Add-On Therapy in Patients with Refractory Status Epilepticus and Postanoxic Encephalopathy: A Real-Life Single-Center Retrospective Cohort Study.

Data on the efficacy of perampanel in refractory status epilepticus (RSE) and postanoxic encephalopathy (PAE) are limited; its use in such conditions is currently off-label. We conducted a retrospective cohort study of consecutive adult patients with RSE, including PAE, exhibiting electroencephalographic patterns indicative of status epilepticus who were treated at our center (January 2018 to December 2022) with assessment of clinical and electroencephalographic outcomes. Thirty-six patients were included in the study, of whom 29 had nonanoxic RSE and 7 had PAE. Within the nonanoxic RSE subgroup, 45% (13 of 29; 95% confidence interval [CI] 27-63%) of study participants were responders, 34% (10 of 29; 95% CI 17-52%) were partial responders, and 21% (6 of 29; 95% CI 6-35%) were nonresponders. In the PAE subgroup (n = 7), no patients fully responded to perampanel; 43% (3 of 7; 95% CI 6-80%) were partial responders, and 57% (4 of 7; 95% CI 20-95%) were nonresponders. Responder and nonresponder study participants exhibited overlapping baseline characteristics. No significant differences in duration of hospitalization were observed between responders and nonresponders in both subgroups. Responders in the RSE subgroup had a median discharge modified Rankin Scale score of 3 (interquartile range 3-4), and nonresponders had a median discharge modified Rankin Scale score of 5 (interquartile range 5-6). Despite limitations from the retrospective design and the small population size, this study suggests that perampanel use in nonanoxic RSE appears to yield promising results at moderate doses, including a tendency toward a better functional outcome at discharge, without significant adverse effects. However, in patients with PAE, the drug seems to show suboptimal performance. Perampanel appears to have promising efficacy as an add-on therapy in nonanoxic RSE. However, in patients with PAE, its efficacy seems to be lower. Further studies are warranted to confirm these observations.

Brain Death Donors on Extracorporeal Membrane Oxygenation Support.

We investigated donors with brain death on extracorporeal membrane oxygenation support, a clinically challenging situation due to hemodynamic instability frequently encountered in these donors, which may threaten organ function. We described our experience with 15 utilized brain death donors on extracorporeal membrane oxygenation support, consecutively admit-ted in our intensive care unit (which is a referral center for extracorporeal membrane oxygenation) from 2018 to 2023. We investigated whether utilization rate for brain death donors on extracor-poreal membrane oxygenation was affected by the introduction of a monitoring hemodynamic schedule during the 6-hour observation period. The utilization rate was 78% in period 1 and 88% in period 2. No statistically significant differences were observed for age, sex, and the incidence of cardiovascular risk factors between period 1 and period 2. The cause of death was postanoxic encephalopathy in all but 1 donor, who was on venovenous extracorporeal membrane oxygenation for refractory respiratory failure and developed cerebral hemorrhage. Number of organs per donor was 2 in all the population with no significant differences between period 1 and period 2. In the overall population, 15 livers were transplanted, 11 kidneys, 1 heart, and 1 pancreas. In our population, left ventricular ejection fraction severe dysfunction was observed in all donors except in the donor on venovenous extracorporeal membrane oxygenation; the organ from this donor was deemed unsuitable for transplant. No significant differences were observed in hemodynamic data between the 2 subgroups. All donors were on 2 vasoactive drugs (norepinephrine and vasopressin) to maintain adequate perfusion (mean arterial pressure >60 mm Hg). Three donors were oligoanuric (due to postarrest acute renal failure). In our series of 15 consecutive brain death donors on extracorporeal membrane oxygenation, a strict monitoring regimen during the 6-hour obser-vation period was associated with a higher utilization rate.

Preservation of thalamocortical circuitry is essential for good recovery after cardiac arrest.

Continuous electroencephalographam (EEG) monitoring contributes to prediction of neurological outcome in comatose cardiac arrest survivors. While the phenomenology of EEG abnormalities in postanoxic encephalopathy is well known, the pathophysiology, especially the presumed role of selective synaptic failure, is less understood. To further this understanding, we estimate biophysical model parameters from the EEG power spectra from individual patients with a good or poor recovery from a postanoxic encephalopathy. This biophysical model includes intracortical, intrathalamic, and corticothalamic synaptic strengths, as well as synaptic time constants and axonal conduction delays. We used continuous EEG measurements from hundred comatose patients recorded during the first 48 h postcardiac arrest, 50 with a poor neurological outcome [cerebral performance category ] and 50 with a good neurological outcome ( ). We only included patients that developed (dis-)continuous EEG activity within 48 h postcardiac arrest. For patients with a good outcome, we observed an initial relative excitation in the corticothalamic loop and corticothalamic propagation that subsequently evolved towards values observed in healthy controls. For patients with a poor outcome, we observed an initial increase in the cortical excitation-inhibition ratio, increased relative inhibition in the corticothalamic loop, delayed corticothalamic propagation of neuronal activity, and severely prolonged synaptic time constants that did not return to physiological values. We conclude that the abnormal EEG evolution in patients with a poor neurological recovery after cardiac arrest may result from persistent and selective synaptic failure that includes corticothalamic circuitry and also delayed corticothalamic propagation.

Post anoxic myoclonic encephalopathy syndrome or Lance- Adams: Case report

Introduction: Lance Adams syndrome (LAS) a post anoxic myoclonic encephalopathy, an infrequently described entity since 1963, currently less than 200 cases have been reported1, characterized by myoclonic limb-acting movements and cerebellar ataxia with generally preserved higher mental functions, which typically appears hours or days after a cerebral hypoxia event (prolonged hypotension, cardiorespiratory arrest) and certain structures of the brain stem, cerebellum and diencephalon are thought to be involved in myoclonus due to hypoxia1-5.

Temporal recovery and delayed decline of cognitive functions in patients with hypoxic encephalopathy after cardiac arrest

AbstractBackgroundNeuropsychological recovery is important for survivors’ quality of life after cardiac arrest. However, most studies on cognitive symptoms after cardiac arrest examined cognitive functions within one year after onset.AimTo investigate long‐term changes in cognitive functions in individuals with hypoxic encephalopathy after cardiac arrest.MethodsWe retrospectively recruited survivors of cardiac arrest who demonstrated cognitive dysfunction at the chronic stage. The inclusion criteria were follow‐up period of more than 3 years with multiple neuropsychological examinations and brain MRI/CT within 1 year after onset.ResultsFive patients showed various cognitive dysfunctions 1 year after onset, and the follow‐up periods were 3 to 13 years. Four patients showed temporal recovery of cognitive functions over a period of a few years followed by gradual deterioration afterward. The youngest patient, 48 years of age at the final assessment, demonstrated gradual improvement without clear evidence of deterioration for 4 years. Brain magnetic resonance imaging (MRI) revealed hyperintense areas at the acute stage in 2 patients, and mild cortical atrophy and cerebral hypoperfusion were observed in 3 patients. Delayed cognitive decline in our cases differs in length of the course from that in previously reported “delayed” postanoxic encephalopathy, which appears several days to weeks after onset.ConclusionsCognitive functions in survivors of cardiac arrest recovered for a few years and then gradually deteriorated, which suggests hypoxic changes induce long‐term impact on cerebral functions.

In-hospital and long-term mortality in patients with arrhythmic storm

Abstract Funding Acknowledgements Type of funding sources: Foundation. Main funding source(s): Beca para la Formación e Investigación en Cuidados Críticos Cardiológicos concedida por la Asociación de Cardiopatía Isquémica y Cuidados Críticos Cardiológicosde la SEC Introduction Available data on arrhythmic storm (AS) is usually obtained from retrospective observational studies based on series of patients (pts) with ICD or who undergo ablation. Therefore, selection bias limits the evidence regarding mortality and prognosis of this entity. Purpose/ Methods Describe in-hospital and long-term mortality of pts admitted between 2006 and 2020 for AS in the Acute Cardiac Care Unit (ACCU) of 2 tertiary hospitals in Spain. Results A total of 190 episodes of AS in 169 pts were retrospectively analysed. Baseline characteristics are depicted in Table 1. In-hospital mortality was 18.9%. Mortality in STEMI related AS was 44.2%, while in the rest of aetiologies was 6.1% (p < 0.001). In-hospital cause of death was heart failure or cardiogenic shock (32.4%), refractory AS (20.6%), cardiac arrest due to pulseless activity (8.8%), severe postanoxic encephalopathy (14.7%), septic shock (8.8%), others (14.7%). long-term follow-up was obtained in 154 pts. Among those patients who survived after the first episode of AS, median follow up was 2.85 years. Long term mortality was 49.7%. Long-term survival did not differ among STEMI related AS (8.30 years, 95% CI 5.62 to 10.98) and the rest of aetiologies (6.91 years, 95% CI 5.75 to 8.07), Log rank 0.33. Kapplan-Meier survival curves are presented in Figure 1. Long-term cause of death was AS (8.3%), heart failure or cardiogenic shock (14.6%), cardiac arrest due to pulseless activity (4.2%), STEMI (2.1%), stroke (8.3%), cancer (10.4%), pneumonia and sepsis (22.9%) and unknown (29.2%). Conclusion In-hospital mortality in patients with AS requiring admission to an ACCU differs depending on the aetiology being worst in STEMI related AS. Long term mortality remains high and do not depend on the ethiology. Baseline CharacteristicsAge (SD) years66.5 (13.3)Male gender (%)141 (83.4)Previous VT ablation38 (22.4)Previous LVEF (SD)37.9 (13.1)Previous coronary artery disease (%)77 (45.5)Hypertrophic myocardiopathy (%)4 (23.7)Dilated myocardiopathy (%)24 (14.2)Previous Myocarditis (%)1 (0.6)Ventricular dysplasia (%)2 (1.2)Canalopathy (%)3 (1.8)ICD carrier (%)95 (55.6)Abstract Figure 1

Neuroprotective Treatment of Postanoxic Encephalopathy: A Review of Clinical Evidence.

Postanoxic encephalopathy is the key determinant of death or disability after successful cardiopulmonary resuscitation. Animal studies have provided proof-of-principle evidence of efficacy of divergent classes of neuroprotective treatments to promote brain recovery. However, apart from targeted temperature management (TTM), neuroprotective treatments are not included in current care of patients with postanoxic encephalopathy after cardiac arrest. We aimed to review the clinical evidence of efficacy of neuroprotective strategies to improve recovery of comatose patients after cardiac arrest and to propose future directions. We performed a systematic search of the literature to identify prospective, comparative clinical trials on interventions to improve neurological outcome of comatose patients after cardiac arrest. We included 53 studies on 21 interventions. None showed unequivocal benefit. TTM at 33 or 36°C and adrenaline (epinephrine) are studied most, followed by xenon, erythropoietin, and calcium antagonists. Lack of efficacy is associated with heterogeneity of patient groups and limited specificity of outcome measures. Ongoing and future trials will benefit from systematic collection of measures of baseline encephalopathy and sufficiently powered predefined subgroup analyses. Outcome measurement should include comprehensive neuropsychological follow-up, to show treatment effects that are not detectable by gross measures of functional recovery. To enhance translation from animal models to patients, studies under experimental conditions should adhere to strict methodological and publication guidelines.

Gardnerella vaginalis Is a Rare Cause of Ventilator-Associated Pneumonia: A Case Report and Literature Review

Gardnerella vaginalis ( G. vaginalis ) is a commensal bacterium of the vaginal flora, facultative anerobic with Gram-variable, frequently implicated in cases of vaginosis or even infections of the genitourinary tract, rarely responsible for systemic infections and very exceptionally isolated in bronchopulmonary damage. We report here a case of G. vaginalis pneumonia in a 45-year-old man admitted to the intensive care unit for cardiorespiratory arrest (CRA) by hanging, whose course was unfavorable following severe post-anoxic encephalopathy. During his hospitalization, the patient presented ventilator-associated pneumonia (VAP) with identification of G. vaginalis at a significant threshold on the protected distal bronchial sampling (PDBS). Antibiotic therapy with cefotaxime and metronidazole had a good response to this infection. In this observation, we discuss the pathogenic role and identification of G. vaginalis at the pulmonary level. J Med Cases. 2021;12(4):134-137 doi: https://doi.org/10.14740/jmc3645

A Rare Case of Gastric Cystic Pneumatosis Associated With Drug-Induced Gastric Injury

A 47-year-old man with history of cocaine addiction was hospitalized after cardiac arrest. Cardiopulmonary resuscitation associated with subsequent doses (3+6+6 mg) of ephedrine was performed. Upon intensive care unit admission, he presented with postanoxic encephalopathy, hyperpyrexia, disseminated intravascular coagulation, and multiorgan failure. Drug screening detected benzoylecgonine (57 ng/mL–1), ephedrine (73 ng/mL–1), 3,4-methylenedioxymethamphetamine, 3,4-methylenedioxyamphetamine, delta-9-tetrahydrocannabinol, and morphine.

Past Life Experiences and Neurological Recovery: The Role of Cognitive Reserve in the Rehabilitation of Severe Post-Anoxic Encephalopathy and Traumatic Brain Injury.

Patients with an equivalent clinical background may show unexpected interindividual differences in their outcome. The cognitive reserve (CR) model has been proposed to account for such discrepancies, but its role after acquired severe injuries is still being debated. We hypothesize that inappropriate investigative methods might have been used when dealing with severe patients, which have very likely reduced the possibility of observing meaningful influences in recovery from severe traumas. To overcome this issue, the potential neuroprotective role of CR was investigated, considering a wider spectrum of clinical symptoms ranging from low-level brain stem functions necessary for life to more complex motor and cognitive skills. In the present study, data from 50 severe patients, 20 suffering from post-anoxic encephalopathy (PAE) and 30 with traumatic brain injury (TBI), were collected and retrospectively analyzed. We found that CR, diagnosis, time of hospitalization, and their interaction had an effect on the clinical indexes. When the predictive power of CR was investigated by means of two machine learning classifier algorithms, CR, together with age, emerged as the strongest factor in discriminating between patients who reached or did not reach successful recovery. Overall, the present study highlights a possible role of CR in shaping the recovery of severe patients suffering from either PAE or TBI. The practical implications underlying the need to routinely considered CR in the clinical practice are discussed.

Serum neurofilament light chain as a prognostic marker in postanoxic encephalopathy

Functional outcome in patients with postanoxic encephalopathy after cardiac arrest (CA) often remains unclear, and there is a strong need of new prognostication measures. We aimed at investigating serum neurofilament light (NfL) chain concentration in patients with a postanoxic encephalopathy after CA and its prognostic potential.Serum samples were prospectively collected at different time points after CA in consecutive patients admitted to the intensive care unit (ICU) of Ticino Cardiocentre (Lugano, Switzerland) between June 2017 and March 2018. Serum NfL concentration was measured using a single molecule array (SIMOA) assay. The association of NfL levels with time to return of spontaneous circulation (ROSC), serum neuronal specific enolase (NSE) concentration, time between CA and sample collection, electroencephalogram (EEG) pattern and clinical outcome (death status at one month) were explored.Fourteen patients experiencing 15 CAs were included in the study (median age = 58 (57–68) years, 8 males). Median serum NfL concentration was 1027.0 (25.5–6033.7) pg/ml. There were positive associations between serum NfL and time to ROSC (rho = 0.60, p < 0.0001), NSE concentration (rho = 0.76, p < 0.0001), and severity of brain damage as estimated by EEG, with the highest concentrations measured in patients with suppressed electrical activity (14,954.0 [9006.0–25,364.0] pg/ml). Neurofilament light concentration remained high in samples collected up to 17 days after CA. Median NfL levels were higher among dead than alive patients at one month (6401.7 [3768.5–15,573.3] vs 25.5 [25.2–75.4] pg/ml). High NfL levels performed better than NSE in predicting death status at one month (NfL area under the curve (AUC) = 0.98, 95% confidence interval (CI) = 0.94–1.00; NSE AUC = 0.80, 95% CI = 0.67–0.94).These results support the potential inclusion of serum NfL in the battery of prognostication measures to be used in patients with postanoxic encephalopathy in ICU settings.This article is part of the Special Issue “Proceedings of the 7th London-Innsbruck Colloquium on Status Epilepticus and Acute Seizures"

Biomarkers in acute brain trauma: A narrative review

Biomarkers have been used to diagnose, prognose, evaluate, and identify the severity and outcomes in traumatic brain injury (TBI) patients. This study explored if it is possible to predict the outcome of TBI patients by estimating the biomarkers in cerebrospinal fluid and serum. We searched data bases and literature about biomarkers, and found forty epidemiologic studies from 92 potentially relevant articles. However, limited data are available about postanoxic encephalopathy. It showed that presently, neurofilament, S100B, glial fibrillary acidic protein, and ubiquitin carboxyl terminal hydrolase-L1 seemed to have the best potential as diagnostic biomarkers for distinguishing focal and diffuse injury, whereas C-Tau, neuron-specific enolase, S100B, glial fibrillary acidic protein, and spectrin breakdown products appear to be candidates for reflective biomarkers of TBI. Point-of-care biomarkers are needed in TBI which is one of the most important additional risk factors in road traffic injuries. In a holistic approach, more researches about biomarkers of TBI are required. These biomarkers are very useful for treatment of patients with TBI.

Postmortem histopathology of electroencephalography and evoked potentials in postanoxic coma

Early EEG patterns and SSEP responses are associated with neurological recovery of comatose patients with postanoxic encephalopathy after cardiac arrest. However, the nature and distribution of brain damage underlying the characteristic EEG and SSEP patterns are unknown. We relate EEG and SSEP findings with results from histological analyses of the brains of eleven non-survivors. With restoration towards continuous rhythms within 24 h after cardiac arrest, no signs of structural neuronal damage were observed. Absent SSEP responses were always accompanied by thalamic damage. Pathological burst suppression patterns were associated with a variable degree of neuronal damage to cortex, cerebellum and hippocampus. In patients with additional thalamic involvement, burst-suppression with identical bursts was observed, a characteristic EEG pattern presumably reflecting residual activity from a relatively isolated and severely compromised cortex.

Giant somatosensory evoked potentials are uncommon in patients with post-anoxic coma and paroxysmal electroencephalographic activity

Objectives Post-anoxic encephalopathy (PAE) is a severe neurological condition associated with poor outcome. As part of a multi-modal evaluation, electrophysiological investigations such as electroencephalography (EEG) and somatosensory evoked potentials (SSEPs) have been shown to be reliable outcome predictors in the assessment of comatose survivors, particularly with PAE [3] . The aim of the study was firstly to evaluate the feasibility of performing SSEPs in post-anoxic comatose patients with paroxysmal activity on EEG and secondly to assess the relationship between EEG cortical hyperexcitability and giant cortical N20 SSEPs responses. Methods In this retrospective study between 2016 and 2018, patients with PAE, paroxysmal activity on EEG and available median nerve SSEPs data were included in the analysis. Paroxysmal activity was identified on the EEG performed in the last 48 h preceding SSEPs. We evaluated the N20 amplitude from baseline, and P14-N20 and N20-P24 peak to peak amplitudes. Giant SSEPs were defined as a N20 exceeding 2.7 μV or N20–N24 exceeding 5.5 μV [2] or a late giant component exceeding 5 μV [1] . Results Twenty-one patients were included; 14 men (67%) mean age 66 ± 18 years. A total of 62% of PAE cases were due to cardiac arrest. Nineteen patients died following withdrawal of life support, one died spontaneously and one patient survived. Three patterns of EEG paroxysmal activity were identified: continuous rhythmic activity (n = 3), periodic generalized discharges (GPDs) on a low frequencies background (n = 12) and GPDs on a flat background (burst-suppression) (n = 6). SSEPs were giant in 3 patients (14%), normal in 7 patients (34%), reduced in 3 patients (14%) and absent bilaterally in 8 (38%). Conclusions Our study shows that performing SSEPs is feasible in PAE patients with EEG paroxysmal activity. Giant SSEPs are uncommon in these patients. The EEG cortical hyperexcitability reflects different stages of brain injury, as it can be associated with preserved (even giant), or absent SSEPs.

F86. EEG findings and prognosis in post-anoxic encephalopathy: A Brazilian experience

Prognostication after cardiac arrest (CA) poses a challenge to physicians, as it may lead to futile treatment in some cases, and withdrawal of life support therapy (WLST) in others. Clinical and neurophysiological data – electroencephalogram (EEG) and somatosensory evoked potential (SSEP) – are used as prognostic features. In this study, we aimed at analyzing data of patients who survived CA, in a hospital setting in Brazil, where care is not withdrawn even in patients with expected poor neurological outcome. We reviewed clinical and neurophysiological data of patients who had EEG after CA from 2006 to 2016. We considered background suppression, burst-suppression, periodic discharges, and status epilepticus (SE) as ‘malignant’ EEG patterns. Neurologic disability was measured according to the modified Rankin scale (mRS). Scores from 4 to 6 were considered poor outcome. 32 patients had EEG after CA. Age ranged from 47 to 98 years (mean 71.6). The majority of patients had in-hospital CA (75%) and the most common cause was hypoxia. 37% received therapeutic hypothermia (TH) as standard care. 73% of patients had poor outcome; 63% of these had a ‘malignant’ EEG pattern after CA. However, 45% of patients who had favorable outcome also had a ‘malignant’ EEG pattern after CA. Patients who received TH presented more ‘malignant’ EEG patterns, compared with those who did not (66% vs 50%). ‘Malignant’ EEG patterns were seen in most of the patients, regardless of CA local (in-hospital 54% vs out-of-hospital 62%). Our results emphasize that good outcome may be achieved even if face of ‘malignant’ EEG patterns, and this should be considered when WLST is evaluated.

Extracorporeal cardiopulmonary resuscitation for refractory in-hospital cardiac arrest

Despite recent improvement in cardiac arrest management, in-hospital cardiac arrest (IHCA) remains associated with poor outcome. Whereas its usefulness for out-of-hospital cardiac arrest seems poor, extracorporeal cardiopulmonary resuscitation (e-CPR; i.e. veno-arterial extracorporeal membrane oxygenation (VA-ECMO) under cardiopulmonary resuscitation) could be a life-saving strategy for refractory IHCA. To describe the characteristics and outcomes of refractory IHCA patients supported by e-CPR in our institution. Retrospective cohort study of data prospectively collected. All patients implanted with a VA-ECMO for refractory IHCA from 2007 to 2017 were included. VA-ECMO was implanted at the cardiac arrest site by trained cardiac surgeons from our mobile circulatory assistance unit. After ECMO implantation, patients were all referred and managed in our ICU. A 1-yr follow-up phone call was given to each survivor. During the study period, 97 patients (mean age 50.9 ± 14.8 yrs) received e-CPR for refractory IHCA. 80.4% of IHCA had a cardiac origin. VA-ECMO was implanted in our ICU for 37% of them, in the cardiology department for 30%, in another hospital for 23%. Survival rate was 19.6% at hospital discharge, 15% at 1-yr follow-up, with a 1-yr CPC score of 1 [1–2]. Main causes of in-ICU deaths were multiple organ failure (71%) and post-anoxic encephalopathy (12%). Compared to 1-yr non-survivors, 1-yr survivors had similar no- and low-flow, their initial rhythm was more frequently shockable (69.2% versus 33.8%, respectively, P = 0.03) and their day-1 SOFA score was significantly lower (13 [10–14] versus 15 [12–17], respectively, P = 0.02). e-CPR in refractory IHCA is associated with a 15% 1-yr survival rate. Survivors have a good 1-year CPC score. Next step is to determine prognosis factors to select the patients the most likely to benefit from this technique.

The interrelation between clinical presentation and neurophysiology of posthypoxic myoclonus.

ObjectivePosthypoxic myoclonus (PHM) in the first few days after resuscitation can be divided clinically into generalized and focal (uni‐ and multifocal) subtypes. The former is associated with a subcortical origin and poor prognosis in patients with postanoxic encephalopathy (PAE), and the latter with a cortical origin and better prognosis. However, use of PHM as prognosticator in PAE is hampered by the modest objectivity in its clinical assessment. Therefore, we aimed to obtain the anatomical origin of PHM with use of neurophysiological investigations, and relate these to its clinical presentation.MethodsThis study included 20 patients (56 ± 18 y/o, 68% M, 2 survived, 1 excluded) with EEG‐EMG‐video recording. Three neurologists classified PHM into generalized or focal PHM. Anatomical origin (cortical/subcortical) was assessed with basic and advanced neurophysiology (Jerk‐Locked Back Averaging, coherence analysis).ResultsClinically assessed origin of PHM did not match the result obtained with neurophysiology: cortical PHM was more likely present in generalized than in focal PHM. In addition, some cases demonstrated co‐occurrence of cortical and subcortical myoclonus. Patients that recovered from PAE had cortical myoclonus (1 generalized, 1 focal).InterpretationHypoxic damage to variable cortical and subcortical areas in the brain may lead to mixed and varying clinical manifestations of myoclonus that differ of those patients with myoclonus generally encountered in the outpatient clinic. The current clinical classification of PHM is not adequately refined to play a pivotal role in guiding treatment decisions to withdraw care. Our neurophysiological characterization of PHM provides specific parameters to be used in designing future comprehensive studies addressing the potential role of PHM as prognosticator in PAE.

Synaptic densities in hypoxia exposed and electrically stimulated primary neural cultures

Synaptic densities in hypoxia exposed and electrically stimulated primary neural cultures

O76 EEG continuity features predict outcome in postanoxic encephalopathy

Objectives In postanoxic encephalopathy, a rapid restoration of EEG background continuity predicts a good neurological outcome. Patterns with sharp amplitude transitions, such as burst-suppression with identical bursts, have a clear association with a poor outcome. We aim to capture these visual observations by two quantitative measures, in order to improve predictive accuracy. Methods We defined EEG background continuity as the fraction of signal without suppressions (segments with amplitudes μ V for >0.5 s). The burst-suppression contrast ratio was defined as the mean amplitude ratio between “bursts” (segments not classified as suppressions) and suppressions. Features were extracted from continuous EEG recordings in patients with postanoxic coma, using 5-min epochs for each hour between 0 and 72 h after cardiac arrest. Epochs with muscle artifacts were rejected automatically. The algorithm was optimized for a random set of 50 patients, and tested on an independent set of 410 patients. Outcome was assessed at 6 months after cardiac arrest and defined as “good” (Cerebral Performance Category 1–2) or “poor” (CPC 3–5). Results In the test set, EEG background continuity predicted good outcome best at 13 h after cardiac arrest, with sensitivity of 0.50 (95%-CI: 0.44–0.56) and specificity of 0.91 (95%-CI: 0.86–0.94). The burst-suppression contrast ratio predicted poor outcome best at 15 h after cardiac arrest, with sensitivity of 0.46 (95%-CI: 0.40–0.52) and specificity of 1.00 (95%-CI: 0.98–1.00). Discussion The quantitative measures outperform visual EEG assessment in terms of predictive accuracy. Still, they remain closely related to key features of visual EEG assessment, in contrast to other commonly used quantitative EEG features. A visual check of the EEG in the burst-suppression contrast ratio calculation remains essential, to rule out unwanted effects of high-amplitude artifacts. Conclusions Quantitative measures of EEG continuity reliably predict outcome in postanoxic encephalopathy. Significance The presented continuity features provide an objective, rapid, and reliable tool to assist in EEG interpretation in the ICU.

Predictive value of EEG in postanoxic encephalopathy: A quantitative model-based approach

IntroductionThe majority of comatose patients after cardiac arrest do not regain consciousness due to severe postanoxic encephalopathy. Early and accurate outcome prediction is therefore essential in determining further therapeutic interventions. The electroencephalogram is a standardized and commonly available tool used to estimate prognosis in postanoxic patients. The identification of pathological EEG patterns with poor prognosis relies however primarily on visual EEG scoring by experts. We introduced a model-based approach of EEG analysis (state space model) that allows for an objective and quantitative description of spectral EEG variability. MethodsWe retrospectively analyzed standard EEG recordings in 83 comatose patients after cardiac arrest between 2005 and 2013 in the intensive care unit of the University Hospital Zürich. Neurological outcome was assessed one month after cardiac arrest using the Cerebral Performance Category. For a dynamic and quantitative EEG analysis, we implemented a model-based approach (state space analysis) to quantify EEG background variability independent from visual scoring of EEG epochs. Spectral variability was compared between groups and correlated with clinical outcome parameters and visual EEG patterns. ResultsQuantitative assessment of spectral EEG variability (state space velocity) revealed significant differences between patients with poor and good outcome after cardiac arrest: Lower mean velocity in temporal electrodes (T4 and T5) was significantly associated with poor prognostic outcome (p<0.005) and correlated with independently identified visual EEG patterns such as generalized periodic discharges (p<0.02). Receiver operating characteristic (ROC) analysis confirmed the predictive value of lower state space velocity for poor clinical outcome after cardiac arrest (AUC 80.8, 70% sensitivity, 15% false positive rate). ConclusionModel-based quantitative EEG analysis (state space analysis) provides a novel, complementary marker for prognosis in postanoxic encephalopathy.