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Introduction Standardized EEG patterns according to the American Clinical Neurophysiology Society (ACNS) (“highly malignant”, “malignant” and “benign”) demonstrated good correlation with outcome after cardiac arrest (CA). However, this approach relates to EEGs after target temperature management (TTM), and correlation to other recognized outcome predictors remains unknown. Objectives To investigate the relationship between categorized EEG and other outcome predictors, during and after TTM, at different temperatures. Methods In a prospective adult CA registry between 01.2014 and 06.2017, EEG at day one and two after CA were reclassified into pre-defined categories. Correlations between EEG and clinical, biochemical, neurophysiological outcome predictors, and prognosis (CPC at three months; good: 1–2), were assessed. Results Of 203 CA episodes, 31.5% were managed targeting 33 °C, 60.6% targeting 36 °C, and 7.9% with spontaneous temperature. “Highly malignant” EEG was found in 36.7% of patients at day one (predicting poor prognosis with 91% specificity −95%CI: 83%–97%-, and 63% sensitivity −95% CI: 53%–72%), and 27.1% at day two. “Benign” EEG occurred in 19.2% at day one (sensitivity to good prognosis: 35% −95%CI: 26%–46%-, positive predictive value: 89% −95% CI: 75%–97%), and in 33.2% at day two. Categorized EEG showed robust correlations with all prognostic predictors. Results were similar between EEGs recorded at day one or two, and, especially for poor prognosis, across TTM targets. Discussion Standardized EEG categorization after CA shows strong correlation with other outcome predictors, without marked variation across EEG recording time or TTM targets, underscoring its prognostic role in a multimodal approach.

Background: Non-invasive, easy-to-use bedside tools to estimate prognosis in unresponsive patients with postanoxic brain injury are needed. We assessed the usefulness of otoacoustic emissions as outcome markers after cardiac arrest. Methods: Distortion product otoacoustic emissions (DPOAE) and transient evoked otoacoustic emissions (TEOAE) were measured in cardiac arrest patients whose prognosis was deemed to be poor following standard neurological assessment (n = 10). Ten patients with myocardial infarction without prior loss of consciousness served as controls. Results: Compared to controls with myocardial infarction, cardiac arrest patients with poor neurological prognosis had significantly less often preserved DPOAE (9.2 vs. 40.8% positive measurements; OR 0.15 (CI 0.07-0.30); p < 0.0001). Partially preserved DPOAE were noted in 4 cardiac arrest patients. TEOAE were not statistically different between the two groups. Conclusions: Despite their convenience, otoacoustic emissions cannot be used as reliable prognostic markers in cardiac arrest survivors. This is because we identified 4 cases with partially preserved otoacoustic emissions in a sample of 10 unresponsive post-cardiac arrest patients whose neurological condition was so poor that active treatment was withdrawn. However, we suggest that future research should address if decaying outer hair cell function over time may serve as a proxy for evolving ischemic brain damage.

These past few years have seen an increasing role of MRI in the investigation of neonatal cerebral anoxic-ischemic pathology. This is due not only to greater precision in diagnosing lesion extension, but also to earlier detection of lesions with the diffusion of weighted imagery. The aim of this iconographic review is to illustrate the main MRI aspects of anoxic-ischemic encephalopathy in a pedagogical way. After a brief physiopathology reminder, the different cerebral lesions are studied in a first chapter on the premature newborn pathology and a second chapter on full-term newborn pathology.

Data from MRI can be used to generate detailed maps of central nervous system anatomy and functional activation. Here, we review new research that integrates advanced MRI acquisition and analysis to predict and track recovery following severe traumatic brain injury (TBI) or anoxic ischemic encephalopathy (AIE) following cardiac arrest.Diffusion tensor MRI studies of comatose TBI patients demonstrate specific distributions of white matter damage that are robustly associated with long-term functional outcomes. In unconscious patients with AIE, whole brain diffusion restriction has prognostic significance, as do regional changes in diffusion restriction or anisotropy. Results using functional MRI suggest that coma following TBI and cardiac arrest is associated with disconnections within cerebral architectures associated with arousal and conscious perception. The relation between these disconnections and postinjury recovery is being explored in ongoing cohorts.MRI of the brain is feasible in critically ill patients following TBI or cardiac arrest, revealing patterns of structural damage and functional disconnection that can help predict outcome in the long term. Prospective studies are needed to validate these findings and to identify relationships between MRI-defined alterations and specific postinjury cognitive and behavioural phenotypes.

Item does not contain fulltext PURPOSE: To analyze white matter pathologic abnormalities by using diffusion-tensor (DT) imaging in a multicenter prospective cohort of comatose patients following cardiac arrest or traumatic brain injury (TBI). MATERIALS AND METHODS: Institutional review board approval and informed consent from proxies and control subjects were obtained. DT imaging was performed 5-57 days after insult in 49 cardiac arrest and 40 TBI patients. To control for DT imaging-processing variability, patients' values were normalized to those of 111 control subjects. Automated segmentation software calculated normalized axial diffusivity (lambda1) and radial diffusivity (lambda perpendicular) in 19 predefined white matter regions of interest (ROIs). DT imaging variables were compared by using general linear modeling, and side-to-side Pearson correlation coefficients were calculated. P values were corrected for multiple testing (Bonferroni). RESULTS: In central white matter, lambda1 differed from that in control subjects in six of seven TBI ROIs and five of seven cardiac arrest ROIs (all P < .01). The lambda perpendicular differed from that in control subjects in all ROIs in both patient groups (P < .01). In hemispheres, lambda1 was decreased compared with that in control subjects in three of 12 TBI ROIs (P < .05) and nine of 12 cardiac arrest ROIs (P < .01). The lambda perpendicular was increased in all TBI ROIs (P < .01) and in seven of 12 cardiac arrest ROIs (P < .05). Cerebral hemisphere lambda1 was lower in cardiac arrest than in TBI in six of 12 ROIs (P < .01), while lambda perpendicular was higher in TBI than in cardiac arrest in eight of 12 ROIs (P < .01). Diffusivity values were symmetrically distributed in cardiac arrest (P < .001 for side-to-side correlation) but not in TBI patients. CONCLUSION: DT imaging findings are consistent with the known predominance of cerebral hemisphere axonal injury in cardiac arrest and chiefly central myelin injury in TBI. This consistency supports the validity of DT imaging for differentiating axon and myelin damage in vivo in humans. 01 februari 2014

Despite advances in the management of cardiac arrest, mortality remains very high and persistence of coma often leads to withdrawal of life support. Accurate prediction of neurologic outcome early after resuscitation is important for directing goals of medical care. This chapter reviews the pathophysiology of anoxic-ischemic brain injury and the clinical, biochemical, radiographic and electrophysiologic tests used to predict neurologic outcome following cardiac arrest as well as the ethical issues that can arise during prognostication.

The combined effect of vascular occlusion and anoxia was used to produce lesions in the rat brain. Histological and histochemical techniques were employed in order to ascertain the early cellular changes. One could demonstrate unequivocal pallor and a spongy appearance of the cortical neuropil, indicating edema, as early as 2.5 hours. The earliest changes in the neurons were characterized by a reduction in number of the lysosomes rather than an enlargement of this cytoplasmic organelle. The appearance of “cytolysomes” was sporadic and haphazard. They were not as large as other workers have demonstrated. The earliest changes demonstrated with the oxidative enzymatic techniques were present in the neuropil and this would indicate that the structures far from the cell body (dendrites, glial processes and axons) are affected first. Ischemic neurons showed persistent enzymatic activity after more than 24 hours. The reactive astrocytes, present in old lesions, showed a most intense reaction with the oxidative enzymatic techniques.

• Although the human brain stem is considered relatively invulnerable to ischemic anoxia, evaluation of 16 cases of a single acute asphyxial episode either at or following birth indicates that such involvement is a frequent and characteristic aspect of anoxic encephalopathy in the infant. Ischemic cell change, neuronal loss, and nuclear or reticular formation gliosis were present in the brain stem of all but one infant. At least two topographic patterns of anoxic encephalopathy exist: (1) a rostrocaudal pattern of decreasing vulnerability, with the cerebral cortex being most sensitive and the brain stem least sensitive, and (2) a pattern of brain stem and thalamic damage. Of the two, the latter pattern appears to follow most acute asphyxial episodes in the human neonate and infant.