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Abstract Background To assess in comatose patients after cardiac arrest (CA) if amplitudes of two somatosensory evoked potentials (SSEP) responses, namely, N20-baseline (N20-b) and N20–P25, are predictive of neurological outcome. Methods Monocentric prospective study in a tertiary cardiac center between Nov 2019 and July-2021. All patients comatose at 72 h after CA with at least one SSEP recorded were included. The N20-b and N20–P25 amplitudes were automatically measured in microvolts (µV), along with other recommended prognostic markers (status myoclonus, neuron-specific enolase levels at 2 and 3 days, and EEG pattern). We assessed the predictive value of SSEP for neurologic outcome using the best Cerebral Performance Categories (CPC1 or 2 as good outcome) at 3 months (main endpoint) and 6 months (secondary endpoint). Specificity and sensitivity of different thresholds of SSEP amplitudes, alone or in combination with other prognostic markers, were calculated. Results Among 82 patients, a poor outcome (CPC 3–5) was observed in 78% of patients at 3 months. The median time to SSEP recording was 3(2–4) days after CA, with a pattern “bilaterally absent” in 19 patients, “unilaterally present” in 4, and “bilaterally present” in 59 patients. The median N20-b amplitudes were different between patients with poor and good outcomes, i.e., 0.93 [0–2.05]µV vs. 1.56 [1.24–2.75]µV, respectively (p 2 µV predicted good outcome with a specificity of 73% and a moderate sensitivity of 39%, although an N20–P25 > 3.2 µV was 93% specific and only 30% sensitive. A low voltage N20-b

Background: To assess in comatose patients after cardiac arrest (CA) if amplitudes of two somatosensory evoked potentials (SSEP) responses, namely, N20-baseline (N20-b) and N20–P25, are predictive of neurological outcome. Methods: Monocentric prospective study in a tertiary cardiac center between Nov 2019 and July-2021. All patients comatose at 72 h after CA with at least one SSEP recorded were included. The N20-b and N20–P25 amplitudes were automatically measured in microvolts (µV), along with other recommended prognostic markers (status myoclonus, neuron-specific enolase levels at 2 and 3 days, and EEG pattern). We assessed the predictive value of SSEP for neurologic outcome using the best Cerebral Performance Categories (CPC1 or 2 as good outcome) at 3 months (main endpoint) and 6 months (secondary endpoint). Specificity and sensitivity of different thresholds of SSEP amplitudes, alone or in combination with other prognostic markers, were calculated. Results: Among 82 patients, a poor outcome (CPC 3–5) was observed in 78% of patients at 3 months. The median time to SSEP recording was 3(2–4) days after CA, with a pattern "bilaterally absent" in 19 patients, "unilaterally present" in 4, and "bilaterally present" in 59 patients. The median N20-b amplitudes were different between patients with poor and good outcomes, i.e., 0.93 [0–2.05]µV vs. 1.56 [1.24–2.75]µV, respectively (p < 0.0001), as the median N20–P25 amplitudes (0.57 [0–1.43]µV in poor outcome vs. 2.64 [1.39–3.80]µV in good outcome patients p < 0.0001). An N20-b > 2 µV predicted good outcome with a specificity of 73% and a moderate sensitivity of 39%, although an N20–P25 > 3.2 µV was 93% specific and only 30% sensitive. A low voltage N20-b < 0.88 µV and N20–P25 < 1 µV predicted poor outcome with a high specificity (sp = 94% and 93%, respectively) and a moderate sensitivity (se = 50% and 66%). Association of "bilaterally absent or low voltage SSEP" patterns increased the sensitivity significantly as compared to "bilaterally absent" SSEP alone (se = 58 vs. 30%, p = 0.002) for prediction of poor outcome. Conclusion: In comatose patient after CA, both N20-b and N20–P25 amplitudes could predict both good and poor outcomes with high specificity but low to moderate sensitivity. Our results suggest that caution is needed regarding SSEP amplitudes in clinical routine, and that these indicators should be used in a multimodal approach for prognostication after cardiac arrest. [ABSTRACT FROM AUTHOR]

Purpose: To evaluate the predictive value of EEG reactivity assessment and confounders for neurological outcome after cardiac arrest.Methods: All consecutive patients admitted in a tertiary cardiac arrest center between 2007 and 2016 still alive 48 h after admission with at least one EEG recorded during coma. EEG reactivity was defined as a reproducible waveform change in amplitude or frequency following standardized stimulation. Each EEG was classified based on American Clinical Neurophysiology Society nomenclatures and classified in highly malignant (including status epilepticus), malignant, or benign EEG. We assessed the predictive values of EEG reactivity and sedation effect for neurologic outcome at ICU discharge using the Cerebral Performance Category scale (with CPC 1-2 assumed as favorable outcome and CPC 3-4-5 considered as poor outcome).Results: Among 428 patients, a poor outcome was observed in 80% patients. The median time to EEG recording was 3 (1-4) days and 51% patients had a non-reactive EEG. The positive predictive value (PPV) of a non-reactive EEG to predict an unfavorable outcome was 97.1% (IC95% 93.6-98.9), increasing to 98.3% (IC95 94.1-99.8) when the EEG had been performed without sedation. In multivariate analysis, a non-reactive EEG was associated with poor outcome (OR 12.6 IC95% 4.7-33.6; p < 0.001). In multivariate analysis, concomitant sedation was not statistically associated with EEG non-reactivity. The PPV of a benign EEG to predict favorable outcome was 49.7% (IC95% 41.5-57.9), increasing to 66.2% (IC95% 54.3-76.8) when EEG was recorded earlier, with ongoing sedation.Conclusions: After cardiac arrest, absence of EEG reactivity was predictive of unfavorable outcome. By contrast, a benign EEG was slightly predictive of a favorable outcome. Reactivity assessment may have important implications in the neuroprognostication process after cardiac arrest and could be influenced by sedation. [ABSTRACT FROM AUTHOR]

Aim: To investigate the relation between brain ischemia and persistent vegetative state after severe traumatic brain injury. Methods: The 66 patients with severe brain injury were divided into two groups: The persistent coma group (coma duration ≥10 d) included 51 patients who had an admission Glasgow Coma Scale (GCS) of 5-8 and were unconscious for more than 10 d. There were 15 patients in the control group, their admission GCS was 5-8, and were unconscious for less than 10 d. The brain areas, including frontal, parietal, temporal, occipital lobes and thalamus, were measured by Single Photon Emission Computed Tomogrophy (SPECT). Results: In the first SPECT scan, multiple areas of cerebral ischemia were documented in all patients in both groups, whereas bilateral thalamic ischemia were presented in all patients in the persistent coma group and were absented in the control group. In the second SPECT scan taken during the period of analepsia, with an indication that unilateral thalamic ischemia were persisted in 28 of 41 patients in persistent coma group(28/41,68.29%). Conclusion: Persistent coma after severe brain injury is associated with bilateral thalamic ischemia. [ABSTRACT FROM AUTHOR]

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