Neurocritical Care最新文献

Background: The modified Fisher score is commonly used after aneurysmal subarachnoid hemorrhage (aSAH) to estimate hemorrhage burden and support early prognostication, although its accuracy in predicting cognitive outcomes remains limited. This study compares the predictive value of the subjective asessment of aSAH volume through the modified Fisher score with an objetive volumetric quantification in prognosticating cognitive outcomes.

Methods: This retrospective observational study included patients with aSAH between 2009 and 2024 and good functional recovery (modified Rankin score ≤ 2) at least 6 months after aSAH. Cognitive outcomes were assessed using Montreal Cognitive Assessment scores normalized to population data, with poor outcomes defined as Montreal Cognitive Assessment scores < 25th percentile for normative data. A semiautomated method was used to quantify hemorrhage volume from presentation on computed tomography scans. Logistic regression, receiver operating characteristic curves, and mediation analyses were conducted to evaluate the potential relationship between aSAH volume, clinical variables, and cognitive outcomes.

Results: A total of 142 patients with aSAH were included in the study, with 30% of patients (43/142) experiencing poor cognitive outcomes. The objective quantification of hemorrhage volume demonstrated a superior predictive performance compared with the modified Fisher score in determining poor cognitive outcomes (area under the curve 0.75 vs. 0.66, p = 0.037). An aSAH volume cutoff of 24 mL yielded a sensitivity of 72% and a specificity of 60% in predicting poor cognitive outcomes. Mediation analysis revealed partial mediation by vasospasm in the relationship between hemorrhage volume and poor cognitive outcomes.

Conclusions: There is a high rate of cognitive impairment among survivors with aSAH with good functional recovery. Volume quantification outperformed the modified Fisher score in predicting cognitive outcomes after aSAH. aSAH volumes more than 24 mL are linked to worse outcomes, with vasospasm contributing to this association.

Background: Traumatic spinal cord injury (TSCI), a severe central nervous system injury, despite treatment advances, critically ill patients with TSCI face high short-term mortality. This study leverages machine learning to integrate standard intensive care unit (ICU) indicators, identifying 7-day high-mortality risk patients with TSCI to optimize treatment.

Methods: Using critically ill patients with TSCI data from the Medical Information Mart for Intensive Care 2.2 database, this study employs the Boruta and LASSO regression algorithms to identify key features, developing a 7-day mortality risk prediction model in critically ill patients with TSCI using ten machine learning algorithms including Adaptive Boosting, Categorical Boosting, Gradient Boosting Machine, k-Nearest Neighbors, Light Gradient Boosting Machine, Logistic Regression, Neural Network, Random Forest (RF), Support Vector Machine, and Extreme Gradient Boosting. Model Performance is evaluated via receiver operating characteristic curves, calibration curves, decision curve analysis, accuracy, sensitivity, specificity, precision, and F1 score, whereas Shapley Additive Explanations ensure model interpretability. External validation with ICU data from the First Affiliated Hospital of Xinjiang Medical University further assesses the model's generalizability.

Results: This study, collecting data from 261 and 45 critically ill patients with TSCI from the Medical Information Mart for Intensive Care database and the First Affiliated Hospital of Xinjiang Medical University's ICU, respectively, identified ten key features for model development, in which the RF model consistently outperformed others across raw and Synthetic Minority Over-sampling Technique-balanced synthetic datasets in receiver operating characteristic curves, calibration curves, decision curve analysis, and performance metrics. Shapley Additive Explanation analysis highlighted minimum body temperature, lowest systolic blood pressure, and Charlson Comorbidity Index as critical predictors in the RF model. External validation initially demonstrated the model's robustness and clinical applicability, leading to an online calculator that enables clinicians to estimate the 7-day survival probability of critically ill patients with TSCI.

Conclusions: The RF model exhibits favorable performance in predicting 7-day mortality risk among critically ill patients with TSCI, indicating its potential utility in supporting clinical decision-making.

Background: Traumatic brain injury (TBI) often results in tau hyperphosphorylation, a key pathological feature of neurodegenerative diseases such as Alzheimer's disease. Hypothermia (HT) is a promising therapeutic intervention for TBI, but the underlying molecular mechanisms remain unclear. This study investigates the role of RNA-binding motif protein 3 (RBM3) in mediating the neuroprotective effects of HT on tau phosphorylation and its involvement in glycogen synthase kinase 3 beta (GSK-3β) and AMP-activated protein kinase (AMPK) signaling.

Methods: We used a TBI mouse model to assess the effects of HT on tau phosphorylation using Western blotting and immunohistochemistry. The phosphorylation status of GSK-3β (Ser9) and AMPK (Thr172) was also analyzed to explore key signaling pathways. RBM3 expression was modulated using RBM3 short hairpin RNA (knockdown) and adenovirus-RBM3 plasmid (overexpression) to determine its role in HT-induced changes in tau phosphorylation.

Results: Hypothermia treatment significantly reduced tau hyperphosphorylation in TBI mice compared with controls. Western blotting revealed a significant increase in GSK-3β Ser9 phosphorylation (p < 0.01) and AMPK Thr172 phosphorylation (p < 0.05) in the HT group. Manipulation of RBM3 expression showed that both RBM3 knockdown and overexpression affected the extent of tau dephosphorylation mediated by HT. Specifically, RBM3 overexpression enhanced the protective effects of HT, whereas knockdown diminished its efficacy.

Conclusions: Our findings suggest that RBM3 is a crucial mediator of the neuroprotective effects of hypothermia in TBI, acting through modulation of GSK-3β and AMPK signaling pathways. These results provide new insights into the molecular mechanisms of TBI treatment and highlight RBM3 as a potential therapeutic target for neurodegenerative diseases associated with tauopathies. Limitations include the need for further validation in clinical models.

Background: There is little research on venous thromboembolism (VTE) prophylaxis (PPX) timing of the higher rebleeding risk groups based on size and type of traumatic brain injury (TBI) due to exclusion from previous observational studies, which prohibits the facilitation of an evidence-based strategy. We aim to determine the effect of VTE PPX timing on the high rebleeding risk TBI population based on the modified Berne Norwood Criteria.

Methods: This retrospective cohort study used the American College of Surgeons Trauma Quality Program Participant Use File from 2017 to 2022. The study population consisted of adult patients who received chemical or mechanical PPX with no missing times and had a blunt high rebleeding risk TBI stratified by a comorbid history of anticoagulation or bleeding disorder with excluded polytrauma. There was a total of 12 exposure groups based on VTE PPX timing with the outcomes of interest being intensive care unit (ICU) stay, ventilation days, and mortality.

Results: A total of 13,016 patients were included in the exploratory analysis. Early initiation of chemical VTE PPX (within ≤ 24 h) was associated with a reduced likelihood of prolonged ICU stay and ventilation days, regardless of prior anticoagulation use or bleeding disorder. In contrast, inferior vena cava filter placement within the > 24-h to < 72-h window was associated with increased ICU and ventilation duration.

Conclusions: This study highlights the benefits of initiating chemical VTE PPX within 24 h for patients wih high rebleeding risk TBI, demonstrating significant reductions in ICU stays and ventilation days without an increase in mortality rates. Additionally, although inferior vena cava filters are associated with longer ICU stays and increased ventilation days, this may reflect the greater severity and potential mortality risk of the conditions being treated.

Background: External ventricular drain (EVD)-associated infections (EVDAI) remain a relevant complication of acute hydrocephalus treatment following aneurysmal subarachnoid hemorrhage (aSAH). Whether radiological quantity and anatomical distribution of subarachnoid and ventricular blood impact EVDAI rates has not been thoroughly studied to date.

Methods: This was a retrospective (2009-2023) analysis of patients with aSAH undergoing emergency ventriculostomy. Univariable and multivariable logistic regression analyses were used to assess the association between the Barrow Neurological Institute (BNI) grading scale for subarachnoid hemorrhage and the intraventricular hemorrhage (IVH) score for extent and anatomical distribution of intracerebral bleeding with EVDAI risk. Cox regression analysis was employed to investigate the relationship between hemorrhage extent and the timing of EVDAI onset.

Results: One hundred and ninety-four patients with aSAH received 228 EVDs with a total of cumulative 2,258 EVD days. Overall EVDAI rates were 14% (27/194) per patient and 12% (27/228) per EVD. EVDAI was associated with a larger subarachnoid blood clot (BNI grade 4; odds ratio 6.66, 95% confidence interval 2.04-21.68; p = 0.002) and higher IVH scores (odds ratio 1.33, 95% confidence interval 1.05-1.69; p = 0.02). Intracerebral hemorrhage was more frequently localized in the posterior fossa in the EVDAI group (20% vs. 0%, p = 0.004). Multivariable analysis confirmed a positive independent correlation with larger blood clots. Cox regression demonstrated earlier EVDAI onset in association with higher BNI grades and IVH scores.

Conclusions: Both the quantity and radiological distribution of subarachnoid and ventricular blood positively correlate with EVD-associated nosocomial meningitis, eventually accelerating an earlier infection onset. These findings should help guide future research on EVDAI prevention in patients with aSAH.

Background: Consciousness recovery after severe traumatic brain injury (sTBI) can take minutes to years. Despite this variability, we hypothesized that we could identify subgroups with distinct temporal recovery trajectories and that these subgroups would have distinct clinical features.

Methods: We conducted a retrospective cohort study to analyze recovery trajectories for patients with sTBI (Glasgow Coma Scale [GCS] score ≤ 8) admitted to Stony Brook University Hospital from 2010 to 2019. Patients meeting our criteria for recovery (GCS score ≥ 13) were classified into cohorts using the slopes of their recovery trajectories. We then characterized these groups by their clinical features, neuroimaging, and electroencephalography (EEG).

Results: A total of 501 patients with sTBI (348 men, mean age 51 years) were included in this study. Of these, 299 recovered. After analyzing their recovery rates, two distinct groups emerged, (1) fast recovery (n = 215) and (2) slow recovery (n = 84), with a median recovery time of 6 (interquartile range [IQR] 2-12) vs. 33 (IQR 27-44.75) days. Slow recovery patients had higher Injury Severity Scores (median 30 [IQR 25-41.75] vs. 24 [IQR 16-30]; 95% confidence interval [CI] 4.4495-10.6105; P < 0.001), more thalamic injury on neuroimaging (normalized volume [voxels] - 0.664 vs. 1.74; R² = 0.781; P < 0.016), and impaired interhemispheric connectivity on EEG (phase-locking value 0.35 vs. 0.44; 95% CI 0.055-0.14; P < 0.001).

Conclusions: Recovery after sTBI falls into two broad categories, distinguishable by injury severity, thalamic injury, and disrupted interhemispheric connectivity. This model accounts for heterogeneity in TBI outcomes and represents progress toward identifying targets for future neuromodulatory therapeutic development.

Background: Many traumatic brain injury (TBI) treatment protocols, including the Lund concept, advocate the highest point of the subarachnoid space (typically the vertex) as the zero-reference point for intracranial pressure (ICP) and the level of the right atrium as the zero-reference point for mean arterial blood pressure (MAP). In 2017, at the Department of Neurosurgery in Lund, Sweden, the zero-reference points for ICP and MAP were both changed to the external auditory meatus (EAM), thus altering the calculated cerebral perfusion pressure (CPP) levels. We hypothesized that the ICP and MAP levels obtained from the different zero-reference points resulted in altered neurocritical care management and/or patient outcome.

Methods: We conducted a retrospective analysis of ICP, CPP, MAP, medical management, mortality, and outcome in two different patient cohorts with severe TBI treated at the Department of Neurosurgery, Skåne University Hospital, Lund, Sweden, between 2013 and 2016 and 2018 and 2022.

Results: We collected more than 31,000 measurements from 49 patients between 2013 and 2016 and 53 patients between 2018 and 2022. Age and injury severity were similar in both groups. Mortality and treatment outcome according to the Glasgow Outcome Scale - Extended were similar. Mean ICP levels were higher (p < 0.0001) after the reference point was changed to the EAM. The use of clonidine (65% vs. 49%; p = 0.17) and metoprolol (50% vs. 13%; p = 0.0002) decreased, and the use of norepinephrine increased (42% vs. 98%; p < 0.0001) after changing the reference points.

Conclusions: Higher ICP levels were observed when the reference point was changed to the EAM. The use of metoprolol was reduced, and there was a significant increase in the use of norepinephrine. These results show the impact of zero-reference point placement, which should be reported in TBI studies analyzing ICP and CPP management.

Background: This study aims to explore the predictors of poor outcomes by analyzing the clinical characteristics and prognosis of adult patients with severe forms of autoimmune encephalitis (AE) requiring intensive care unit (ICU) admission.

Methods: A retrospective analysis was conducted on 134 adult patients diagnosed with definite or possible AE and admitted to the neurology ICU between January 2015 and December 2023. Neurological outcomes at 6 and 12 months were assessed using the modified Rankin scale (mRS). The study further analyzed the relationship between their clinical characteristics, auxiliary examinations, and prognosis.

Results: A total of 134 adult patients with AE requiring ICU admission were included. The 6- and 12-month survival rates were 91.8% and 91.5%, respectively. At 6 months, 72.4% (97 of 134) of patients had favorable outcomes (mRS score ≤ 2), whereas 27.6% (37 of 134) had poor outcomes (mRS score ≥ 3). Compared with the favorable group, patients in the poor outcome group were older (42.92 vs. 30.71 years, p = 0.002), had a higher incidence of tumors (24.3% vs. 4.1%, p < 0.001), and were more likely to require mechanical ventilation (67.6% vs. 26.8%, p < 0.001). They also had lower Glasgow Coma Scale scores on ICU admission (p = 0.006), higher Acute Physiology and Chronic Health Evaluation II scores (p = 0.006), elevated cerebrospinal fluid glucose (p = 0.004) and protein levels (p = 0.029), higher autoantibody seronegativity (32.4% vs. 13.4%, p = 0.011), lower glucocorticoid use (p = 0.038), and longer ICU stays (p = 0.031). Multivariate logistic regression identified age (p = 0.001), presence of tumor (p = 0.03), mechanical ventilation (p = 0.025), antibody negativity (p = 0.042), and ICU length of stay (p = 0.000) as independent predictors of poor prognosis.

Conclusions: These factors may help identify high-risk patients with AE early, enabling timely and targeted interventions to improve outcomes.