Neurocritical Care最新文献

Background: Brain magnetic resonance imaging (MRI) has been investigated as a neuroprognostication (NP) test after out-of-hospital cardiac arrest (OHCA); however, most studies have focused on predicting poor neurologic outcomes or death.

Methods: We examined the ability of a composite brain MRI score ("NP score") to predict neurologic outcomes in an OHCA cohort (2017-2023) who underwent brain MRI within 2-7 days post arrest and survived to hospital discharge. NP scores (range 0-214) were calculated from diffusion weighted imaging and fluid attenuated inversion recovery signals in prespecified neuroanatomical regions. We categorized neurologic outcomes as "independent" (Cerebral Performance Categories [CPC] 1-2), "dependent" (CPC 3), and "vegetative state" (CPC 4). We conducted correlation analyses and used computational modeling for probabilities to identify transition points between the outcome categories.

Results: Forty-two OHCA survivors were included (median age 47 years; 74% male, 43% shockable rhythm; 88% underwent targeted temperature management). At hospital discharge, 50% (n = 21) had recovered to independent, 24% (n = 10) were dependent, and 26% (n = 11) remained in a vegetative state. MRIs were obtained at a median of 4 days post arrest, (interquartile range 3-5). NP scores (range 0-136, median 11.5, interquartile range 0-41.5, intraclass correlation coefficient 0.89) strongly correlated with CPC (r_s = 0.69, p < 0.001) and were significantly different between CPC groups (p < 0.001); thresholds of 15 and 54 were identified as transition points between independent-dependent and dependent-vegetative state, respectively. Among survivors with bilaterally intact somatosensory evoked potentials, median NP scores were 0, 29, 68.5 for independent, dependent, and vegetative state patients, respectively.

Conclusions: Quantitative brain MRI-based scoring may predict neurologic outcomes at discharge among OHCA survivors. External validation in larger prospective multicenter cohorts, assessment of long-term outcomes, and examination of the score in deceased patients are needed to establish the prognostic value and address concerns about generalizability.

Transcranial Doppler (TCD) is increasingly used in pediatric acute care with emerging point-of-care ultrasound (POCUS) applications. However, no standardized definition distinguishes POCUS TCD from diagnostic/consultative TCD. This scoping review aims to (1) examine how the terminology "POCUS TCD" is used in pediatric literature, (2) describe physiologic indications driving TCD use in pediatric acute care settings, and (3) compare contexts of performance and operational characteristics across these indications. A comprehensive scoping review was conducted following published guidelines. Databases were searched from inception to June 2024 for studies addressing TCD use in children (≤ 18 years) in emergency departments, inpatient services, or intensive care units. Full-text eligibility and data extraction were performed in duplicate by independent reviewers. Of 4,066 screened studies, 660 full texts were assessed, and 307 studies met eligibility criteria (258 original studies and 49 reviews, guidelines, or surveys). The term "POCUS TCD" was mentioned in only 3% of original studies and 26% of included reviews and guidelines, which were mostly published after 2018. Eleven physiologic indications for TCD use were identified, and specific subtypes of context of use emerged. TCD operational characteristics varied widely and were often incompletely reported. However, notable differences were observed across physiologic indications, particularly in TCD extent, operator type, and use of point-of-care machines. The terminology "POCUS TCD" is infrequently used in current pediatric research, and most studies do not specify the type of TCD performed or intended. Significant differences in the context of performance and operational characteristics across physiologic indications suggest the coexistence of distinct forms of TCD in current clinical practice despite the lack of explicit distinction between POCUS and diagnostic/consultative TCD. Standardizing terminology and improving reporting of operational contexts in future research will be essential to support safe and effective clinical integration of TCD in pediatric critical care.

Background: Measuring reliable intracranial pressure (ICP) is critical for patients with acute brain injuries. The aim of this study was to evaluate zero drift of the intraparenchymal strain gauge Pressio transducer (Sophysa, Orsay, France) in clinical conditions.

Methods: A prospective observational multicenter study was conducted in four French intensive care units of university hospitals. Patients with acute brain injuries were included if they needed ICP measurement using the Pressio transducer. The zero drift was measured at the explantation of the sensor. ICP-related adverse events were also collected.

Results: Between January 1, 2018, and March 31, 2020, 235 patients were included in this study for a monitoring time of 2,180 days. The zero drift assessment was determined in 223 transducers (95%). The median duration of ICP monitoring was 8 days (interquartile range [IQR] 4 to 13 days). The median zero drift was 1 mm Hg (IQR 1 to 3 mm Hg), and a weak correlation was observed between the duration of ICP monitoring and zero drift (ρ = 0.141; P = 0.0357), which lacks clinical significance. Zero drifts higher than 5 mm Hg were found in 10% of transducers. Four patients (1.8%) had ICP-related hematomas, with no clinical impact, and none had ICP-related brain infection. Failures or technical dysfunctions of the monitoring were found in six patients (2.6%).

Conclusions: The Pressio catheter from the Sophysa system exhibited a minor zero drift after a median monitoring period of 8 days. The transducer's precision was comparable to that of other ICP devices using strain gauge technology.

Background: Traumatic brain injury (TBI) is a major life-threatening event. In addition to neurological deficits, it can lead to long-term impairments of cognitive function. The vagus nerve (VN) provides a direct communication conduit between the central nervous system and the periphery, and modulation of the inflammatory reflex via electrical stimulation of the vagus nerve (VNS) shows efficacy in ameliorating pathology in neurodegenerative diseases. Our objective was to investigate the impact and underlying mechanism of VNS for cognitive impairment in a rat model of TBI.

Methods: Male rats were implanted with VNS electrodes on the left VN 1 week prior to controlled cortical impact. Mitochondrial permeability transition pore blocker cyclosporin A (CsA) and stimulator of interferon genes (STING) agonist 2'3'-cGAMP were delivered by intranasal administration or intraventricular injection. Post-VNS assessments included Morris water maze, Nissl staining, hematoxylin and eosin staining, Western blotting, quantitative polymerase chain reaction, mitochondrial membrane potential, and enzyme-linked immunosorbent assay.

Results: We found that VNS treatment significantly improved cognitive impairment, increased mitochondrial membrane potential, reduced accumulation of cytosolic mitochondrial DNA, attenuated cyclic GMP-AMP synthase (cGAS)-STING pathway, suppressed nucleotide-binding domain, leucine-rich-containing family, pyrin domain-containing-3 (NLRP3) inflammasome activation, and partially reversed hippocampus neuronal damage and loss caused by TBI. However, 2'3'-cGAMP delivery significantly abrogated these effects of VNS. In addition, CsA also showed neuroprotective effects, including improved cognitive impairment, decreased levels of cGAS, phosphorylated STING, and suppressed the expressions of NLRP3 inflammasome and pyroptosis-pertinent components containing cleaved Caspase-1, ASC, and N-terminal Gasdermin D. CsA also inhibited interleukin-1β and interleukin-18 proinflammatory cytokine concentration.

Conclusions: Stimulation of the VN attenuates the pyroptosis and neuroinflammatory cascades in the rat of the TBI model by regulating the mitochondrial DNA/cGAS/STING /NLRP3 pathway.

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.