Neurocritical Care最新文献

Background: The receptor tyrosine kinase AR4-type receptor in erythropoietin-producing hepatocellular carcinoma (EphA4) has been linked to disruption of the blood-brain barrier (BBB) and hemorrhagic transformation after acute ischemic stroke. Here, we explored whether EphA4 may be involved in parenchymal hematoma (PH) after ischemic stroke.

Methods: Data were analyzed from patients who were admitted to West China Hospital of Sichuan University within 48 h of stroke onset between January 2017 and December 2019. EphA4 levels in serum were measured within 24 h after admission, and baseline computed tomography perfusion was performed immediately upon admission. Potential relationships of EphA4 levels or ipsilateral flow extraction product (FED) with occurrence of PH were explored using logistic regression.

Results: Of the 578 patients (337 men) analyzed, who were a median age of 69 years old, 56 (9.69%) developed PH. Serum EphA4 levels were higher in patients with PH than in those without PH (44.96 vs. 37.86 ng/mL, P = 0.036). After adjustment for confounders, higher serum EphA4 levels (≥ 32.21 ng/mL) were significantly associated with PH (odds ratio [OR] 3.84, 95% confidence interval [CI] 1.66-8.90, P = 0.002). Among the 230 patients in whom brain perfusion was analyzed using computed tomography perfusion, ipsilateral FED was significantly associated with PH after adjusting for confounders (OR 2.43, 95% CI 1.63-3.63, P < 0.001). The two parameters of EphA4 level and ipsilateral FED interacted in their association with PH (P_interaction = 0.037): higher EphA4 level was associated with PH in those with higher ipsilateral FED (OR 1.04, 95% CI 1.01-1.07, P = 0.006), not in those with lower FED.

Conclusions: Elevated EphA4 levels in serum are associated with higher risk of PH after ischemic stroke, especially among patients showing greater permeability of the BBB as reflected in higher ipsilateral FED on computed tomography perfusion.

Background: Early postoperative cerebral infarction (ePCI) following spontaneous intracerebral hemorrhage (ICH) is a severe complication. This study aimed to develop and validate a cisterns and cortical sulci effacement (CCSE) score for predicting ePCI and to compare its predictive performance with that of established clinical scoring systems.

Methods: Data on spontaneous ICH from two centers were retrospectively analyzed. The visibility of 10 cisterns and the left/right cortical sulci was assessed on preoperative computed tomography scans (scored as 0 = visible, 1 = not visible), and the total sum constituted the CCSE score. Interrater and intrarater reliability were assessed using Cohen's κ coefficient. Logistic regression and subgroup analyses were conducted to explore the association between CCSE and ePCI. Predictive performance was evaluated using receiver operating characteristic curves, and restricted cubic splines were used to assess potential nonlinearity.

Results: From a cohort of 3,968 consecutive patients with spontaneous ICH from May 2015 to September 2022, 637 individuals (mean age 57.3 years [SD 12.5]; 71.3% male) were included in the final analysis, with 71 (11.1%) developing ePCI. The CCSE score showed excellent intrarater (κ = 0.93) and interrater (κ = 0.86) reliability and was strongly associated with ePCI risk (odds ratio 2.14 per point, 95% confidence interval [CI] 1.80-2.53, p < 0.001). Subgroup analyses confirmed the robustness of the association. The CCSE score outperformed traditional scores, including the Glasgow Coma Scale, Original Intracerebral Hemorrhage Scale, and Modified Intracerebral Hemorrhage A score (area under the curve = 0.91; 95% CI 0.86-0.95). Additionally, a nonlinear relationship was identified (p for nonlinearity = 0.002), with a CCSE score threshold ≥ 4.02 for risk discrimination.

Conclusions: The CCSE score may be a reliable and practical tool for predicting ePCI in patients with supratentorial ICH.

Background: Intracranial compliance (ICC) reflects the balance among intracranial volume components. Recent technological advances enable continuous, noninvasive assessment of ICC in neurocritical care settings. In this study, we aimed to correlate noninvasive ICC parameters derived from intracranial pressure (ICP) waveform morphology with the established amplitude-pressure index (RAP index), which is calculated using invasive ICP monitoring.

Methods: Patients with traumatic brain injury underwent ventricular ICP monitoring. Simultaneously, ICP values and waveform characteristics were recorded using an external skull microdynamics sensor (brain4care) that provides surrogate waveform parameters, including the P2/P1 ratio and time-to-peak (TTP). The RAP index was calculated using dedicated software based on ICP values and pulse amplitude and was used to categorize patients into three groups: (1) adequate ICC, (2) compromised ICC, and (3) exhausted ICC. Noninvasive parameters (P2/P1 ratio and TTP) were then analyzed in relation to RAP index groupings.

Results: A total of 61 patients were included. Group 1 (adequate ICC) had a median ICP of 12.3 ± 5.4 mm Hg, a P2/P1 ratio of 1.06 ± 0.3, and a TTP of 0.18 ± 0.09 s. Group 2 (compromised ICC) had a median ICP of 13 ± 6.4 mm Hg, a P2/P1 ratio of 1.15 ± 0.32, and a TTP of 0.23 ± 0.07 s. Group 3 (exhausted ICC) had a median ICP of 19.45 ± 5.9 mm Hg, a P2/P1 ratio of 1.31 ± 0.26, and a TTP of 0.25 ± 0.05 s. Regression analysis revealed a statistically significant association between the noninvasive parameters and RAP index-based ICC classification (p < 0.0001).

Conclusions: This study demonstrates a significant correlation between the RAP index and noninvasive ICP waveform-derived parameters, such as the P2/P1 ratio and TTP. These findings suggest that such noninvasive measures may serve as reliable indicators of ICC status. The critical ICP cut-off per RAP was 19.45 mmHg, below the current threshold for therapy escalation according to TBI guidelines. Although further prospective validation is required, this approach has the potential to facilitate earlier intervention before ICC deterioration and enable noninvasive monitoring, possibly improving outcomes in neurocritical care.

Trial registration: NCT03144219. Registered 15 June 2017, http://www.

Clinicaltrials: gov/NCT03144219 .

Clinical trial registration: ClinicalTrials.gov identifier: NCT03144219.