Frontiers in Neurology最新文献

Background: Patient-reported outcome measures (PROMs) are increasingly used for symptom monitoring and care delivery, yet their prognostic value for identifying patients at higher risk for mortality in neurological populations is unclear. This systematic review evaluated whether PROMs predict mortality and/or survival in adults with neurological conditions.

Methods: We systematically searched MEDLINE, Embase, and the Cochrane Central Register of Controlled Trials (January 2002-November 2024) for studies incorporating PROMs into mortality or survival prediction models across 10 neurological conditions: motor neuron disease, diabetic neuropathy, nervous system cancers, Alzheimer's and other dementias, Guillain-Barré syndrome, epilepsy, headache, multiple sclerosis, Parkinson's disease, and stroke. Screening, data extraction, and risk-of-bias assessment followed the CHARMS and PRISMA guidelines. Findings were descriptively summarized.

Results: Of 6,218 abstracts reviewed, 49 studies met the inclusion criteria. Most evaluated stroke (n = 16), nervous system cancers (n = 14), or motor neuron disease (n = 9). None evaluated headache, diabetic neuropathy, Guillain-Barré syndrome, or epilepsy. Of the included studies, 26 used generic PROMs, 19 used condition-specific PROMs, and 4 included both. Across conditions, PROMs independently predicted mortality in three-quarters of studies, with the strongest evidence observed in nervous system cancers and motor neuron disease. By instruments, EORTC QLQ in brain cancers and SF-36 in stroke showed the most consistent prognostic utility. Among studies with mixed findings by domain, physical health components were more likely to predict mortality than emotional components.

Conclusion: PROMs independently predict mortality in several neurological conditions, though prognostic value varied by condition and instrument type. Future studies should evaluate their additive value and feasibility for integration into prognostic models in routine care.

Objective: To investigate the correlation between the neutrophil-to-apolipoprotein A1 ratio (NAR) and disease severity, long-term prognosis, and risk of relapse in patients with anti-N-methyl-D-aspartate receptor (anti-NMDAR) encephalitis.

Methods: This study included 125 patients with anti-NMDAR encephalitis as a retrospective cohort. Baseline clinical, laboratory, and imaging data was collected. Spearman's correlation analysis was used to evaluate correlations between NAR, disease severity, and C-reactive protein (CRP) levels. Logistic regression and Cox proportional hazards models were used to analyze independent associations between NAR and poor prognosis and recurrence, respectively. The predictive performance of NAR was evaluated using receiver operating characteristic (ROC) curves. Mediation analysis was used to explore potential pathways of action. Sensitivity and subgroup analyses were performed to verify the reliability of the results.

Results: The final modified Rankin's score (mRS) score and recurrence rate were significantly higher in the high-NAR group than in the low-NAR group (both p < 0.05). NAR significantly and positively correlated with the initial mRS score (r = 0.308, p < 0.001) and CRP level (r = 0.486, p < 0.001). Multivariate analysis showed that NAR was an independent risk factor for poor prognosis (OR = 1.19, 95% confidence interval (CI): 1.02-1.38, p = 0.026) and recurrence (Hazard ratio (HR) = 1.13, 95% CI: 1.02-1.24, p = 0.017). ROC curve analysis showed that the area under the curve (AUC) for predicting poor prognosis with NAR was 0.724, the optimal cutoff value was 10.34, and the specificity was 92.2%. Mediation analysis showed that disease severity partially mediated the relationship between NAR and prognosis (effect rate, 41.7%).

Conclusion: NAR is an independent predictor of poor disease prognosis and risk of recurrence in patients with anti-NMDAR encephalitis. Its high specificity helps identify high-risk patients early and accurately, giving this biomarker long-term prognostic value.

Purpose: This study aimed to investigate the diagnostic value of somatosensory evoked potentials (SEPs) in patients with paroxysmal sympathetic hyperactivity (PSH) and to identify independent predictors of the condition.

Methods: A retrospective cohort study was conducted on 123 patients with prolonged disorders of consciousness (PDOC) admitted to the Critical Care Rehabilitation Department of Nanjing Jiangning Hospital between August 2022 and August 2024. Patients were classified into PSH-positive (PSH+) and PSH-negative (PSH-) groups according to the Paroxysmal Sympathetic Hyperactivity Assessment Measure (PSH-AM). Demographic, clinical, and SEPs parameters were collected. Univariate and multivariate logistic regression analyses were employed to examine the association between these variables and PSH. The predictive performance was evaluated using receiver operating characteristic (ROC) curve analysis.

Results: A total of 123 patients with prolonged disorders of consciousness were enrolled in the study. Among these, 34 patients (27.64%) were classified into the PSH + group and 89 patients (72.36%) into the PSH - group. Multivariate logistic regression analysis identified younger age (OR = 0.96, 95% CI: 0.92-0.99, p = 0.02), male patient (OR = 0.28, 95% CI: 0.09-0.75, p = 0.02), and reduced N20-P25 amplitude (OR = 0.34, 95% CI: 0.13-0.70, p = 0.01) as independent predictors of PSH. Using a cut-off value of 1.19 μV for the N20-P25 amplitude, the area under the curve (AUC) for discriminating PSH was 0.811 (95% CI: 0.71-0.912), yielding a sensitivity of 79.7% and a specificity of 75%. The combination of these three predictors improved the AUC to 0.846 (95% CI: 0.75-0.942). After adjusting for potential confounders, partial correlation analysis demonstrated a significant negative correlation between N20-P25 amplitude and PSH-AM score (adj. r = -0.30, p = 0.003).

Conclusion: A reduced N20-P25 amplitude may serve as an independent and objective electrophysiological biomarker for the early prediction of PSH. In combination with younger age and male patient, it contributes to the identification of high-risk populations and offers valuable guidance for clinical management.

Background: Accurate prediction of functional recovery after thoracolumbar fracture with incomplete spinal cord injury (SCI) remains challenging. We aimed to identify independent predictors and develop a validated model for 12-month functional outcome.

Methods: In this single-center, retrospective cohort study (January 2018-December 2024), consecutive adults (≥18 years) with acute T11-L2 fractures and admission American Spinal Injury Association Impairment Scale (AIS) grade B, C, or D were enrolled. Functional recovery was defined as ≥1 AIS grade improvement plus ≥10-point Spinal Cord Independence Measure version III (SCIM-III) gain at 12 months. Candidate predictors (n = 23) were selected a priori based on literature review and expert consensus. Missing data (<8% per variable) were multiply imputed (m = 20). Multivariable logistic regression with Firth's correction and backward elimination guided by Akaike Information Criterion was used. Model discrimination [optimism-corrected area under the curve (AUC) 0.87] and calibration (Hosmer-Lemeshow test) were assessed by 1,000 bootstrap resamples. Pre-specified subgroup analyses examined age, AIS grade, surgical timing and lesion length.

Results: Among 1,032 eligible patients, 206 (20.0%) achieved functional recovery. Eight predictors were independently associated: admission AIS grade (OR 4.5 per grade, 95% CI 3.5-5.8), motor score (OR 1.05 per point, 1.03-1.07), intact posterior ligamentous complex (OR 2.3, 1.6-3.2), decompression ≤ 24 h (OR 1.9, 1.4-2.7), non-smoking (OR 1.7, 1.2-2.4), Charlson Comorbidity Index = 0 (OR 1.5, 1.1-2.1), shorter intramedullary T2 lesion length (OR 0.96 per mm, 0.95-0.97) and rehabilitation intensity ≥3 h/day (OR 1.4, 1.0-1.9). The final model demonstrated an optimism-corrected AUC of 0.87 (95% CI: 0.85-0.89) and calibration characteristics with a calibration slope of 1.02, an intercept of 0.01, and a Hosmer-Lemeshow p-value of 0.18 during internal validation. Predictive effects were stronger in younger, AIS B/C patients and when surgery was performed early.

Conclusion: A parsimonious eight-factor model showed robust discrimination and satisfactory calibration in internal validation for 12-month functional recovery after thoracolumbar incomplete SCI, enabling individualized prognostication. External validation in independent multicenter cohorts is required before clinical implementation and treatment decision-making.

Aim: This study aimed to investigate the neuroprotective mechanisms of mechanical thrombectomy (MT) by evaluating its effects on the neurovascular unit (NVU) and correlating these effects with dynamic changes in serum biomarkers in patients with acute ischemic stroke (AIS).

Methods: A prospective cohort of 128 AIS patients with anterior circulation large vessel occlusion was enrolled. Participants were divided into MT (n = 68) and intravenous thrombolysis (IVT) (n = 60) groups. Serum levels of neurofilament light chain (NfL), glial fibrillary acidic protein (GFAP), interleukin-1β (IL-1β), and tumor necrosis factor-α (TNF-α) were measured at baseline (T0), 24 h (T1), and 72 h (T2) post-treatment. Clinical outcomes included recanalization rate (mTICI grade), NIHSS improvement, and 90-day modified Rankin Scale (mRS) score.

Results: The MT group showed significantly higher recanalization rates (94.1% vs. 36.7%, p < 0.001) and greater neurological improvement (median NIHSS improvement: 8 vs. 4, p < 0.001) compared to the IVT group. Serum NfL, GFAP, IL-1β, and TNF-α levels were markedly lower in the MT group at T1 and T2 (all p < 0.01). Strong correlations were identified between T2 NfL/GFAP levels and clinical outcomes (NIHSS improvement: r = -0.728/-0.663; 90-day mRS: r = 0.705/0.641; all p < 0.001).

Conclusion: Successful recanalization with MT is associated with mitigated axonal injury, astrocyte activation, and neuroinflammation, findings consistent with better preservation of NVU integrity. Serum NfL and GFAP represent promising biomarkers for predicting stroke prognosis and tailoring therapeutic strategies.

For many years, clinical and surgical pathologists have searched for explanations as to why human tissue is altered, why mass lesions are observed or why the function of an organ is disrupted. One way to answer these questions has been to assess tissue with the naked eye and/or using light- or electron-microscopes, and to compare what is seen in the lesioned tissue with what is seen in normal tissue. Lesions have then been described and named primarily by clinical and surgical pathologists. The practice of sampling tissue for assessment has led to the creation of biobanks-archives of tissue samples that have been analysed and stored for future use. With appropriate ethical approval, these tissue archives have been used extensively for research; over the past decades, our knowledge of various tissue alterations has increased almost exponentially. Below, we have briefly summarised some aspects of work carried out in the field of pathology and its limitations, with particular emphasis on brain pathology.

Objective: To investigate clinical factors associated with unstable intracranial plaques and examine the relationship between pre-stroke statin use and plaque instability using high-resolution magnetic resonance imaging (HR-MRI).

Methods: In this retrospective cross-sectional study, we enrolled 116 patients with acute anterior circulation cerebral infarction (within 7 days of onset) due to symptomatic intracranial atherosclerosis, all of whom underwent HR-MRI during hospitalization. Based on pre-stroke statin exposure, patients were grouped into a no-statin group and a statin-treatment group; based on culprit-plaque enhancement, they were further divided into enhancement and non-enhancement groups. Using HR-MRI, we systematically evaluated vascular morphometrics of the culprit artery (vessel area, lumen area, degree of stenosis, and remodeling index) and plaque activity parameters (enhancement grade).

Results: Eighteen patients (15.5%) had used statins prior to stroke onset. Compared with the no-statin group, the statin group had significantly lower total cholesterol (TC), low-density lipoprotein cholesterol (LDL-C), and non-high-density lipoprotein cholesterol (non-HDL-C) (p = 0.001, p < 0.001, p < 0.001). Infarct-pattern distributions differed between groups (p = 0.023): in the statin group, deep-only infarcts (50.0%) and cortical-only infarcts (33.3%) were more frequent, whereas large cortical/cortical-deep infarcts predominated in the no-statin group (50.0%). Plaque enhancement was less frequent in the statin group (p = 0.015) multivariable logistic regression, identified body mass index (BMI) (p = 0.021; OR = 1. 157; 95% CI: 1.023-1.309) and lack of statin use (p = 0.028; OR = 3.351; 95% CI: 1.143-9.823) as independent factors associated with plaque enhancement.

Conclusion: Pre-stroke statin therapy stabilizes intracranial plaques by lowering lipids and suppressing plaque enhancement. It independently protects against enhancement and is associated with fewer large cortical infarctions, whereas elevated BMI is an independent risk factor for enhancement.

Objective: This real-world study evaluated the efficacy and safety of telitacicept, a dual BAFF/APRIL inhibitor, in patients with generalized myasthenia gravis (MG).

Methods: In this retrospective study, 17 myasthenia gravis patients on stable background therapy received weekly subcutaneous telitacicept (160-240 mg). Efficacy was evaluated at 12/24 weeks using a primary composite endpoint (≥2-point MG-ADL and ≥3-point QMG reduction). A pre-specified Bayesian analysis, updating a conservative prior with observed data, was employed to determine the posterior probability of treatment success and its 95% credible interval. Safety and steroid-sparing effects were also assessed.

Results: Of the 15 patients evaluable for efficacy (≥12 weeks treatment), 12 (80.0%) met the composite efficacy endpoint. Significant improvements were observed: mean MG-ADL decreased from 8.0 ± 4.4 to 4.2 ± 3.1 (p < 0.01); mean QMG decreased from 13.8 ± 5.5 to 7.6 ± 4.3 (p < 0.01). A robust steroid-sparing effect was demonstrated: the mean daily prednisone dose decreased by 76.0% (10.41 ± 7.30 mg to 2.50 ± 3.21 mg, p < 0.05), with 3 patients achieving complete withdrawal. Five patients attained Minimal Symptom Expression. Bayesian analysis yielded a posterior mean efficacy rate of 66.67% (95% CrI: 49.99-81.43%), with a probability (P) of exceeding 50% efficacy at 97.49%. Treatment was well-tolerated: only mild, transient AEs occurred (one injection-site reaction, one gastrointestinal event leading to withdrawal), and no serious adverse events (SAEs) were reported.

Conclusion: This real-world study utilizing Bayesian analysis provides evidence supporting a high probability of efficacy for telitacicept in AChR-Ab-positive MG, demonstrating significant symptom improvement, substantial steroid-sparing effects, and favorable safety. These findings complement prior randomized controlled trial data and support the use of telitacicept in clinical practice. Study limitations include retrospective design and small sample size.