Search Results (45)

Background/Objectives: Clinical outcomes after traumatic brain injury (TBI) remain difficult to predict, highlighting the need for more sensitive diagnostic and prognostic biomarkers, particularly in polytrauma. This study aimed to identify TBI-specific proteomic signatures in plasma and extracellular vesicles (EV)-enriched fractions of critically injured trauma patients. Methods: Seventy-five severely injured adult trauma patients (ISS ≥ 16) were included: isolated severe TBI (TBI; AIS_head ≥ 4, other AIS ≤ 1, n = 23), polytrauma with TBI (PT-TBI; AIS_head ≥ 4, n = 22), and polytrauma without TBI (PT; AIS_head = 0, n = 30). 24 age- and sex-matched healthy volunteers served as controls. Neat plasma and EV-enriched fractions were profiled using HPLC-MS/MS. Differentially expressed proteins (DEP) were analyzed bioinformatically, and associations with clinical parameters were assessed using Spearman’s correlation. Results: The EV-enriched plasma fraction yielded more DEPs than neat plasma (846 vs. 258). Most DEPs were linked to polytrauma, with plasma reflecting metabolism and EVs showing translation and protein catabolism signatures. Among TBI-context proteins, EV-associated NRCAM and AQR and plasma IGHV1-69D, MASP1, PON1, and IGFBP7 remained significantly associated with TBI after adjustment for confounder. Notably, only EV-associated proteins correlated with injury-related clinical parameters. AQR negatively correlated with GCS (r = −0.51, p < 0.0001), while elevated NRCAM, AQR, and plasma MASP1 were associated with neurological deterioration and neurosurgical intervention. Conclusions: EV-enriched plasma proteomics enhances biomarker discovery in polytrauma, revealing distinct pathways and greater sensitivity than whole plasma. While most changes reflect systemic injury, EV-associated NRCAM and AQR, along with plasma MASP1, show TBI-specific associations with neurological status, highlighting their potential as candidate TBI biomarkers for further study. Full article

Background: While trefoil factor 3 (TFF3) has been linked to cardiovascular disease, its role in peripheral artery disease (PAD) remains largely unexplored. In this prospective study, we assessed three pre-selected circulating biomarkers and found that TFF3 demonstrated the strongest association with the presence of PAD. Building on this finding, we integrated plasma TFF3 concentrations with clinical characteristics to construct predictive models aimed at identifying individuals with PAD and estimating their risk of major adverse limb events (MALE) over a two-year follow-up period. Methods: A total of 476 individuals were prospectively recruited, including 312 patients with PAD and 164 controls without PAD. At study entry, circulating concentrations of TFF3, oncostatin M (OSM), and brain-derived neurotrophic factor (BDNF) were quantified, and all participants were subsequently monitored for a two-year period. The primary endpoint was the occurrence of MALE within two years, comprising acute limb ischemia, major amputation, or lower extremity revascularization by either open surgical or endovascular approaches. PAD diagnosis served as the secondary outcome and was established by an ankle–brachial index (ABI) ≤ 0.9 or toe–brachial index (TBI) ≤ 0.67 in the presence of reduced or absent pedal pulses. For predictive model development, the cohort was randomly divided into training (70%) and testing (30%) sets. A random forest algorithm incorporating clinical variables and plasma TFF3 levels was developed and optimized using 10-fold cross-validation. Model discrimination was quantified using the area under the receiver operating characteristic curve (AUROC). For prognostic evaluation, patients were classified into low- and high-risk groups based on the optimal ROC-derived probability threshold of 0.60, and MALE-free survival between groups was assessed using Cox proportional hazards regression. Results: Among the three candidate biomarkers evaluated, only TFF3 demonstrated a significant association with PAD. Patients with PAD exhibited higher circulating TFF3 concentrations than those without PAD (7.27 ± 3.36 vs. 5.89 ± 2.67 pg/mL; p < 0.001), whereas OSM and BDNF showed no significant differences between groups. Over the two-year follow-up period, MALE occurred in 28 patients (9%). Predictive models combining plasma TFF3 measurements with clinical variables achieved strong performance for both PAD detection and 2-year MALE risk estimation, yielding AUROCs of 0.79 and 0.85, respectively. Furthermore, patients classified as high risk by the model experienced a significantly increased hazard of MALE during follow-up (HR 1.12, 95% CI 1.10–1.19; p = 0.003). Variable importance analysis revealed that TFF3 was the most influential predictor of MALE, followed by age and smoking history. Conclusions: Combining plasma TFF3 levels with readily available clinical characteristics enabled the development of a predictive model with good discriminatory ability for both PAD diagnosis and estimation of 2-year MALE risk. Such an approach may enhance risk stratification by identifying patients at elevated risk earlier in their disease course, thereby informing decisions related to vascular testing, referral for specialist evaluation, and implementation of targeted treatment strategies. Full article

Background: Traumatic brain injury (TBI) remains a major cause of neurological morbidity and mortality. Mitochondria, being embedded as one of the key organelles disrupted after injury, play a central role in regulating neuronal metabolism, oxidative balance, and cell survival, hence the growing interest in their role after TBI. Methods: We present a narrative review of the literature on mitochondrial dysfunction after TBI to highlight the potential role in diagnosis, monitoring, prognostication and treatment strategies. Following SANRA guidelines we conducted a synthesis of 159 selected references published between 1997 and 2026, including 70 references published from 2020 onward. Results: Mitochondrial dysfunction underpins bioenergetic failure through the impairment of critical regulatory pathways, including oxidative phosphorylation, dysregulated reactive oxygen species production, and dysregulated calcium handling. These changes trigger downstream processes of oxidative damage, epigenetic and proteomic remodeling, and activation of regulated cell death pathways such as apoptosis, necroptosis, and ferroptosis in the context of an inflammatory milieu. As such, mitochondrial-derived molecules (such as mitochondrial DNA and microRNA) are emerging candidate biomarkers of TBI severity and prognosis. Additionally, therapeutic approaches under investigation include inhibition of the mitochondrial permeability transition pore, mitigation of mitochondrial oxidative stress using targeted antioxidants, restoration of NAD⁺-dependent metabolic pathways, and metabolic support through ketogenic interventions. Conclusions: Mitochondrial biology is advancing our understanding of TBI and offers a promising framework for improving its management. Full article

Severe traumatic brain injury (TBI) is a leading cause of mortality and long-term disability in polytrauma (PT) patients, and its clinical outcome remains difficult to predict due to clinical heterogeneity and secondary injury mechanisms. Current diagnostic and prognostic approaches based on clinical assessment and imaging are limited, particularly in PT where neurological evaluation is often impaired. This study aimed to compare plasma- and extracellular vesicle (EV)-associated microRNA (miRNA) signatures in patients with severe TBI and healthy controls to identify their potential as minimally invasive biomarkers and to improve understanding of molecular responses. For profiling circulating miRNAs, blood samples were collected at ≤3 h and at 48 h after admission. In the screening phase, plasma samples of n = 15 patients with severe isolated TBI (Abbreviated Injury Scale [AIS]Head ≥ 4, all other AIS ≤ 1) and n = 15 age- and sex-matched healthy controls were pooled (n = 5/pool) and subjected to next-generation sequencing (NGS). In the following validation phase, n = 25 severely injured trauma patients (Injury Severity Score [ISS] ≥ 16) were enrolled and stratified into PT without TBI (PT; AISHead = 0; n = 13) and isolated TBI (n = 12). Differentially expressed candidate miRNAs identified in the screening phase were validated in individual plasma and EV samples using reverse transcription droplet digital polymerase chain reaction (RT-ddPCR). Functional enrichment and pathway analyses were performed using miRNet. NGS identified more differentially expressed miRNAs in plasma (ER: 103; 48 h: 65) than in EVs (Emergency Room [ER]: 14; 48 h: 32). Functional enrichment analysis indicated associations with pathways related to cellular stress, senescence, growth factor signaling, transcriptional regulation, and apoptosis. In validation, 12 of 16 plasma and 10 of 15 EV-miRNAs were confirmed as differentially expressed in TBI patients; among these, three plasma and four EV miRNAs differed between TBI and PT. After adjustment, most plasma miRNAs were associated with injury severity rather than group status. EV miRNA profiles showed heterogeneous patterns, with miR-1469 associated with TBI group status in adjusted analysis, while miR-1237-5p was linked to injury severity and other EV miRNAs showed no consistent group-specific effects. Plasma miRNAs mainly correlated with systemic injury markers, whereas EV miR-1469 showed a moderate association with the Glasgow Coma Scale (GCS). Overall, circulating miRNA profiles after injury appear to be predominantly influenced by systemic trauma severity rather than TBI-specific effects. Plasma miRNAs mainly reflected general injury burden, whereas EV-associated miRNAs showed more heterogeneous patterns, with miR-1469 emerging as a candidate associated with TBI after adjustment for clinical covariates. These findings suggest that EV-derived miRNAs, particularly miR-1469, may provide more targeted signals related to brain injury and warrant further investigation. Full article

Traumatic brain injury (TBI) is a major cause of death and disability, mainly in persons under 45 years of age and it remains clinically challenging due to its heterogeneous pathophysiology and unpredictable course. Except from the initial mechanical damage, secondary injury —largely driven by neuroinflammation—plays a critical role in outcome and extent of recovery. Cytokines are central mediators of this immune response and have therefore been extensively studied as potential biomarkers for TBI diagnosis, need of imaging and prognosis. Among pro-inflammatory cytokines, IL-1β is rapidly upregulated after TBI and contributes to blood–brain barrier disruption and secondary damage. Furthermore, experimental studies suggest that IL-1 inhibition could be neuroprotective. IL-6 is up to date the most extensively studied cytokine and shows strong associations with injury severity, neuroimaging abnormalities, mortality and long-term functional outcomes across multiple adult and pediatric studies. Nevertheless, results vary depending on the biological compartment and timing. Anti-inflammatory IL-10 levels correlate with injury severity and has shown promise in distinguishing CT-positive from CT-negative mild TBI patients, potentially reducing unnecessary imaging, though findings are inconsistent. Other cytokines, including IL-17, TNF-α, IL-8, IL-9, and IL-15, have been correlated to post-traumatic neuroinflammation and may have diagnostic or prognostic value. Overall, IL-6 and IL-10 currently appear to be the most promising cytokine as biomarkers, however future research should focus on standardized cytokines assessment methods and possible use of multimarker panels. Full article

Background/Objectives: Prognostication in traumatic brain injury (TBI) remains challenging. The urine-to-serum osmolality (U/S) ratio may reflect hypothalamic–pituitary axis integrity, a critical but underexplored prognostic domain. We investigated whether the U/S ratio provides early prognostic value and enhances prediction when combined with conventional severity markers. Methods: This retrospective study included 128 adult TBI patients admitted to a neurosurgical intensive care unit (ICU) with simultaneous osmolality measurements within 6 h of admission. The primary outcome was ICU mortality; the secondary outcome was poor neurological outcomes (Glasgow Outcome Scale 1–3). Results: ICU mortality was 14.1% (18/128), and poor neurological outcome occurred in 41.8% (46/110). Non-survivors had significantly lower U/S ratios than survivors (1.09 ± 0.58 vs. 1.70 ± 0.68, p < 0.001). For ICU mortality, U/S ratios (AUC = 0.803) showed similar discriminative ability to GCS (AUC = 0.806). For poor neurological outcomes, the U/S ratio (AUC = 0.768) significantly outperformed both GCS (AUC = 0.641, p = 0.038) and the Acute Physiology and Chronic Health Evaluation (APACHE) II score (AUC = 0.553, p < 0.001). Combining the U/S ratio with GCS improved mortality prediction (AUC = 0.890), as did combinations with the APACHE II score (AUC = 0.847). The U/S ratio remained independently associated with ICU mortality and poor neurological outcomes after adjusting for GCS or APACHE II scores. Quartile analyses revealed a dose–response relationship, with ICU mortality of 34.4% in Q1 versus 3.1% in Q4 (p for trend < 0.001). Prognostic value was preserved in patients receiving osmotic therapy (n = 86). Conclusions: The U/S ratio is a simple, readily available biomarker that independently predicts mortality and poor neurological outcomes in TBI patients. Particularly for neurological outcome predictions, it outperforms GCS or the APACHE II score alone. Combined with established severity scores, it may serve as a practical bedside tool reflecting hypothalamic–pituitary function in neurocritical care. Full article

Despite significant advances in neurosurgical and critical care, traumatic brain injury (TBI) remains a major cause of morbidity and mortality. Surgical treatment of intracranial hemorrhagic lesions can only target the primary mechanical injuries and their immediate consequences but fails to address the biochemical pathological cascade that unfolds during the second injury. This review synthesizes current knowledge regarding the use of several biomarkers in diagnosis and prognosis assessment. A structured literature search was conducted by querying the PubMed database. Articles evaluating diagnostic and prognostic biomarkers in adult TBI were screened according to Prisma guidelines, and data regarding biomarkers type, cut-off values, and correlations with the outcome were extracted and summarized. Among Central Nervous System (CNS)-Specific markers, S100 calcium-binding protein (S100B) emerged as a remarkably strong negative predictor for Computed Tomography (CT)-visible intracranial lesions (NPV = 97.3–100%), whereas glial fibrillary acidic protein (GFAP) yielded both high NPV and brain specificity. Coagulation parameters such as the international normalized ratio (INR) and fibrinogen were independently correlated with mortality and unfavorable outcomes. Fibrinogen displayed a bidirectional relationship with increased mortality risk at both low (<2 g/L) and high (>4.5 g/L) values. In conclusion, biomarkers quantify the otherwise invisible progression of secondary traumatic brain injury that persists even after successful surgery. Full article

Traumatic brain injury (TBI) is a major global health concern and a leading cause of mortality and disability. Head computed tomography (CT) remains indispensable for the detection of intracranial hemorrhage; however, its indiscriminate use in mild trauma increases radiation exposure, cumulative oncogenic risk, and healthcare costs. Consequently, there is growing interest in tools capable of improving sensitivity in mild or early-stage TBI. Protein-based biomarkers are promising complements to conventional assessment. Molecules such as glial fibrillary acidic protein (GFAP), ubiquitin C-terminal hydrolase L1 (UCH-L1), S100 calcium-binding protein B (S100B), and neurofilament light chain (NfL) reflect astroglial activation, neuronal injury, and axonal damage, enabling objective evaluation of neurotrauma. Beyond protein biomarkers, metabolomic and lipidomic approaches capture alterations associated with early metabolic distress, oxidative stress, mitochondrial dysfunction, and membrane disruption following TBI. High-resolution mass spectrometry studies have identified reproducible metabolite and lipid signatures correlating with injury severity and functional outcomes. Longitudinal profiling further reveals dynamic metabolic trajectories that distinguish secondary injury progression from stabilization, supporting predictive modeling and risk stratification. Together, these advances pave the way toward precision medicine in neurotrauma. Nevertheless, variability in assay performance and sampling timing continues to limit widespread clinical adoption. Future research should prioritize methodological standardization, analytical validation, and the integration of multi-omic data with machine learning–based predictive models. Full article

Traumatic brain injury (TBI) is a major global health problem and a leading cause of long-term neurological disability. TBI produces a spectrum of persistent symptoms, including cognitive impairment, mood and behavioral disturbances, sleep disruption, fatigue, and autonomic dysregulation. Chronic pain is among the most debilitating sequelae, affecting physical, emotional, and social functioning. The etiology of post-TBI pain is multifactorial, arising from initial structural and biochemical injury to the nervous system, maladaptive neuroplastic changes, neuroinflammation, and psychological comorbidities that amplify pain perception and chronicity. This review explores the complex pathophysiology of post-TBI pain and outlines a multidisciplinary framework for management. Pain syndromes are classified according to the International Association for the Study of Pain’s mechanistic framework as nociceptive pain (resulting from tissue injury and inflammation), neuropathic pain (due to lesion or disease of the somatosensory nervous system), and nociplastic pain (arising from altered nociceptive processing without clear evidence of tissue or nerve damage). Many patients exhibit mixed pain phenotypes driven by neuroinflammation and central sensitization. Pharmacologic approaches, including anti-inflammatory agents, anticonvulsants, and antidepressants, require cautious titration due to TBI-related comorbidities. Equally essential are non-pharmacologic strategies such as physical and occupational therapy, cognitive behavioral therapy, and neuromodulation techniques, which target both biomechanical and psychosocial contributors. Emerging innovations, machine learning for prognostication, blood biomarkers for structural injury, and neuro-reparative agents, represent the next frontier in personalized management. Effective care for post-TBI pain requires an integrated strategy that combines mechanistic classification, multidisciplinary treatments, and advancing diagnostic technologies. Full article

Background/Objectives: Traumatic brain injury (TBI) is a major global cause of death and disability, with long-term cognitive, behavioral, and functional consequences. Despite its high burden, management is complicated by heterogeneous presentations and limited evidence. This review summarizes recent advances in monitoring, therapeutic strategies, neuroprotection, and rehabilitation, while highlighting future directions toward individualized and globalized care. Methods: This paper is a narrative review of clinical trials, systematic reviews, and observational studies, focusing on invasive and non-invasive monitoring, pharmacologic and non-pharmacologic interventions, neuroprotective agents, stem cell therapy, and advanced rehabilitation modalities. Results/Findings: Our review focuses on emerging monitoring techniques, including brain tissue oxygenation, cerebral microdialysis, and multimodal strategies, that provide detailed insights but lack standardized application. Interventions such as anti-inflammatory agents, hypothermia, hyperosmolar therapies, and metabolic suppression show mixed efficacy, with few therapies supported by high-level evidence. Novel agents like erythropoietin and progesterone demonstrate neuroprotective potential in preclinical models but remain inconclusive in clinical trials. Stem cell therapies and extracellular vesicle approaches are promising in early studies. Rehabilitation is expanding with virtual reality, robotics, and neurostimulation to promote neuroplasticity. Personalized medicine approaches incorporating biomarkers and machine learning may refine prognostication and guide therapy. Global inequities persist, particularly in low-resource settings. Conclusions: TBI care is shifting toward individualized, multimodal, and technology-driven strategies. While emerging therapies show promise, high-quality randomized trials and global implementation strategies are needed to improve outcomes and reduce disparities. Full article

Background: Amino acid biomarkers have a crucial influence on our understanding of brain injury mechanisms, and their plasma concentrations may indicate neurological damage and recovery patterns. Pediatric mild traumatic brain injury (mTBI) assessment particularly benefits from such molecular indicators, as clinical presentations can be subtle and variable. However, current diagnostic and prognostic tools lack reliable biochemical markers that can track the temporal evolution of injuries and recovery. Methods: We conducted a prospective longitudinal cohort study involving 36 pediatric mTBI patients and 44 controls to characterize the temporal evolution of key amino acids and their derived indices. Blood samples were collected at 3, 6, 12, and 24 h and at 7, 14, and 28 days post-injury, with amino acids quantified using high-performance liquid chromatography. Results: Our analysis revealed significant temporal changes in glutamate, glutamine, and glycine concentrations, with glutamate peaking at day 7 before declining, while glutamine showed steady increases throughout. The GLN/GLU ratio demonstrated an early excitatory imbalance followed by astrocytic compensation, and the GLX ratio indicated progressive recovery. Conclusions: These patterns represent continuous neurochemical processes involving excitotoxicity and glial regulation, suggesting potential utility as biomarkers for mTBI diagnosis and monitoring. While further validation using larger cohorts is needed, these findings provide compelling evidence of the efficacy of using amino acid profiles to track pediatric mTBI progression and recovery. Full article

Mild traumatic brain injury (mTBI) remains a clinical challenge, particularly in cases with normal computed tomography (CT) findings but persistent or evolving symptoms. Conventional diagnostic approaches relying solely on clinical criteria and neuroimaging often lack adequate sensitivity and may lead to unnecessary radiation exposure. Recent advances in biomarker research have identified several blood-based proteins such as glial fibrillary acidic protein (GFAP), ubiquitin carboxy-terminal hydrolase L1 (UCH-L1), S100 calcium-binding protein B (S100B), Tau protein, neuron-specific enolase (NSE), and neurofilament light chain (NFL) as potential tools for improving diagnostic precision and guiding clinical decisions. In this study, we synthesize current evidence evaluating the diagnostic and prognostic utility of these biomarkers using sensitivity, specificity, negative predictive value (NPV), and area under the receiver operating characteristic curve (AUC). GFAP and UCH-L1 have shown high sensitivity in detecting intracranial lesions and are now FDA-cleared for emergency department triage within 12 h of injury. While S100B remains widely investigated, its low specificity limits its application beyond select clinical scenarios (i.e., in patients without polytrauma). Additionally, Tau, NSE, and NFL are emerging as prognostic markers, with studies suggesting associations with persistent symptoms and long-term neurocognitive outcomes. Overall, the integration of biomarker-based data into clinical workflows may enhance early mTBI diagnosis, reduce reliance on imaging, and enable individualized follow-up and prognostic stratification. Future research should refine optimal sampling windows and explore multimarker panels to maximize diagnostic and prognostic performance. Full article

Diffuse axonal injury (DAI) is one of the most severe consequences of traumatic brain injury (TBI), characterized by widespread axonal damage in the cerebral white matter. DAI plays a crucial role in determining clinical outcomes, significantly contributing to long-term disability and mortality in severe cases. Despite advancements in neuroscience and clinical management, the diagnosis and prognosis of DAI remain challenging due to its complex pathophysiology and the difficulty of detecting axonal damage in its early stages. This study critically analyzes the clinical and post-mortem methodologies used to assess DAI, highlighting their strengths and limitations. Traditional histopathological grading systems provide valuable insights into disease progression, yet their correlation with long-term functional outcomes remains controversial. Advanced neuroimaging techniques, such as diffusion-weighted MRI, have improved lesion detection, although their routine clinical application is still limited. Additionally, emerging approaches involving biomarkers and artificial intelligence-based models hold promise for enhancing diagnostic accuracy and prognostic predictions. By synthesizing current knowledge on DAI, this work aims to outline a comprehensive framework for improving diagnosis and outcome assessment. Furthermore, it seeks to foster collaboration among clinicians and researchers, ultimately advancing the understanding of DAI and refining strategies to improve patient care. Full article

Background: Traumatic brain injury (TBI) remains a significant contributor to global mortality and long-term neurological disability. Accurate prognostic biomarkers are crucial for enhancing prognostic accuracy and guiding personalized clinical management. Objective: This review assesses the prognostic value of arterial spin labeling (ASL), a non-invasive MRI technique, in adult and pediatric TBI, with a focus on quantitative cerebral blood flow (CBF) and arterial transit time (ATT) measures. A comprehensive literature search was conducted across PubMed, Embase, Scopus, and IEEE databases, including observational studies and clinical trials that applied ASL techniques (pCASL, PASL, VSASL, multi-PLD) in TBI patients with functional or cognitive outcomes, with outcome assessments conducted at least 3 months post-injury. Results: ASL-derived CBF and ATT parameters demonstrate potential as prognostic indicators across both acute and chronic stages of TBI. Hypoperfusion patterns correlate with worse neurocognitive outcomes, while region-specific perfusion alterations are associated with affective symptoms. Multi-delay and velocity-selective ASL sequences enhance diagnostic sensitivity in TBI with heterogeneous perfusion dynamics. Compared to conventional perfusion imaging, ASL provides absolute quantification without contrast agents, making it suitable for repeated monitoring in vulnerable populations. ASL emerges as a promising prognostic biomarker for clinical use in TBI. Conclusion: Integrating ASL into multiparametric models may improve risk stratification and guide individualized therapeutic strategies. Full article

Background/Objectives: Nutritional support in neurosurgical patients is challenging due to severe brain injury, neurological disease, or post-surgical complications. This study aimed to assess outcomes of long-term enteral nutrition via endoscopic gastrostomy (PEG) in these patients over a 22-year period. Methods: A single-center retrospective (2001–2023) study was conducted on patients referred for PEG. Included patients presented severe traumatic brain injury (TBI), stroke, brain tumor, or other neurosurgical conditions. Demographic, anthropometric, and clinical data were collected. Results: A total of 196 patients were included (105 men); 57% were under 65 years. The main diagnoses were stroke (41.8%), TBI (35.2%), and brain tumors (19.9%). The median time from diagnosis to PEG was 94 days. At the time of PEG, only 38.5% were underweight. Outcomes: A total of 132 deaths (75.4%) occurred, while 21 patients resumed oral feeding (10.7%), 22 patients remained PEG-fed (12.6%), and 21 patients were lost to follow-up (10.7%). Most surviving PEG-fed patients had experienced stroke (77%). Median post-PEG survival was 11.5 months and 88% survived >1 month. Higher albumin, transferrin, and cholesterol levels at the time of PEG were associated with longer survival. Albumin (p < 0.001) and transferrin (p < 0.01) were significantly associated with reduced short-term mortality. Conclusions: Despite limited overall survival, reflecting the clinical severity of the diseases, most patients were adequate survivors, and PEG-feeding proved to be appropriate and useful for neurosurgical patients. While most patients had normal-to-high BMI, low serum biomarkers reflected acute illness. Higher serum albumin level was associated with better outcomes, supporting its potential prognostic value. Full article