Neuroinflammation mediated by microglia and excessive oxidative stress are key pathological processes driving the progression of brain injuries such as intracerebral hemorrhage (ICH) and traumatic brain injury (TBI). Modulating lactate transport has emerged as a promising approach to mitigate M1 microglia polarization and alleviate neuroinflammation. Liposomal nanoparticles provide a safe and efficient platform for drug delivery. Here, we developed reactive oxygen species (ROS) responsive MiRCM nanoparticles that co-deliver monocarboxylate transporter 1 (MCT1) inhibitor AR-C155858 and a ROS-scavenging PPS core, modified with CAQK and MG1 peptides for brain injury site and microglia targeting. MiRCM nanoparticles demonstrated ROS-induced degradation and controlled drug release, effectively protecting AR-C155858 from enzymatic degradation. In vitro and in vivo experiments exhibited that MiRCM nanoparticles selectively accumulated at injured brain regions and in M1-type microglia, where they scavenged ROS, inhibited lactate efflux, suppressed M1 microglia polarization and reduced inflammatory cytokine production in ICH and TBI models. Consequently, MiRCM treatment protected neurons, reduced astrocyte activation, preserved blood-brain barrier integrity, enhanced endogenous antioxidant enzyme activities, and alleviated neurological deficits in both ICH and TBI models. RNA sequencing further confirmed downregulation of inflammatory pathways. Moreover, biosafety evaluations revealed no significant histopathological or biochemical abnormalities in major organs, indicating good biocompatibility. In summary, this study offers a new MiRCM nanoparticle that effectively modulates lactate transport and eliminates ROS to suppress microglia M1 polarization and neuroinflammation, ultimately enhancing neural protection and functional recovery after ICH and TBI.

Subthalamic nucleus deep brain stimulation (STN DBS) is an established treatment for advanced Parkinson's disease (PD), whereas the posterior subthalamic area (PSA) has been proposed as an alternative target for tremor-dominant cases. However, their underlying therapeutic mechanisms have not been directly compared. Leveraging the single-trajectory dual-target DBS technique, this work utilizes high-field 3.0 T resting-state functional magnetic resonance imaging data and spectral dynamic causal modeling to investigate the differential modulatory effects of PSA and STN stimulation on effective connectivity within both cortico-basal ganglia and cerebello-thalamo-cortical networks. We show that both PSA and STN stimulation suppress cortico-cerebellar connectivity and cortico-subthalamic hyperdirect connectivity, while enhancing STN self-inhibition. Compared with STN stimulation, PSA stimulation provides a greater reduction in cortico-cerebellar coupling but a greater increase in striato-STN connectivity. Moreover, changes in hyperdirect pathway coupling correlate with motor improvement in response to both PSA and STN stimulation. Furthermore, hyperdirect pathway and cerebellar connectivity were significantly associated with motor impairment and resting tremor severity, respectively, regardless of hemisphere or DBS target. Taken together, these findings suggest that PSA and STN stimulation share common network-level mechanisms but differ in their relative modulation of cortico-cerebellar pathway. The present study may offer theoretical guidance for future individualized DBS targeting in treating tremor-dominant PD.

Abstract Subarachnoid hemorrhage (SAH) resulted from intracranial aneurysm (IA) rupture is an especially severe form of stroke. Endothelial dysfunction represents the initiating event of IA pathogenesis. Understanding the role of endothelial cells (ECs) underlying formation of IAs is helpful to seek for pharmaceutical treatment strategy. Based on single-cell RNA sequencing, proteomics, and metabolic analysis, we discovered a change in cell population in IA samples, majorly in ECs and macrophages (MPs). Abnormal ECs exhibit senescence and death in IA samples, which is absent in the control arterial samples. Cross-analysis of multi-omics revealed that CALM1, a calcium detector involved in mechanotransduction, is downregulated in the abnormal ECs. CALM1 knockdown leads to senescence and inhibits the proliferation and maturation of ECs under turbulent flow. Through high-throughput virtual screening, this work identified compound ZC04329651 as a potent CALM1 activator in maintaining the stability of endothelial cell junctions and attenuating cellular senescence. Thus, our findings showed compound ZC04329651 up-regulate the expression of CALM1 to restore ECs, which maybe a promising pharmacological treatment strategy for IAs.

To identify specific, sensitive, and non-invasive circulating protein biomarkers that could facilitate the diagnosis of brain metastasis (BrM) and improve risk prediction for BrM among patients with non-small cell lung cancer (NSCLC). We performed data-independent acquisition mass spectrometry (DIA-MS)-based proteomic profiling of 14 tissue specimens obtained from 7 patients, together with 89 serum samples from NSCLC and NSCLC-BrM cohorts, to identify candidate biomarkers associated with BrM. A total of 12,808 proteins were identified in the tissue proteome and 6041 proteins in the serum proteome, representing an extensive proteomic analysis of lung cancer with BrM reported to date. Using integrated analyses, we identified a four-protein classifier that served as biomarkers for predicting the risk of NSCLC metastasis to the brain. Notably, PSMA4, LAP3, and LZIC were consistently downregulated in both the sera and tissues of patients with NSCLC-BrM compared with those with NSCLC without BrM. These biomarkers were subsequently validated by ELISA in an additional cohort, demonstrating high concordance with the PRM results. Immunohistochemical analyses further supported the utility of these proteins in distinguishing BrM from primary brain tumors. The integrated analysis of tissue and serum proteomics across the cohorts supports the potential value of proteomics-guided, biomarker-assisted diagnosis and risk prediction in BrM and may help enable more accurate stratification and more targeted treatment strategies.

BackgroundIntracerebral hemorrhage (ICH) represents one of the most severe forms of cerebrovascular injury, characterized by high mortality and lasting neurological dysfunction. Neural stem cells (NSCs), which are indispensable for neurogenesis, are mainly distributed in the hippocampus, a brain region essential for learning and memory. However, alterations in hippocampal NSCs following ICH and the mechanisms that mediate these changes remain poorly defined. The present study investigates the effects of ICH on hippocampal NSCs, focusing on the regulatory role of MTHFD2 in maintaining mitochondrial redox homeostasis through NADPH metabolism.MethodsBoth in vivo and in vitro ICH models were used, including a collagenase-induced mouse model and a hemin-treated NSC model, to examine molecular and cellular responses of hippocampal NSCs to hemorrhagic injury. Western blotting, RNA sequencing, CUT&Tag profiling, and ChIP-qPCR were employed to analyze the related pathways.ResultsWe found that NSCs exhibited a time-dependent response after ICH, showing initial activation followed by gradual functional exhaustion and increased apoptosis. ICH induced persistent endoplasmic reticulum stress and significantly upregulated MTHFD2, a mitochondrial enzyme essential for one-carbon metabolism. Mechanistically, MTHFD2 was required to maintain mitochondrial integrity and redox homeostasis by regulating NADPH levels. Knockdown of MTHFD2 reduced NSC proliferation, increased apoptosis, and worsened cognitive impairment in ICH mice. Exogenous NADPH supplementation partially restored these changes, emphasizing the importance of redox balance in NSC survival and function.ConclusionsOur findings identify MTHFD2 as a key metabolic regulator supporting NSC adaptation to ICH through NADPH-dependent mitochondrial mechanisms. Targeting mitochondrial redox metabolism may provide a potential strategy for preserving NSC function and improving cognitive recovery after ICH.

Deep brain stimulation (DBS) for treatment-resistant depression (TRD) is challenged by significant individual variability in efficacy and unclear neural circuit mechanisms. To address this, a cross-species, multi-level electrophysiological study was conducted to elucidate the core underlying pathophysiology and reveal the precise therapeutic mechanisms of DBS. Based on the clinical trial (NCT04530942), this study focuses on the bed nucleus of the stria terminalis-nucleus accumbens (BNST-NAc) circuit, and it is hypothesized that the fundamental pathology of the depressive state lies in the persistent hyperactivity of BNST neurons, which disrupts the high-fidelity signal communication capacity of this circuit. In a mouse model, a key communication pattern, inhibitory period isolated spikes (IPIS), was first identified within the excitation/inhibition (E/I) cycle. This pattern involves slow-wave oscillations creating a high signal-to-noise ratio window for the firing of single or few action potentials, thereby enabling efficient inter-regional communication. Subsequently, it was found that chronic stress-induced pathological hyperactivity of BNST neurons in stress-susceptible animals specifically disrupts the inhibitory periods of network activity, thereby dismantling IPIS-mediated cross-regional neural synchrony and leading to circuit dysfunction. The therapeutic mechanism of DBS was verified to involve precisely suppressing the pathological hyperactivity of the BNST, thereby restoring the network's inhibitory periods and re-establishing the efficient signal transmission pathway mediated by IPIS. In a closed-loop DBS paradigm, only continuous stimulation and stimulation precisely locked to the inhibitory periods produced antidepressant effects and most effectively restored cross-regional communication. Furthermore, in a cohort of human TRD patients, local field potential (LFP) data were recorded during BNST-NAc DBS treatment, and LFP biomarkers corresponding to the restoration of circuit function were identified. To more directly validate changes in E/I cycles in the human brain, an innovative cross-species algorithm was developed to decode functional excitatory and inhibitory periods from macroscopic human LFP signals. It was confirmed that the therapeutic response to DBS is associated with an increased proportion of inhibitory periods and the functional recovery of the BNST-NAc circuit, providing direct quantitative evidence for the theory that DBS restores E/I balance in the human brain. Finally, a double-blind, crossover randomized controlled trial (RCT) involving 18 participants confirmed that active DBS clinically alleviated depressive symptoms (an average of 9.4 reduction). Open-label data were used for model development, while RCT data served as an independent validation set. Model ablation study within a deep learning framework confirmed that E/I cycle features provide significantly higher informative value than spectral models, establishing these dynamics as the primary electrophysiological determinants of the clinical state. This study integrates mechanistic research with clinical validation, providing evidence for precision and personalized closed-loop DBS therapy.

BACKGROUND:Astrocytes participate in both neuropathological and protective processes following traumatic brain injury (TBI) and undergo various characteristic changes, including phenotypic transformation, transcriptional reprogramming, and functional diversification. METHODS:A comprehensive literature review was conducted in PubMed using key terms "astrocytes" and "traumatic brain injury", and we integrated this existing evidence from transcriptomic analyses to mechanistic studies to elucidate the role and underlying mechanisms of astrocytes in TBI pathophysiology. RESULTS:Transcriptomic analyses reveal distinct astrocyte phenotypes: neurotoxic A1 astrocytes and neuroprotective A2 astrocytes. Beyond this binary framework, single-cell studies have identified intermediate astrocyte states, underscoring the need for more nuanced functional profiling. TBI triggers astrocyte activation via classic signaling pathways in response to mechanical stress, damage-associated molecular patterns (DAMPs), and cytokines. These pathways-TLR4/NF-κB, JAK/STAT3, and MAPK-form an interactive signaling network, enabling astrocytes to integrate diverse injury signals into coordinated responses that drive subsequent pathological effects. Dysregulation of astrocytic ion channels and transporters disrupts ionic homeostasis, exacerbating cytotoxic and vasogenic edema. Mitochondrial dysfunction and reactive oxygen species overproduction further amplify neuronal damage through lipid peroxidation and excitotoxicity. Interactions between astrocytes and microglia, macrophages, and endothelial cells promote neuroinflammation, blood-brain barrier disruption, synaptic and axonal dysfunction, and neuronal apoptosis via mediators such as matrix metalloproteinases, vascular endothelial growth factor, and adhesion molecules. Additionally, reactive astrocytes inhibit neural regeneration through glial scar formation and secretion of inhibitory molecules. CONCLUSIONS:By combining mechanistic studies with translational perspectives, this review highlights that astrocytes act as central mediators of secondary injury and repair in TBI pathology. Given the context-dependent nature of astrocyte signaling, future therapeutic strategies should aim to reprogram astrocyte responses with temporal and cell-type precision rather than pursuing broad inhibition. Also, targeting astrocyte-specific pathways, such as the TLR4 and NF-κB pathways, may mitigate secondary injury and improve outcomes. This underscores the therapeutic potential of modulating astrocyte responses in the treatment of TBI.

Intracerebral hemorrhage (ICH) is a severe subtype of stroke linked to high morbidity and mortality rates. However, the underlying mechanisms of neuronal injury post-ICH remain poorly understood. In this study, we investigated sphingolipid metabolism alterations in neurons using lipidomics and explored the regulatory mechanisms involved. Western blot and live-cell imaging were applied to detect mitochondrial quality and mitophagy level. We found a significant upregulation of ceramide synthase 6 (CERS6)-related C16 ceramide biosynthesis after hemin treatment. Knockdown of CERS6 notably ameliorated mitochondrial dysfunction and reduced neuronal apoptosis. Additionally, impaired neuronal mitophagy was observed after hemin treatment, which was restored by CERS6 knockdown. Mechanistically, CERS6 impaired mitophagy by interacting with sequestosome 1, leading to mitochondrial dysfunction and neuronal apoptosis. Our study explored the relationship between ceramide metabolism and mitophagy in neurons, revealing the pro-apoptotic role of CERS6 while providing a potential therapeutic target for patients with ICH.

ObjectivePediatric Cushing’s disease (CD) is exceptionally rare and poses significant diagnostic and therapeutic challenges. This study aimed to review the diagnostic features and to evaluate the long-term surgical outcomes of transsphenoidal surgery (TSS) in Pediatric CD patients at a single tertiary center in China over two decades.MethodsA retrospective analysis included 22 pediatric CD patients (10 male, 12 female; mean age 15.8 ± 2.5 years) who underwent TSS between 2002 and 2022. Diagnosis was established through a multidisciplinary protocol involving standardized biochemical testing (LDDST, HDDST), bilateral inferior petrosal sinus sampling (BIPSS) with desmopressin stimulation (n=19), and high-resolution pituitary MRI. Microscopic TSS (MTSS) was performed before 2016 (n=11) and endoscopic TSS (ETSS) thereafter (n=11). Surgical strategy was guided by MRI and BIPSS findings. Immediate remission was defined as a postoperative serum cortisol nadir <5 μg/dL or normal 24-h urinary free cortisol (UFC). Recurrence was defined as the reappearance of hypercortisolism after remission. Mean follow-up was 29.4 months (range 2-129).ResultsMRI identified the adenoma in 18/22 patients (81.8%; 16 microadenomas, 2 macroadenomas). BIPSS indicated lateralization in 14/19 patients (73.7%), with concordance between BIPSS and MRI lateralization in 57.9% (11/19) of cases. Immediate postoperative remission was achieved in 20 patients (90.9%). The two non-remitters (one macroadenoma, one MRI- and pathology-negative) received additional therapies. Among the 20 patients with initial remission, 2 (10.0%) developed recurrence (one microadenoma, one MRI-negative) during follow-up. The sustained long-term remission rate was 81.8% (18/22).ConclusionTranssphenoidal surgery represents a highly effective first-line treatment for pediatric CD, achieving high rates of immediate (90.9%) and long-term remission (81.8%) in a specialized center. A meticulous diagnostic approach incorporating BIPSS is crucial, particularly for MRI-negative cases. While recurrence occurred in a minority of patients, primarily those with microadenomas, durable disease control is attainable for the majority with appropriate surgical management. The transition to endoscopic techniques was feasible and effective.

Interventional MRI (i-MRI) has been used for improving the accuracy and safety of brain intervention. The surgical navigation system that provides guidance before and during the intervention is crucial for the operation, especially for robot-assisted neurosurgery. Here we present a Surgical Planning for Brain Intervention (SPBI) software system. SPBI provides a series of functionalities to improve the safety and precision of brain intervention, including brain tissue segmentation, vessel segmentation, fiber tracking, and intervention path planning. Multimodal brain MR images from healthy volunteers were used for demonstration of the functionalities. Codes and sample data are open-sourced and publicly available.

Stereotactic neurointervention is a common procedure for biopsy, injection, ablation, and implantation of electrodes for deep brain stimulation. Guided by preoperative imaging, conventional approaches are mostly performed manually, lacking operation stability and interactive feedback. The intraoperative magnetic resonance imaging (MRI) guidance enables both structural and functional assessment during operation, permitting interactive adaptation to tissue deformation and avoidance of critical anatomical regions. Here, we report an MRI-guided robotic system for stereotactic neurointervention. A macro-micro hybrid pneumatic-hydraulic actuated stereotactic robot with a large range of motion and high precision is developed. This is coupled with a compact bioinspired soft actuator for target intervention. A global-focal MRI sequence is proposed for interactive navigation, closed-loop control, and precise targeting. Validation is performed with phantom, cadaveric, and in vivo animal studies, showing positional accuracies of 0.39, 0.68, and 0.14 millimeters, respectively, demonstrating superior performance compared to the current state of the art in robotic-assisted stereotactic neurointervention.

This study aims to elucidate the mechanism by which YAP mediates the activity of vascular endothelial cells (ECs) in the biological process of intracranial aneurysms (IAs) and to provide a novel target for noninvasive IAs treatment. Single-nuclei RNA profiling of aneurysmal cells revealed that ECs within aneurysms exhibit an intermediate identity between arterial and venous/capillary cells, rather than clustering within the normal arterial population. These specific human ECs showed downregulated YAP expression under turbulent flow. Immunostaining of human IA tissues demonstrated reduced YAP and increased phosphorylated YAP (p-YAP) compared with superficial temporal artery walls. Using YAP-knockdown human brain microvascular endothelial cells (HBMECs), we observed elevated expression of senescence markers p21 and p16, accompanied by diminished proliferation and migration capacities. Furthermore, SPI1 (also known as PU.1) overexpression alleviated EC degeneration induced by turbulent flow through suppression of YAP phosphorylation. Collectively, our findings indicate that turbulent flow markedly reduces YAP expression while promoting its phosphorylation, thereby accelerating endothelial senescence. Importantly, SPI1 overexpression effectively mitigated turbulent-flow-induced endothelial senescence, suggesting that SPI1 may serve as a potential therapeutic target for preventing aneurysmal progression.

BackgroundCushing's Disease (CD) is a rare clinical syndrome characterized by excessive secretion of adrenocorticotrophic hormone, leading to significant functional and structural brain alterations as observed in Magnetic Resonance Imaging (MRI). While traditional statistical analysis has been widely employed to investigate these MRI changes in CD, it has lacked the ability to predict individual-level outcomes.PurposeTo address this problem, this paper has proposed an interpretable machine learning (ML) framework, including model-level assessment, feature-level assessment, and biology-level assessment to ensure a comprehensive analysis based on structural MRI of CD.MethodsThe ML framework has effectively identified the changes in brain regions in the stage of model-level assessment, verified the effectiveness of these altered brain regions to predict CD from normal controls in the stage of feature-level assessment, and carried out a correlation analysis between altered brain regions and clinical symptoms in the stage of biology-level assessment.ResultsThe experimental results of this study have demonstrated that the Insula, Fusiform gyrus, Superior frontal gyrus, Precuneus, and the opercular portion of the Inferior frontal gyrus of CD showed significant alterations in brain regions. Furthermore, our study has revealed significant correlations between clinical symptoms and the frontotemporal lobes, insulin, and olfactory cortex, which also have been confirmed by previous studies.ConclusionsThe ML framework proposed in this study exhibits exceptional potential in uncovering the intricate pathophysiological mechanisms underlying CD, with potential applicability in diagnosing other diseases.

BackgroundCushing disease (CD) is a rare clinical neuroendocrine disease. CD is characterized by abnormal hypercortisolism induced by a pituitary adenoma with the secretion of adrenocorticotropic hormone. Individuals with CD usually exhibit atrophy of gray matter volume. However, little is known about the alterations in topographical organization of individuals with CD. This study aimed to investigate the structural covariance networks of individuals with CD based on the gray matter volume using graph theory analysis.MethodsHigh-resolution T1-weighted images of 61 individuals with CD and 53 healthy controls were obtained. Gray matter volume was estimated and the structural covariance network was analyzed using graph theory. Network properties such as hubs of all participants were calculated based on degree centrality.ResultsNo significant differences were observed between individuals with CD and healthy controls in terms of age, gender, and education level. The small-world features were conserved in individuals with CD but were higher than those in healthy controls. The individuals with CD showed higher global efficiency and modularity, suggesting higher integration and segregation as compared to healthy controls. The hub nodes of the individuals with CD were Short insular gyri (G_insular_short_L), Anterior part of the cingulate gyrus and sulcus (G_and_S_cingul-Ant_R), and Superior frontal gyrus (G_front_sup_R).ConclusionsSignificant differences in the structural covariance network of patients with CD were found based on graph theory. These findings might help understanding the pathogenesis of individuals with CD and provide insight into the pathogenesis of this CD.

Recent investigations have revealed that oxidative stress can lead to neuronal damage and disrupt mitochondrial and endoplasmic reticulum functions after intracerebral hemorrhage (ICH). However, there is limited evidence elucidating their role in maintaining neuronal homeostasis. Metabolomics analysis, RNA sequencing, and CUT&Tag-seq were performed to investigate the mechanism underlying the interaction between the PERK/ATF4 branch of the endoplasmic reticulum stress (ERS) and mitochondrial one-carbon (1C) metabolism during neuronal resistance to oxidative stress. The association between mitochondrial 1C metabolism and the PERK/ATF4 branch of the ERS after ICH was investigated using transcription factor motif analysis and co-immunoprecipitation. The findings revealed interactions between the GRP78/PERK/ATF4 and mitochondrial 1C metabolism, which are important in preserving neuronal homeostasis after ICH. ATF4 is an upstream transcription factor that directly regulates the expression of 1C metabolism genes. Additionally, the GRP78/PERK/ATF4 forms a negative regulatory loop with MTHFD2 because of the interaction between GRP78 and MTHFD2. This study presents evidence of disrupted 1C metabolism and the occurrence of ERS in neurons post-ICH. Supplementing exogenous NADPH or interfering with the PERK/ATF4 could reduce symptoms related to neuronal injuries, suggesting new therapeutic prospects for ICH.

Brain metastases (BrMs) and gliomas are two typical human brain tumors with high incidence of mortalities and distinct clinical challenges, yet the understanding of these two types of tumors remains incomplete. Here, a multidimensional proteomic landscape of BrMs and gliomas to infer tumor-specific molecular pathophysiology at both tissue and plasma levels is presented. Tissue sample analysis reveals both shared and distinct characteristics of brain tumors, highlighting significant disparities between BrMs and gliomas with differentially activated upstream pathways of the PI3K-Akt signaling pathway that have been scarcely discussed previously. Novel proteins and phosphosites such as NSUN2, TM9SF3, and PRKCG_S330 are also detected, exhibiting a high correlation with reported clinical traits, which may serve as potential immunohistochemistry (IHC) biomarkers. Moreover, tumor-specific altered phosphosites and glycosites on FN1 are highlighted as potential therapeutic targets. Further validation of 110 potential noninvasive biomarkers yields three biomarker panels comprising a total of 19 biomarkers (including DES, VWF, and COL1A1) for accurate discrimination of two types of brain tumors and normal controls. In summary, this is a full-scale dataset of two typical human brain tumors, which serves as a valuable resource for advancing precision medicine in cancer patients through targeted therapy and immunotherapy.

Corticotroph pituitary neuroendocrine tumors (PitNETs), associated with Cushing's disease (CD), have limited treatment options other than surgical resection. Bone morphogenetic protein 4 (BMP4), a potential therapeutic target, is decreased in patients with CD. Previous studies have identified BMPSB4 as a potent agonist of the BMP4 signaling pathway. Here, we investigated the effect of BMPSB4 on the corticotroph PitNET cell line AtT20/D16v-F2 and explored the underlying mechanisms and therapeutic potential. We verified the low expression patterns of BMP4 and downstream p-SMAD1/5/9 in CD samples at the transcriptional and protein levels. In addition, BMPSB4 activated SMAD1/5/9 in a time- and concentration-dependent manner, with concomitant inhibitory effects on AtT20/D16v-F2 cells. Further RNA sequencing, transmission electron microscopy (TEM), and transfection with the mRFP-EGFP-LC3 adenoviral vector revealed that BMPSB4 induced cellular autophagy, which was the basis for the inhibitory effect of BMPSB4. Moreover, we demonstrated that autophagy induced by BMPSB4 was achieved through the SMADs-dependent pathway. In vivo, BMPSB4 inhibited tumor growth and significantly reduced adrenocorticotrophin (ACTH) and corticosterone (CORT) secretion, thereby alleviating the CD phenotype. In conclusion, this study identified BMPSB4 as an effective therapeutic agent for CD. BMPSB4 activates autophagy through a SMADs-dependent pathway, which in turn promotes autophagy-mediated cell death. Our work further elucidates the mechanism of the BMP4 signaling pathway in CD and suggests broad prospects for the development and application of BMPSB4 in CD therapy.

Background Schwannomas are the most common intrathoracic neurogenic tumors. In the past, they were often treated by traditional open surgery. Video-assisted thoracic surgery (VATS) has also been used for some large tumors. Recently, minimally invasive posterior neurosurgical technique provides a new option for some of these tumors. Method Here, we describe the specific steps involved in the O-arm guided minimally invasive removal of intrathoracic epidural schwannoma, as well as its advantages and limitations. Conclusion O-arm guided minimally invasive resection of intrathoracic epidural schwannoma is safe and effective and causes little damage.

Objectives Pituitary abscess (PA) accounts for only 0.3-0.5% of sellar masses, and the lack of specific clinical symptoms makes diagnosing PA difficult without a surgical biopsy. In clinical practice, PA is often mistaken for cystic pituitary adenoma, craniopharyngioma, and Rathke's cyst. Thus, this study aims to investigate challenges in diagnosing PA and evaluate the importance of combining intraoperative surgery with postoperative antibiotic treatment.Methods We conducted a retrospective analysis of 19 patients diagnosed with PA through histopathology. All patients underwent transsphenoidal surgery (TSS) for pituitary adenomas after undergoing comprehensive preoperative evaluations, including routine tests, endocrine assay, and imaging examination. Furthermore, we compared different treatments for pituitary abscess (PA) to determine the most effective approach for achieving a favorable prognosis.Results The most prevalent symptom of PA was headache, especially in the frontal-temporal and vertex regions, ranging from mild to moderate severity. Hypopituitarism-related symptoms were also frequently observed, including hypaphrodisia, cold sensitivity, fatigue, weight loss, polyuria, and amenorrhea. Twelve patients exhibited abnormalities in endocrinology examinations. Diagnosing PA correctly is challenging. In our study, none of the patients were correctly diagnosed with PA prior to surgery, and many sellar lesions were misdiagnosed. The favorable prognosis was largely attributed to surgical intervention and active postoperative antibiotic therapy.Conclusions Given the lack of clarity in preoperative diagnosis, typical intraoperative findings and effective antibiotics treatment are more indicative of the correct diagnosis than other tests. In terms of therapy, optimal surgical intervention and active postoperative antibiotic treatment contribute to resolving the challenges posed by PA.