Diabetic foot ulceration and deep tissue destruction result from concurrent lower-limb neurological and vascular damage in patients with diabetes mellitus, imposing a substantial burden on health and quality of life. Conventional medical strategies that focus on metabolic control and hemodynamic improvement offer limited benefit for refractory ulcers dominated by diabetic peripheral neuropathy, making surgical intervention essential. Neurosurgical techniques provide an individualized approach for different pathogenic subtypes through decompression of entrapped nerves, spinal cord stimulation for analgesia and microcirculatory enhancement, and comprehensive wound care. This review summarizes current clinical classification, differential diagnostic considerations, and neurosurgical treatment principles, emphasizing the value of multidisciplinary collaboration and neuromodulation technology in optimizing integrated management of diabetic foot.
Professional Committee of Traumatic Brain Injury, World Association of Chinese Neurosurgeon, Collaborative Group for Expert Consensus of Cranioplasty for Skull Defect
Skull defects remaining after decompressive craniectomy can lead to a lack of protection for brain tissue, disruption of cranial cavity integrity, resulting in limited recovery of neurological function, as well as affecting patients' appearance and psychological health. However, skull defect repair involves multiple factors such as scalp healing, bone resorption, postoperative cerebrospinal fluid dynamics changes, and the need for neurological functional compensation. The timing of repair, material selection, and surgical strategies remain controversial. Based on evidence-based medical evidence and the experience of multidisciplinary experts, the China Expert Consensus Collaboration Group on Cranioplasty organized domestic experts. Through literature analysis and expert experience integration, and using the Delphi method, this consensus was developed to provide standardized guidance for cranioplasty.
To explore the neuroprotective effects and mechanisms of intermittent fasting (IF) on ischemia/reperfusion (I/R) injury in mice.
Methods
A total of 150 healthy male C57BL/6J mice were randomly divided into three groups using a random number table: sham surgery group (Sham group), ischemia/reperfusion group (I/R group), and intermittent fasting group (IF group), with 50 mice in each group. The I/R group underwent right middle cerebral artery occlusion (MCAO) to establish a focal cerebral I/R model; the IF group implemented a 16/8 intermittent fasting regimen based on the I/R group; the Sham group only isolated the blood vessels without inserting the filament. All mice were fasted for 12 h prior to surgery with free access to water. After 30 d, the neurological function of the mice was assessed using the modified neurological severity score (mNSS), motor function was evaluated using the rotarod test, learning and memory function was assessed using the novel object recognition test, brain edema was measured using the dry/wet weight method, brain infarct volume was calculated using Image-J software, neuronal injury was detected using Nissl staining, and levels of reactive oxygen species (ROS), malondialdehyde (MDA), glutathione (GSH), and total antioxidant capacity (T-AOC) in brain tissue were measured using commercial kits. Gene expression levels of NADPH quinine oxidoreductase-1 (NQO-1), heme oxidase-1 (HO-1), and glutathione peroxidase 4 (GPX4) in brain tissue were detected by qPCR and Western blot, and the levels of nuclear factor-E2-related factor 2 (Nrf2) protein in the nucleus and cytoplasm of brain tissue were measured by Western blot.
Results
The mNSS scores, drop time of the rotating rod test, new object recognition index, degree of brain edema, brain infarct volume, degree of neuronal damage, oxidative stress intensity (ROS, MDA, GSH, and T-AOC levels), nuclear translocation level of Nrf2, and mRNA and protein expression of antioxidant genes NQO-1, HO-1, and GPX4 in Sham group, I/R group, and IF group mice 30 d after I/R were compared, and the differences were statistically significant (P<0.05). The mNSS scores and rotarod drop times of the IF group were significantly lower than those of the I/R group, while the recognition index for new objects was significantly higher in the IF group compared to the I/R group, with statistical significance (P<0.05). The degree of brain edema and brain infarct volume in the IF group were significantly lower than those in the I/R group, and the number of surviving neurons was significantly higher in the IF group compared to the I/R group, with statistical significance (P<0.05). The levels of ROS and MDA in the IF group were significantly lower than those in the I/R group, while the levels of GSH and T-AOC were significantly higher in the IF group compared to the I/R group, with statistical significance (P<0.05). Compared with the I/R group mice, the mRNA levels of NQO-1, HO-1, and GPX4 in the brain tissue, nuclear translocation water of Nrf2, and protein levels of NQO-1, HO-1, and GPX4 in the IF group mice were significantly increased, while the cytoplasmic Nrf2 level was significantly decreased, with statistical significance (P<0.05).
Conclusions
IF significantly improves neurological function damage in I/R mice, and its mechanism may promote Nrf2 pathway to inhibit oxidative stress following I/R injury.
To observe the role of lysosomal-associated membrane protein 1 (LAMP1) in microglial (MG) injury in rats subjected to cerebral ischemic-reperfusion injury (CIRI) and to investigate the impact and mechanism of LAMP1 on autophagy in this model.
Methods
Thirty adult healthy SD rats were selected and the rat model was established using transient middle cerebral artery occlusion (tMCAO) method. The rats were randomly divided into sham group (Sham group), surgical group (tMCAO group), and intervention group (tMCAO+CQ group) according to the random number table method, with 10 rats in each group. Three groups of rats were intraperitoneally injected with sterile physiological saline before surgery, while the tMCAO+CQ group was injected with chloroquine (CQ) lysosome inhibitor 2 h before surgery. CIRI rat model was established, and Sham group was the surgical control group. Five samples were taken from each group for TTC staining, and the remaining five brain tissue specimens were collected for experimental testing in sequence. After collecting brain tissue and extracting the ischemic penumbra tissue, the expression of LAMP1 protein in cells was detected. To investigate the effects of LAMP1 on MG injury and autophagy in a model, enzyme-linked immunosorbent assay (ELISA) was used to detect inflammatory factors [interleukin (IL)-6, tumor necrosis factor alpha (TNF-α), IL-10], and Western blot was used to detect the expression of p62, Cathepsin B, Cathepsin D, and LC3B. In addition, the Longa scoring system was used to evaluate the neurological function of rats 24 h after CIRI, TTC staining was used to measure the volume of cerebral infarction, HE staining was used to observe pathological changes in brain tissue.
Results
Compared with the Sham group, the Longa scores of the tMCAO group and the tMCAO+CQ group were significantly increased, and the cerebral infarction volume was significantly increased. The Longa score of the tMCAO+CQ group was higher than that of the tMCAO group, and the cerebral infarction volume was larger than that of the tMCAO group, with statistical significance (P<0.05). The results of ELISA and Western blot analysis showed that compared with the Sham group, the expression of LAMP1 protein was significantly decreased in the tMCAO group and the tMCAO+CQ group, while the levels of IL-6, TNF-α, LC3B, and Baclin1 protein expression were significantly increased. The levels of IL-10 and p62, LAMP1, Cathepsin B, and Cathepsin D protein expression were significantly decreased, and the differences were statistically significant (P<0.05); Compared with the tMCAO group, the expression of LAMP1 protein in the tMCAO+CQ group decreased significantly, while the levels of IL-6, TNF-α, LC3B, and Beclin1 protein increased. The expression levels of p62 and Cathepsin D protein decreased, and the differences were statistically significant (P<0.05). However, there was no statistically significant difference in the expression levels of Cathepsin B protein (P>0.05).
Conclusions
Inhibiting LAMP1 exacerbates glial cell damage in the rat model and this mechanism may be related to the inhibition of autophagy.
To analyze the influencing factors of bleeding events in patients with anterior circulation intracranial aneurysms after endovascular treatment via transradial approach (TRA).
Methods
Ninety-eight patients with anterior circulation intracranial aneurysms treated with TRA endovascular therapy at Neurosurgery Department of the Second Affiliated Hospital of Nantong University from July 2022 to April 2024 were selected as the study subjects. The patients were divided into the bleeding group (41 cases) and the non-bleeding group (57 cases) according to whether bleeding events occurred after treatment. The general information, past history, preoperative blood test results, and intraoperative operating indicators of the two groups of patients were collected, and single factor and Logistic multifactor regression were used to analyze the influencing factors of bleeding events after TRA endovascular therapy.
Results
Compared with the non-bleeding group, the bleeding group had a higher proportion of patients with the following characteristics: age ≥60 years, hypertension, diabetes mellitus, long-term smoking, guide catheter positioning time ≥12 min, total hemostat release time <1200 min, vascular tortuosity in the arterial access, and hemoglobin level <134.86 g/L (all P<0.05). Multivariate Logistic regression analysis revealed that patient age ≥60 years, history of hypertension, history of diabetes mellitus, long-term smoking history, vascular tortuosity in the arterial access, preoperative hemoglobin level <134.86 g/L, surgical guide catheter positioning time ≥12 min, and total hemostat release time <1200 min were all independent influencing factors for bleeding events during TRA endovascular treatment (all P<0.05).
Conclusions
Patients with anterior circulation intracranial aneurysms who have the following characteristics with the following characteristics, including age≥60 years, history of hypertension, history of diabetes mellitus, long-term smoking history, vascular tortuosity in the arterial access, preoperative hemoglobin level <134.86 g/L, surgical guide catheter positioning time ≥12 min, and total hemostat release time <1200 min have a high risk of bleeding events after TRA endovascular treatment.
To investigate the predictive value of early expression levels of plasma pyruvate kinase M2 (PKM2) for the severity and prognosis of patients with aneurysmal subarachnoid hemorrhage (aSAH).
Methods
A total of 95 aSAH patients admitted to Neurosurgery Department of China Resources Wuhan Iron and Steel General Hospital from September 2021 to May 2023 were prospectively enrolled as aSAH group, while 100 healthy individuals who underwent physical examination in the hospital during the same period were selected as the control group. Enzyme-linked immunosorbent assay (ELISA) was used to measure the PKM2 levels of patients in the aSAH group 12 h after admission, as well as the PKM2 levels of the control group on the day of admission physical examination, and general data and early plasma PKM2 levels were collected and compared between the two groups. The aSAH group was further stratified by disease severity (mild: Hunt-Hess grade Ⅰ-Ⅱ, moderate: Hunt-Hess grade Ⅲ, severe: Hunt-Hess grade Ⅳ) and surgical approach (craniotomy clipping subgroup and endovascular embolization subgroup), with their prognosis evaluated using the modified Rankin scale (mRs) at 90 d after discharge, patients with an mRs score>2 were assigned to the poor prognosis group, and those with an mRs score≤2 to the good prognosis group, and clinical data differences among these subgroups were compared. Additionally, the aSAH patients were divided into the high-expression group (plasma PKM2 level≥190.0 ng/L) and the low-expression group (plasma PKM2 level<190.0 ng/L), and the clinical data of aSAH patients with different plasma PKM2 levels were compared. Receiver operating characteristic (ROC) curve was plotted to assess the predictive value of early plasma PKM2 levels for poor prognosis in aSAH patients.
Results
Early plasma PKM2 levels were significantly higher in the aSAH group than in the control group (P<0.05). Furthermore, significant differences in maximum diameter of aneurysms, plasma PKM2 expression levels, modified Fisher grading, and GCS scores among patients with mild, moderate, and severe aSAH (P<0.05), and the more severe the condition, the higher the plasma PKM2 expression level. In contrast, no statistically significant differences in plasma PKM2 levels or clinical outcomes were found between the different surgical groups (P>0.05). The differences in hypertension history, Hunt-Hess grading, GCS score, modified Fisher grading, and plasma PKM2 expression levels between patients with favorable and unfavorable outcome were statistically significant (P<0.05). The differences in Hunt-Hess grading, GCS score, and modified Fisher grading between patients with high PKM2 expression and those with low PKM2 expression were statistically significant (P<0.05). ROC curve analysis demonstrated that early plasma PKM2 levels effectively predicted unfavorable outcomes in aSAH patients, with an area under the curve of 0.846 (95%CI: 0.764-0.928), a sensitivity of 80.60%, and a specificity of 81.40% at the optimal cut-off value of 190.0 ng/L.
Conclusions
The early expression level of plasma PKM2 is related to the severity and prognosis of aSAH patients, providing certain diagnostic value for predicting disease progression and potentially serving as a new marker for predicting the outcome of aSAH patients.
To explore the independent influencing factors of hospital-acquired pneumonia (HAP) in Neurosurgical Intensive Care Unit (NICU) after emergency craniotomy for acute spontaneous cerebral hemotoma removal, as to provide important reference data for clinic.
Methods
The medical record data of 207 enrolled patients with emergency craniotomy for acute spontaneous cerebral hematoma removal in NICU of Sichuan Provincial People's Hospital from January 2016 to June 2021 were retrospectively analyzed. According to the patients with acute spontaneous intracerebral hemorrhage in NICU, whether they had hospital-acquired pneumonia after emergency craniotomy and hematoma removal, they were divided into infection group and non-infection group. Multiple Logistic regression analysis was used to screen for independent risk factors for HAP in NICU patients with spontaneous intracerebral hemorrhage after emergency craniotomy.
Results
Of the patients enrolled in this study, 127 cases were in the infection group and 80 cases in the non-infection group. There were significant differences between patients in infection and non-infection groups in age, GCS score≤8 on admission, preoperative blood glucose, preoperative albumin, hypertension, operation duration, and postoperative mechanical ventilation. The factors with P<0.1 were included in the multivariate Logstic regression analysis, and the results showed that those with GCS score≤8 on admission, operation duration ≥240 min (4 h), postoperative mechanical ventilation, preoperative blood glucose≥10.0 mmol/L, and preoperative albumin<42.5 g/L were the independent risk factors for HAP in patients with spontaneous intracerebral hemorrhage undergoing emergency craniotomy and hematoma evacuation in NICU.
Conclusions
The independent risk factors for HAP in patients with spontaneous intracerebral hemorrhage undergoing emergency craniotomy and hematoma evacuation in NICU include admission GCS score ≤8, operation duration ≥4 h, postoperative mechanical ventilation, preoperative blood glucose ≥10.0 mmol/L, and preoperative albumin <42.5 g/L. Early screening and corresponding prevention and treatment measures can help reduce the incidence of postoperative HAP and improve long-term prognosis.
To investigate the clinical and imaging characteristics of patients with herniation secondary to critical cerebrospinal fluid hypovolemia (CCSFH) after craniotomy.
Methods
From January 2019 to November 2023, fourteen patients with acute brain injury were admitted to Neurosurgery Department of Beijing Shunyi District Hospital, and experienced cerebral herniation due to CCSFH after craniotomy. Their clinical and imaging characteristics, treatment course, and outcomes were analyzed. Prognosis at six months post-discharge was assessed with the modified Rankin scale (mRS).
Results
CCSFH occurred within 1 to 13 d post-surgery. Seven patients exhibited a decline in consciousness or mental state, with three showing anisocoria. The remaining seven patients had regular pupil sizes, complicating consciousness assessment due to postoperative sedation and analgesia. The midline shift was (10.95±2.90) mm during the CCSFH presentation, ranging from 6.69 to 16.00 mm. Intracranial pressure ranged from 1-11 mmHg (1 mmHg=0.133 kPa) in 5 cases with CCSFH. Four cases underwent decompressive craniectomies owing to delayed CCSFH identification, while 10 cases received conservative treatment. The CCSFH condition was successfully reversed in all patients. Six months post-discharge, 6 cases had mRS scores≤2, and 8 had scores>2.
Conclusions
Post-craniotomy CCSFH often presents with deteriorating consciousness or mental status, and in severe cases, it may lead to transtentorial herniation. CT scans show significant midline shift, but the intracranial pressure remains relatively low. The primary treatment is positioning the patient supine, along with stopping cerebrospinal fluid drainage, halting use of hypertonic diuretics, and administering intravenous hydration, which often leads to good outcomes.
Imbalance between coagulation and fibrinolysis is a key inducer of complications in neurosurgical critical care (such as traumatic brain injury, intracranial hemorrhage, and perioperative period of brain tumors). Novel thrombosis markers (thrombin-antithrombin complex, plasmin-α2-plasmin inhibitor complex, tissue-type plasminogen activator-inhibitor complex, and thrombomodulin) can monitor coagulation activation, fibrinolytic activity, and endothelial injury in an earlier and more sensitive manner. They provide a basis for diagnosis and treatment adjustment (e.g., anticoagulant or antifibrinolytic regimens) and also help predict risks such as thrombosis and rebleeding. The purpose of this review is to clarify the value of these novel markers in the precise diagnosis and treatment of neurosurgical critical care, analyze current application limitations, and propose future research directions. It aims to provide theoretical references for optimizing clinical patient management, reducing secondary brain injury, and improving prognosis, as well as offer directional references for subsequent research.