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OBJECTIVE Twig-like middle cerebral artery (T-MCA) is a rare congenital anomaly that is difficult to distinguish from moyamoya angiopathy (MMA), given the similarity of the angioarchitectures. The aim of this study was to gain insights into the radiological and clinical features of T-MCA and to distinguish this condition from MMA. METHODS A multicenter retrospective study was conducted in 29 patients with T-MCA and 57 patients with MMA. Demographic, radiological, and clinical data were compared between the patients with T-MCA and those with MMA. RESULTS The T-MCA group tended to be older than the MMA group (mean age 47 ± 18 vs 39 ± 22 years). Twenty patients with T-MCA (69%) were initially diagnosed with MMA. All T-MCA cases had twig-like networks and steno-occlusive changes involving the MCA. The T-MCA group had a higher incidence of intracranial aneurysms (35% vs 11%) and coexisting arterial anomalies (48% vs 12%). T-MCA and MMA cases had significant differences in involvement of the internal carotid artery terminus (0% vs 100%) and posterior cerebral artery (0% vs 23%), and in transdural anastomosis (0% vs 51%). T-MCA cases were less likely to present with stroke (59% vs 86%) and more likely to be asymptomatic (28% vs 12%). Of the patients with stroke, those with T-MCA had more hemorrhagic strokes (41% vs 29%) and fewer ischemic strokes (59% vs 71%) compared to those with MMA. CONCLUSIONS This study suggests that T-MCA is a different disease entity from MMA based on significant differences in the radiological and clinical features. Neurosurgeons should recognize this anomaly and understand the key features that differentiate T-MCA from MMA.

The temperature of a strip cast using a vertical type high-speed twin-roll caster was measured by inserting a k-type thermocouple into the strip. The effects of the roll speed and roll load on the cooling rate and temperature at the roll gap were investigated using two aluminum alloys: A383 and Al–4.8%Mg. The thickness of the thermocouple was 0.1 mm, and the sampling time was 0.01 s. The cooling rate increased and the temperature at the roll bite decreased with decreasing roll speed and increasing roll load. The positions of the liquidus and solidus lines were measured, and the reduction of the thickness of the strip was inferred from the roll gap at the solidus line.

A recurrent tumor is defined as a re-emerging subclone originating from an ancestorial clone of the primary neoplasm. Hence, it should be distinguished from de novo tumor emerging from other clones. Herein, we describe an exceptional case in which the locally re-emerging glioma did not share genetic alterations of the primary tumor. While the initial tumor harbored mutations in IDH1 and TERT genes as well as 1p/19q codeletion, the re-emerging tumor did not present any of these genetic abnormalities. Variant calling for tumor samples using whole-genome sequencing revealed that 1696 mutations within the primary tumor faded in the re-emerging tumor, and that 4591 mutations were newly detected in the re-emerging tumor. These results suggested that the initial and re-emerging tumors did not share same clonal origins, although the second tumor appeared adjacent to the old surgical cavity 5 years after the initial surgery. We finally speculated that the re-emerging tumor could be a "de novo glioma" or "radiation-induced glioblastoma following treatment of a diffuse glioma." This case highlights the importance of molecular re-evaluation of clinically diagnosed "recurrent" glioma lesions.

Aim: The adverse events of the CKD4/6 inhibitor abemaciclib are known to be dose dependent. However, its pharmacokinetics vary among individuals. Abemaciclib is reported to be transported by P-glycoprotein (P-gp) and the breast cancer resistance protein (BCRP). Therefore, we evaluated whether ABCB1 and ABCG2 gene polymorphisms could be pharmacokinetic predictive factors of abemaciclib. Methods: A total of 45 patients with breast cancer able to take abemaciclib (150 mg twice daily) for 2 weeks were evaluated to determine the association among abemaciclib concentrations, adverse events, and ABCB1 1236T>C, 2677G>T/A, 3435C>T, and ABCG2 421C>A gene polymorphisms. Results: The trough concentrations of abemaciclib were higher in the group with grade 2 or greater neutropenia, anemia, and thrombocytopenia as compared with the group with grades 0 or 1. No significant association was observed between ABCB1 1236T>C, 3435C>T, and ABCG2 421C>A gene polymorphisms and abemaciclib concentrations. However, in ABCB1 2677G>T/A polymorphisms, the concentrations of abemaciclib tended to be higher in the homozygous group (AA + AT) as compared with that in the wild-type and heterozygous group (GG + GA + GT) [222.8 (80.5–295.8) ng/mL vs. 115.8 (23.6–355.2) ng/mL, P = 0.11]. Hence, the ABCB1 2677G>T/A homozygous group had a significantly higher incidence of abemaciclib withdrawal and dose reduction within 4 weeks as compared than the wild-type and heterozygous group (67% vs. 33%, P = 0.03). Conclusions: The gene polymorphism of ABCB1 2677G> T/A might be a predictor of the pharmacokinetics and tolerability of abemaciclib.

Balloon test occlusion (BTO) can predict the ischemic complication risk associated with arterial occlusion. We present a case of an unruptured, broad-necked internal carotid artery-posterior communicating artery (PcomA) aneurysm that was successfully embolized after super-selective BTO of fetal PcomA with electrophysiological monitoring. The proximal portion of the PcomA was internally occluded without causing major neurological deficits, although we observed a small new infarction in the ipsilateral anterior thalamus postoperatively. We recognized small perforators arising from the proximal PcomA during a previous clipping surgery. Super-selective BTO with electrophysiological monitoring could be useful for functional preservation after infarction from angiographically invisible perforators.

Here, we report two cases showing tumor-like white matter lesions; one case was diagnosed as having inflammatory disease, and the other was diagnosed as having astrocytoma. Their outcomes were completely distinct despite similar pathology. Prior to biopsy, perfusion computed tomography (CT) and magnetic resonance imaging (MRI) were conducted. The two mass-forming lesions were distinct in edema level and vascularity patterns on CT and MRI. However, pathological examination of brain biopsy specimens revealed commonalities, including (1) proliferation of glial cells, (2) perivascular lymphocytic infiltration, and (3) appearance of numerous macrophages. Although atypical astrocytes proliferated in both cases, nuclear atypia was more distinct in case 2 than in case 1. The immunohistochemical results were the same for both cases: isocitrate dehydrogenase 1 (IDH1) R132H mutation was negative, and alpha thalassaemia mental retardation X-linked (ATRX) was retained. Faint immunoreactivity for p53 was observed in a few glial cells, and Ki-67 immunoreactive cells were markedly reduced in numbers (< 1%). Inflammatory reactions were evident in both cases: T cells dominantly infiltrated over B cells in the perivascular area in case 1, whereas both T and B cells infiltrated in case 2. Molecular analysis revealed wild-type IDH1 and IDH2 in both cases. However, a telomerase reverse transcriptase (TERT) sequence mutation was detected in case 2 but not in case 1. Eventually, case 1 was diagnosed as having inflammatory lesions, whereas case 2 was diagnosed as having diffuse astrocytoma associated with inflammatory reactions. The prognosis was favorable for case 1, whereas case 2 died 10 months following biopsy. These data indicated the diagnostic value of molecular analysis, for example, a TERT mutation, in association with the radiological findings. Although in case 2, histopathological evidence did not suggest high-grade glioma, the case met the new diagnostic criteria: "diffuse astrocytic glioma, IDH wild-type, with molecular features of glioblastoma, World Health Organization (WHO) grade IV," according to cIMPACT-NOW, update 3. Thus, interdisciplinary approaches are essential for accurate diagnosis of newly categorized white matter diseases.

Maneuvering motions of a ship in calm water are studied through the concept of MMG model. Governing forces are defined by the use of available empirical formulae that require only main ship particulars as input variables. In order to validate the calculation tool, a full-scale sea experiment was carried out in Osaka Bay using a 17-m twin-screw passenger ferry. Test execution and data measurement were performed through the utilization of an autopilot control unit and satellite compass. The result of a straight running test confirms the acceptable accuracy in addressing the surge motion problem. Reasonable agreement between simulation and experiment is also confirmed for 5 ∘ / 5 ∘ and 10 ∘ / 10 ∘ zig-zag tests despite the strong environmental disturbance. The current model can generally represent the subject ship maneuvering motions and is promising for the application to other ship hulls.

Coagulopathy is often observed in severe traumatic brain injury (sTBI), and hyperfibrinolysis (HF) is associated with a poor prognosis. Although the efficacy of fibrinogen concentrate (FC) in multiple trauma has been reported, its efficacy in sTBI is unclear. Therefore, we delineated severe HF risk factors despite fresh frozen plasma transfusion. Using these risk factors, we defined high-risk patients and determined whether FC administration to this group improved fibrinogen level.In the first part of this study, successive adults with sTBI treated at our hospital between April 2016 and March 2019 were reviewed. Patients underwent transfusion as per our conventional protocol and were divided into two groups based on whether fibrinogen levels of ≥ 150 mg/dL were maintained 3-6 h after arrival to delineate the risk factors of severe HF. In the second part of the study, we conducted a before-and-after study in patients with sTBI who were at a higher risk for severe HF (presence of at least one of the risk factors identified in the first part of the study), comparing those treated with FC between April 2019 and March 2021 (FC group) with those treated with conventional transfusion before FC between April 2016 and March 2019. The primary outcome was maintenance of fibrinogen levels, and the secondary outcome was 30-day mortality.In the first part of the study, 78 patients were included. Twenty-three patients did not maintain fibrinogen levels ≥ 150 mg/dL. A D-dimer level on arrival 50 μg/mL, a fibrinogen level on arrival 200 mg/dL, depressed skull fracture, and multiple trauma were severe HF risk factors. In the second part, compared with 46 patients who were identified as being at high risk for severe HF but were not administered FC (non-FC group), fibrinogen levels ≥ 150 mg/dL 3-6 h after arrival were maintained in 14 of 15 patients in the FC group (odds ratio: 0.07; 95% confidence interval: 0.01-0.59). Although there were significant differences in fibrinogen levels, no significant differences were observed in terms of 30-day mortality between the groups.Coagulation abnormalities on arrival, severe skull fracture, and multiple trauma are severe HF risk factors. FC administration may contribute to rapid correction of developing hypofibrinogenemia.

Background: The pathogenesis and pathophysiology of traumatic coagulopathy during traumatic brain injury is not well understood, and the appropriate treatment strategy for this condition has not been established. This study aimed to evaluate the coagulation phenotypes and their effect on prognosis in patients with isolated traumatic brain injury.Methods: In this multicenter cohort study, we retrospectively analyzed data from the Japan Neurotrauma Data Bank (JNTDB). Adults with isolated traumatic brain injury (head abbreviated injury scale [AIS] >2, any other AIS Results: In total, 556 patients were enrolled, and five coagulation phenotypes were identified. Cluster A (n=129) had the closest to normal coagulation values; cluster B (n=323) had a mild high DD phenotype; cluster C (n=30) had a prolonged PT-INR phenotype with a higher frequency of antithrombotic medication in elderly patients than in younger patients; cluster D (n=45) had a low FBG, high DD, and prolonged APTT phenotype with a high incidence of skull fracture; and cluster E (n=29) had a low FBG and extremely high DD phenotype with high-energy trauma and high incidence of skull fracture. In the multivariable logistic regression analysis, the association of clusters B, C, D, and E with in-hospital mortality yielded the corresponding adjusted ORs of 2.17 (95% CI: 1.22–3.86), 2.61 (95% CI: 1.01–6.72), 10.0 (95% CI: 4.00–25.2), and 24.1 (95% CI: 7.12–81.3), respectively, relative to cluster A.Conclusions: This multicenter observational study identified five different coagulation phenotypes of traumatic brain injury and showed associations of these phenotypes with in-hospital mortality.

To identify the association between skull fracture (SF) and in-hospital mortality in patients with severe traumatic brain injury (TBI).This multicenter cohort study included a retrospective analysis of data from the Japan Trauma Data Bank (JTDB). JTDB is a nationwide, prospective, observational trauma registry with data from 235 hospitals. Adult patients with severe TBI (Glasgow Coma Scale9, head Abbreviated Injury Scale (AIS) ≥ 3, and any other AIS 3) who were registered in the JTDB between January 2004 and December 2017 were included in the study. Patients who (a) were 16 years old, (b) developed cardiac arrest before or at hospital arrival, and (c) had burns and penetrating injuries were excluded from the study. In-hospital mortality was the primary outcome assessed. Multivariable logistic regression analyses were performed to calculate the adjusted odds ratios (ORs) of SF and their 95% confidence intervals (CIs) for in-hospital mortality.A total of 9607 patients were enrolled [median age: 67 (interquartile range: 50-78) years] in the study. Among those patients, 3574 (37.2%) and 6033 (62.8%) were included in the SF and non-SF groups, respectively. The overall in-hospital mortality rate was 44.1% (4238/9607). A multivariate analysis of the association between SF and in-hospital mortality yielded a crude OR of 1.63 (95% CI: 1.47-1.80). A subgroup analysis of the association of skull vault fractures, skull base fractures, and both fractures together with in-hospital mortality yielded adjusted ORs of 1.60 (95% CI: 1.42-1.98), 1.40 (95% CI: 1.16-1.70), and 2.14 (95% CI: 1.74-2.64), respectively, relative to the non-SF group.This observational study showed that SF is associated with in-hospital mortality among patients with severe TBI. Furthermore, patients with both skull base and skull vault fractures were associated with higher in-hospital mortality than those with only one of these injuries.

Chronic subdural hematoma (CSDH) is associated with postoperative recurrence. Although various factors are involved in postoperative recurrence of CSDH, blood flow, especially in the middle meningeal artery (MMA), is considered to play an important role. We investigated whether the degree of signal intensity (SI) of the MMA on time-of-flight magnetic resonance angiography (TOF MRA) and various clinical factors are involved in recurrence of CSDH.The maximum SI of both MMAs was measured on TOF MRA images within 1 month before or after the initial surgery.In total, 185 patients (20 with and 165 without recurrence of CSDH) were included in the analysis. The SI ratio and dementia were significant predictors of recurrence of CSDH (SI ratio: odds ratio [95% confidence interval (CI)] = 1.71 [1.32, 2.22], p 0.0001; dementia: odds ratio [95% CI] = 7.41 [1.83, 30.1], p = 0.005). The estimated regression coefficients in the final model were 6.14 for the SI ratio and 1.28 for dementia. The risk score was derived according to these regression coefficients as follows: score = 5 × SI ratio + 1 (dementia: yes). With a score of 5, the predicted probability of recurrence was 2% [95% CI 0.7, 5.7], whereas with scores of 8 and 10, the probability was 43.3% [27.0, 61.1] and 89.5% [65.7, 97.5], respectively, which increased the risk of recurrence.Patients with an increased SI ratio of the affected MMA on TOF MRA who underwent surgery for CSDH were significantly more likely to experience recurrence.

Purpose: To report a case of vertebral arteriovenous fistula (VAVF) caused by iatrogenic trauma of central venous catheterization (CVC) involving brachiocephalic vein (BCV). Case report: A 79-year-old female was referred for assessment of a vertebral artery (VA) aneurysm at the V1 segment. The patient had no signs other than a vascular murmur on the right neck and was diagnosed 20 years after undergoing CVC. Right vertebral angiography revealed a high-flow shunt from the V1 segment of the right VA and draining into the right BCV. The fistula had a single communication between a pseudoaneurysm and large varix. We diagnosed the patient with CVCinduced VAVF (CIVAVF) involving BCV and obliterated the shunt by selective transarterial and transvenous embolization of the pseudoaneurysm under flow control using a balloon catheter with no complications. Conclusion: This case highlights the point that CIVAVF involving BCV is rare but possible. In addition, there is a possibility that CIVAVF involving BCV does not demonstrate the findings of arterial steal or retrograde venous drainage and is undiagnosed for a long term due to lack of neurological manifestation and other subjective symptoms. We also showed that endovascular treatment can be feasible and useful for CIVAVF involving BCV.

The prognosis of glioblastoma remains poor despite intensive research efforts. Glioblastoma stem cells (GSCs) contribute to tumorigenesis, invasive capacity, and therapy resistance. Leucine-rich repeat-containing G-protein coupled receptor 5 (Lgr5), a stem cell marker, is involved in the maintenance of GSCs, although the properties of Lgr5-positive GSCs remain unclear. Here, the Sleeping-Beauty transposon-induced glioblastoma model was used in Lgr5-GFP knock-in mice identify GFP-positive cells in neurosphere cultures from mouse glioblastoma tissues. Global gene expression analysis showed that Gli2 was highly expressed in GFP-positive GSCs. Gli2 knockdown using lentiviral-mediated shRNA downregulated Hedgehog-related and Wnt signaling pathway-related genes, including Lgr5; suppressed tumor cell proliferation and invasion capacity; and induced apoptosis. Pharmacological Gli inhibition with GANT61 suppressed tumor cell proliferation. Silencing Gli2 suppressed the tumorigenicity of GSCs in an orthotopic transplantation model in vivo. These findings suggest that Gli2 affects the Hedgehog and Wnt pathways and plays an important role in GSC maintenance, suggesting Gli2 as a therapeutic target for glioblastoma treatment.

Purpose The CKD4/6 inhibitor abemaciclib is related to adverse events such as hematological toxicity and increase in serum creatinine levels associated with abemaciclib pharmacokinetics. Increase in serum creatinine levels is considered a result of competition with abemaciclib via organic cation transporter 2 and multidrug and toxic compound extrusion. Therefore, we evaluated the association among serum creatinine levels, serum abemaciclib concentrations, and adverse events and whether increase in serum creatinine levels is a useful indicator for predicting the onset of the adverse events of abemaciclib. Methods In total, the data of 12 patients with breast cancer who were treated with abemaciclib (150 mg twice daily) were evaluated to determine the association between increased serum creatinine levels and abemaciclib concentrations and hematological toxicity. Results Grade 3 neutropenia, thrombocytopenia, and anemia were observed at 4 weeks in four (33%), two (17%), and one (8%) patients, respectively. A significant association was observed between steady-state abemaciclib concentrations and the rate of decrease in neutrophil and platelet counts (r = - 0.80, P = 0.003 and r = - 0.70, P = 0.016, respectively). Compared with baseline levels (0.61 [0.53-0.82] mg/mL), serum creatinine levels significantly increased and reached a steady state in at least 2 weeks (0.84 [0.61-1.02] mg/mL, P = 0.01). However, we did not find a significant association between increase in serum creatinine levels and abemaciclib concentrations and hematological toxicity. Conclusions Abemaciclib concentrations are associated with neutropenia and thrombocytopenia. However, increase in serum creatinine levels may not be a useful predictor for estimating abemaciclib pharmacokinetics and hematological toxicity.

Simultaneous induction of tumor antigen-specific cytotoxic T lymphocytes (CTLs) and helper T lymphocytes (HTLs) is required for an optimal anti-tumor immune response. WT1332, a 16-mer WT1-derived helper peptide, induce HTLs in an HLA class II-restricted manner and enhance the induction of WT1-specific CTLs in vitro. However, in vivo immune reaction to WT1332 vaccination in tumor-bearing patients remained unclear. Here, a striking difference in WT1-specific T cell responses was shown between WT1 CTL + WT1 helper peptide and WT1 CTL peptide vaccines in patients with recurrent glioma. WT1-specific CTLs were more strongly induced in the patients who were immunized with WT1 CTL + WT1 helper peptide vaccine, compared to those who were immunized with WT1 CTL vaccine alone. Importantly, a clear correlation was demonstrated between WT1-specific CTL and WT1332-specific HTL responses. Interestingly, two novel distinct populations of WT1-tetramerlow WT1-TCRlow CD5low and WT1-tetramerhigh WT1-TCRhigh CD5high CTLs were dominantly detected in WT1 CTL + WT1 helper peptide vaccine. Although natural WT1 peptide-reactive CTLs in the latter population were evidently less than those in the former population, the latter population showed natural WT1 peptide-specific proliferation capacity comparable to the former population, suggesting that the latter population highly expressing CD5, a marker of resistance to activation-induced cell death, should strongly expand and persist for a long time in patients. These results demonstrated the advantage of WT1 helper peptide vaccine for the enhancement of WT1-specific CTL induction by WT1 CTL peptide vaccine.

This study aimed to explore the genetic alterations and to identify good responders in the experimental arm in the tumor samples from newly diagnosed glioblastoma (GBM) patients enrolled in JCOG0911; a randomized phase II trial was conducted to compare the efficacy of interferonβ (IFNβ) plus temozolomide (TMZ) with that of TMZ alone. Of 122 tumors, we performed deep targeted sequencing to determine the somatic mutations, copy number variations, and tumor mutation burden; pyrosequencing for O6-methylguanine-DNA methyltransferase (MGMT) promoter methylation; Sanger sequencing for the telomerase reverse transcriptase (TERT) promoter; and microsatellite instability (MSI) testing in 95, 91, 91 and 72 tumors, respectively. We performed a multivariable Cox regression analysis using backward stepwise selection of variables including clinical factors (sex, age, performance status, residual tumor after resection, tumor location) and genetic alterations. Deep sequencing detected an IDH1 mutation in 13 tumors (14%). The MGMT promoter methylation by quantitative pyrosequencing was observed in 41% of the tumors. A mutation in the TERT promoter was observed in 69% of the tumors. While high tumor mutation burden (> 10 mutations per megabase) was seen in four tumors, none of the tumors displayed MSI-high. The clinical and genetic factors considered as independent favorable prognostic factors were gross total resection (hazard ratio [HR]: 0.49, 95% confidence interval, 0.30–0.81, P = 0.0049) and MGMT promoter methylation (HR: 0.43, 0.21–0.88, P = 0.023). However, tumor location at the temporal lobe (HR: 1.90, 1.22–2.95, P = 0.0046) was an independent unfavorable prognostic factor. No predictive factors specific to the TMZ + IFNβ + Radiotherapy (RT) group were found. This additional sub-analytical study of JCOG0911 among patients with newly diagnosed GBM showed that tumor location at the temporal lobe, gross total resection, and MGMT promoter methylation were significant prognostic factors, although no factors specific to IFNβ addition were identified.

Background Spinal subdural hematoma (SSDH), which can cause lower back pain, leg pain, and leg weakness, is rare and will usually be associated with a bleeding tendency, trauma, spinal vascular malformation, intraspinal tumor, or iatrogenic invasion. Only a few cases of SSDH after intracranial chronic subdural hematoma (CSDH) have been reported. We report a case of lumbar SSDH in the absence of predisposing factors after reoperation for recurrent intracranial CSDH, which improved with conservative treatment. Case Description Approximately 1 month after falling, a 63-year-old woman was experiencing left hemiparesis and impaired orientation that was diagnosed as right intracranial CSDH using computed tomography. Surgical treatment of the CSDH led to immediate improvement of her symptoms. On postoperative day 29, the right CSDH had recurred with left hemiparesis, and successful reoperation relieved the symptoms within a few hours postoperatively. However, 1 day after the second operation, very small acute subdural hematomas in regions along the left tentorium cerebelli and left falx cerebri were found on computed tomography. On day 31, she complained of sitting-induced bilateral radiating lower limb pain. Magnetic resonance imaging on day 34 showed an acute SSDH at the L4-L5 level and a sacral perineural cyst filled with hematoma, although her radiating pain was showing improvement. She was treated conservatively and was discharged without symptoms on day 44. Conclusions Although SSDH is rare, it is important for neurosurgeons and physicians to consider the possibility of a SSDH when lower limb pain or paresis occurs after procedures that will result in rapid intracranial pressure alterations such as drainage of an intracranial CSDH.

Background: Fibromuscular dysplasia (FMD) can cause cerebral aneurysms and dissection, which can lead to stroke. Angiographic findings are important in the diagnosis. We report a case of FMD in which the cause of hemorrhage could not be determined by angiography. Case Description: A 73-year-old woman suffered from intracerebral hemorrhage (ICH) associated with FMD without abnormal angiography cerebral vessels. She presented with headache and nausea. Subsequent head-computed tomography-revealed ICH in the left frontal lobe, and contrast-enhanced magnetic resonance imaging revealed a gadolinium-enhancing lesion in the perihematoma area and in the genu of the corpus callosum. Although cerebral angiography revealed a string of beads appearance in the bilateral extracranial internal carotid arteries, no abnormality explaining the hemorrhage was identified. The hematoma was removed and the pathological diagnosis was FMD. In the pathological specimen, various patterns of vulnerable vessels, such as aneurysmal dilatation and obstruction, were observed, which could easily collapse and result in hemorrhage. In the case of ICH of unknown origin, microscopic vessel disruption due to FMD should also be considered. Conclusion: FMD can cause ICH in microscopic vascular lesions that are undetectable on angiography.

Background: The appropriate timing and method of surgery for vertex epidural hematoma (VEDH) are uncertain due to the presentation and slow symptomatic exacerbation caused by bleeding from a venous origin involving the injured superior sagittal sinus (SSS). Coagulation and fibrinolytic disorders that occur after traumatic brain injury also worsen bleeding. For these reasons, it is challenging to decide the surgical procedure and timing of surgery. Case Description: A 24-year-old man involved a car accident and was transported to our emergency department. He was unconscious but not lethargic. Computed tomography showed VEDH overlying the SSS, and hematoma increased temporarily. Due to abnormal coagulation and fibrinolysis at admission, he underwent intentionally delayed surgery after control of coagulation and fibrinolysis. Bilateral parasagittal craniotomy was chosen to ensure hemostasis from the torn SSS. The patient improved without complications and was discharged with no neurological deficit. This case indicates that this surgical strategy is favorable for VEDH with slow symptomatic progression. Conclusion: VEDH is mostly caused by bleeding from the injured SSS secondary to diastatic fracture of sagittal suture. Intentionally delayed surgical intervention using bilateral parasagittal craniotomy after stabilization of coagulation and fibrinolysis is favorable for prevention of further hemorrhage and good hemostasis.

Currently, various posterior surgical techniques are available for cervical spondylotic myelopathy. These techniques include laminoplasty and laminectomy with or without fusion, and are often used in patients with multilevel cervical stenosis. They were developed with the intent to reduce the risk of complications such as injury to the spinal cord and nerve roots, C5 palsy, postlaminectomy membrane, and postoperative kyphosis. Posterior decompression for cervical spondylotic myelopathy is effective in improving neurological function in patients with appropriate surgical indications.

Background and Purpose For removal of childhood posterior fossa tumors, it is important to control bleeding while internally decompressing the tumor. Evaluation of tumor vascularity by preoperative magnetic resonance imaging (MRI) is thought to be effective in predicting and controlling blood loss. In this study, we evaluated the relationship between imaging features, mainly susceptibility-weighted imaging (SWI), and the amount of intraoperative blood loss. Methods Among childhood posterior fossa tumors operated on by the same surgeon between January 2016 and March 2022, 9 cases in which preoperative MRI data could be analyzed and total or subtotal resection was achieved were included. The SWI: intratumoral susceptibility signals (ITSS) grade, an index of tumor vascularity, was used to evaluate the association between the degree of vascularity (ITSS: 0-2 vs. ITSS: 3) and multiple factors, including intraoperative blood loss, in a univariate analysis. In addition, the intraoperative blood loss was analyzed by multivariate analysis. Results There were 3 males and 6 females with a median age of 6 years (5-11). Seven medulloblastomas, one atypical teratoid/rhabdoid tumor, and one ependymoma were included. Univariate analysis showed that patients with higher vascularity (ITSS: 3) had significantly higher intraoperative blood loss (p=0.016) and larger tumor volume (p=0.032). In multivariate analysis with age, degree of contrast enhancement, degree of vascularity, tumor volume, and degree of tumor resection as independent variables, the degree of vascularity was not significantly associated with intraoperative blood loss (p=0.477), but only with tumor volume (p=0.036). Conclusion Although the degree of tumor vascularity may be related to intraoperative blood loss, there was a strong correlation between the degree of vascularity and tumor volume, and multivariate analysis of intraoperative blood loss showed that only tumor volume was a significant factor. Higher tumor vascularity was associated with larger tumor volume, which may result in increased intraoperative bleeding.