Journal of Korean Neurosurgical Society最新文献

Objective: Massive cerebral infarction caused by middle cerebral artery infarction leads to extensive cerebral infarction in one hemisphere, resulting in swelling of the brain and further compression of surrounding normal brain tissue, ultimately leading to a complete cerebral infarction and a mortality rate of about 50-80% for patients. Although early decompressive craniectomy and partial internal decompression can reduce mortality rates, neurosurgeons should strive to achieve lower mortality rates in the face of patients' lives. This study introduces a surgical method with lower mortality rate, which is a rapid internal decompression technique for cerebral hemisphere resection through a flat bone window after decompressive craniectomy (DC) and partial temporal lobe resection.

Methods: From March 2022 to March 2024, 18 patients with extensive cerebral infarction underwent craniotomy and partial temporal lobectomy, craniectomy combined with rapid internal decompression (CCRID). Standard large bone flap craniotomy and anterior temporal lobe resection were performed. Circular electrocoagulation of the arachnoid membrane 1 cm inside the bone window, with sharp cutting, and then rapid resection of necrotic brain tissue outside the bone window (the height of the removed necrotic brain tissue is about 1-2 cm), while electrocoagulating the blood vessels from front to back along the direction of blood vessel formation. Place the drainage tube and intracranial pressure monitoring catheter for 1-2 days. Clinical outcomes were compared to 24 patients who underwent DC combined with partial temporal/frontal pole resection (DCPTR).

Results: The average age of 18 patients was 63 years. The mean cerebral hemisphere resection time was 6.8 minutes with total surgery averaging 2.82 hours. Postoperative ICP averaged 4 mmHg, and the midline shifted back by 0.45 cm. At 3 months, there was one intracerebral hemorrhage, no infections, and a mortality rate of 11.1%. The mean modified Rankin scale score was 4.45. Compared to DCPTR, CCRID showed similar midline shift, shorter surgery time, and lower mortality.

Conclusion: CCRID may represent a viable decompression technique for patients with massive hemispheric infarctions, warranting further consideration for future applications.

Objective: Subdural hematomas (SDHs) are classified clinically and/or radiologically as acute SDH (ASDH), subacute SDH (SSDH), and chronic SDH (CSDH). The management differ depending on their classification, with only the ASDH having a definite accepted surgical guideline. Non-acute SDH, specifically SSDH and CSDH have no clear surgical guidelines but are managed similarly in some literature. This study was conducted to determine if there is a difference in outcomes among surgically managed non-acute SDH in a specific elderly population of retired military personnel.

Methods: This is a pre-pandemic retrospective study that utilized data obtained from January 2016 to April 2019, in a subspecialty tertiary hospital that caters to retired military personnel or veterans, in the Philippines. After chart review and application of inclusion and exclusion criteria, 21 patients were included, all military retirees, with age 56 years old and above. Chart review and electronic database were retrieved to extract relevant information.

Results: In this study, a term 'mixed-type subdural hematoma' (MSDH) was proposed to encompass SDH that have mixed hypo-andhyperdensity on preoperative computed tomography scan and were subsequently found to have bright red liquefied hematoma instead of the classic engine machinery oil fluid found in a CSDH. Based on the observed cohort, nine out of 11 CSDH patients attained the Glasgow outcome scale extended (GOS-E) score of 8 while all the respondents in the MSDH group attained the same GOS-E score underscoring the need for early intervention in patients with non-acute SDH. Moreover, the outcomes of both MSDH and CSDH are comparable with low mortality rate (approximately 9.5%) and immediate postoperative improvement (approximately 90%).

Conclusion: MSDH and CSDH, although classified separately using clinical and/or radiologic means, can collectively be categorized as a non-acute SDH and can be managed safely and effectively with burr hole surgery.

Objective: The aim of this study is evaluating in vivo degradation of photocrosslinkable hyaluronic acid (HA)-based dural sealant (HA photosealant) using magnetic resonance imaging (MRI) and histopathological analysis to assess its biodegradability and effectiveness in preventing cerebrospinal fluid (CSF) leakage.

Methods: HA photosealants were applied to the incised dura in a rat craniectomy and durotomy. The HA photosealant quickly sealed the wound upon low-energy visible light exposure (405 nm, <5 seconds, < 1 J/cm2). The degradation of HA photosealants was tracked through serial MRI scans at 1, 2, and 4 weeks post-application. The remaining area of HA photosealants on the dura was measured using image processing program for volumetric analysis. Additionally, histopathological analyses were performed to evaluate the biocompatibility and effectiveness of the dural repair.

Results: The MRI and histopathological analyses showed that the HA photosealant achieved progressive degradation while successfully preventing CSF leakage without any adverse tissue reactions. The residual area of HA photosealants measured at 2 weeks ranged from 41.35% to 94.88%, with an average of 66.57%. At 4 weeks, a more distinct degradation pattern was observed compared to 2 weeks, showing a residual area of 10.28% to 56.11%. The HA photosealant maintained structural integrity until dural regeneration was completed.

Conclusion: HA photosealant showed gradual degradation in vivo while maintaining mechanical strength until the dura was repaired for preventing CSF leakage without inflammation and toxicity. HA photosealant has great potentials for clinical application for dural repair with biodegradable properties and biocompatibility.

Objective: Acute subdural hematoma (A-SDH) in patients with a Glasgow coma scale (GCS) score of 3 presents significant challenges in clinical decision-making owing to high mortality rates and the likelihood of severe disability. Here, we analyzed data to assess the number of surgical treatments and overall treatment outcomes for patients with A-SDH admitted in a comatose state and discussed the value of such aggressive surgical interventions based on these findings.

Methods: A retrospective analysis was conducted using data from five regional trauma centers in Korea registered with the Korean Neurotrauma Data Bank System. This study included adult patients (aged ≥19 years) admitted between January 2018 and June 2021 to a comatose state due to A-SDH. Patients were classified into death and survivor groups based on their outcomes, and their demographic, clinical, and radiological characteristics were compared. Additionally, patients were divided into a combined group of deaths and vegetative state survivors and a group of remaining survivors to compare the differences and assess the impact of death and vegetative state.

Results: Among a total of 109 patients, the mean age was 59.28 years, and the mortality rate was 80.7%. Among the 21 survivors, 12 (57.1%) remained vegetative. Surgical treatment was performed in 42 patients (38.5%), resulting in a lower mortality rate (64.3%) than conservative treatment (91.0%). However, the rate of the vegetative state was higher in the surgical group (21.4%) than in the conservative group (4.5%). Pupil reactivity was a significant predictor, with mortality rates of 44.4%, 57.1 %, and 85.9% for reactive, unilaterally unreactive, and bilaterally unreactive pupils, respectively. The surgical group had a significantly longer hospital stay (23.69±29.15 days) compared to the conservative group (6.45±13.75 days).

Conclusion: It is time to go one step further from death with the dignity law and have a comprehensive consideration and social consensus on 'how to end life.' A model that can more accurately predict situations in which decompressive surgery should be considered for patients in a comatose state due to A-SDH is required. Neurosurgeons must have a comprehensive understanding of the patient's progress, the anticipated prognosis, and the various financial and psychological burdens on the family and must be able to communicate this information thoroughly.

Objective: This study aimed to assess the safety and efficacy of using the PEAK Plasmablade TMX (PBX) in deep brain stimulation (DBS) of implantable pulse generator (IPG) replacement surgeries, alongside identifying potential risk factors for postoperative complications.

Methods: A prospective study was conducted on 50 patients undergoing IPG replacement with PBX, compared to 150 historical controls. Demographic data, surgical characteristics, and postoperative outcomes were analyzed. Logistic regression was used to identify predictors of surgical complications.

Results: The demographic and clinical profiles of patients in the PBX group were comparable to those in the control group. PBX significantly reduced surgical duration (p=0.005) and did not result in impedance abnormalities. While wound complications did not significantly differ between groups, logistic regression identified diabetes as a significant predictor of wound dehiscence or delayed healing (p=0.012).

Conclusion: The findings support the safety and efficacy of PBX in DBS IPG replacement surgeries, offering advantages such as reduced surgical duration and minimized risk of impedance abnormalities. However, diabetes emerged as a significant predictor of adverse wound outcomes, highlighting the need for tailored preoperative assessment and management strategies.

Constitutional mismatch repair deficiency (CMMRD) is a rare and highly aggressive cancer predisposition syndrome caused by biallelic germline mutations in mismatch repair genes. This condition is characterized by early-onset malignancies across multiple organ systems, including central nervous system tumors, hematological cancers, and gastrointestinal malignancies. CMMRD-associated tumors exhibit hypermutation and microsatellite instability, resulting in a high tumor mutation burden and rendering these malignancies responsive to immune checkpoint inhibitors (ICIs). ICIs targeting programmed cell death protein-1 and programmed cell death ligand 1 have demonstrated remarkable efficacy, particularly in hypermutated tumors, providing durable responses and improving survival outcomes. Advances in genetic and molecular diagnostics have enhanced the ability to identify CMMRD early, allowing for the implementation of comprehensive surveillance programs and improved management strategies. A multidisciplinary and individualized approach is essential for managing CMMRD patients. This review underscores the importance of early diagnosis, surveillance, and emerging therapeutic approaches to improve outcomes and quality of life for individuals and families affected by this devastating syndrome.

Rhabdoid tumor predisposition syndrome (RTPS) is a rare autosomal dominant disorder characterized by an increased risk of developing malignant rhabdoid tumors in early childhood. This syndrome is primarily caused by germline heterozygous loss-of-function pathogenic variants in the SMARCB1 gene (RTPS1) and rarely in the SMARCA4 gene (RTPS2). RTPS is characterized by the development of atypical teratoid rhabdoid tumors of the central nervous system, malignant rhabdoid tumors of the kidney, and/or extrarenal extracranial rhabdoid tumors. The syndrome demonstrates high penetrance, with most tumors developing before age 3 years, and carries a poor prognosis despite intensive multimodal therapy. Early diagnosis through genetic testing, implementation of surveillance protocols, and aggressive treatment approaches are crucial for improving outcomes. This review comprehensively examines the genetic basis, clinical manifestations, surveillance strategies, and current management approaches for RTPS, with particular emphasis on emerging therapeutic options and the importance of multidisciplinary care.

Li-Fraumeni syndrome (LFS) is a rare inherited cancer predisposition syndrome caused by germline mutations in the TP53 tumor suppressor gene. It predisposes affected individuals to a wide spectrum of early-onset malignancies, including sarcomas, breast cancer, brain tumors, and adrenocortical carcinoma. Advances in genetic testing and risk management strategies have enhanced the identification and clinical management of LFS patients. Comprehensive surveillance has demonstrated increased survival rates through proactive screening. Beyond surveillance, research is exploring novel approaches such as liquid biopsy for early cancer detection and chemoprevention strategies, including metformin trials, to mitigate cancer risk. This review discusses the molecular basis, clinical spectrum, surveillance strategies, and emerging research in LFS.