Byung Sup Kim, Yuil Kim, Doo-Sik Kong, Do-Hyun Nam, Jung-Il Lee, Yeon-Lim Suh, and Ho Jun Seol
The authors conducted this retrospective study to investigate the clinical outcomes of intracranial solitary fibrous tumor (SFT) and hemangiopericytoma (HPC), defined according to the 2016 WHO classification of central nervous system (CNS) tumors.
Histopathologically proven intracranial SFT and HPC cases treated in the period from June 1996 to September 2014 were retrospectively reviewed and analyzed. Two neuropathologists reviewed pathological slides and regraded the specimens according to the 2016 WHO classification. Factors associated with progression-free survival (PFS) and overall survival (OS) were statistically evaluated with uni- and multivariate analyses.
The records of 47 patients—10 with SFT, 33 with HPC, and 4 with anaplastic HPC—were reviewed. A malignant transition from conventional SFT to WHO grade III SFT/HPC was observed in 2 cases, and 13 HPC cases were assigned grade III SFT/HPC. Mean and median follow-ups were 114.6 and 94.7 months, respectively (range 7.1–366.7 months). Gross-total resection (GTR) was significantly associated with longer PFS and OS (p = 0.012 for both), and adjuvant radiation therapy versus no such therapy led to significantly longer PFS (p = 0.018). Extracranial metastases to the liver, bone, lung, spine, and kidney occurred in 10 patients (21.3%). Grade III SFT/HPC was strongly correlated with the development of extracranial metastases (p = 0.031).
The 2016 WHO classification of CNS tumors reflected the different types of pathological malignant progression and clinical outcomes better than prior classifications. Gross-total resection should be the primary treatment goal in patients with SFT/HPC, regardless of the pathological grade, and radiation can be administered as adjuvant therapy for patients with SFT/HPC that shows an aggressive phenotype or that is not treated with GTR.
Jae Taek Hong, Tae Hyung Kim, Il Sup Kim, Seung Ho Yang, Jae Hoon Sung, Byung Chul Son, and Sang Won Lee
The aim of this study was to analyze the exact location of the internal carotid artery (ICA) relative to the C-1 lateral mass and describe the effect of age on the tortuosity of the ICA.
The authors analyzed 641 patients who had undergone CT angiography to evaluate the location of the ICA in relation to the C-1 lateral mass. Each patient was assigned to 1 of 3 age groups (< 41 years, 41–60 years, and > 60 years of age). The degree of lateral positioning of the ICA was classified into 4 groups: Group 1 (lateral to the C-1 lateral mass), Group 2 (lateral half of the lateral mass), Group 3 (medial half of the lateral mass), or Group 4 (medial to the lateral mass). The anteroposterior relationship of the ICA was classified into Group A (posterior to the anterior tubercle) or Group B (anterior to the anterior tubercle). Distances from the ICA to the midline, anterior tubercle, and anterior cortex of the lateral mass were measured. Distances between the lateral margin of the lateral mass and the longus capitis muscle were also evaluated.
The prevalence of the ICA located in front of the lateral mass (Groups 2 and 3) was 47.4% overall. The position of the ICA changes with age due to vessel tortuosity. Only 18.3% of patients in the youngest age group (< 41 years of age) had an ICA in front of the lateral mass (Group 2 or 3 area). However, this percentage increased in the older 2 groups (43.5% in the 41–60 year old group, and 57% in the > 60-year-old age group). The mean distance from the midline to the ICA was 22.6 mm, and the mean distance from the ICA to the C-1 anterior tubercle and the ventral cortex of the lateral mass was 4.7 and 4.5 mm, respectively. Moreover, the ICA is more prone to injury during bicortical C-1 screw placement when the longus capitis muscle is hypotrophic and does not cover the entire ventral surface of the lateral mass.
Elderly patients have a higher incidence of a medially located ICA that may contribute to the risk of injury to the ICA during bicortical C-1 screw or C1–2 transarticular screw placement. Although the small number of reported cases of ICA injury does not allow for determination of a direct relationship with specific anatomical characteristics, the presence of unfavorable anatomy does warrant serious consideration during evaluation for C-1 screw placement in elderly patients.
Ho Jun Yi, Jung Eun Lee, Dong Hoon Lee, Young Il Kim, Chul Bum Cho, Il Sup Kim, Jae Hoon Sung, and Seung Ho Yang
Perilesional edema is a predominant mechanism underlying secondary brain injury after traumatic brain injury (TBI). Perilesional edema is characterized by inflammation, production of proinflammatory cytokines, and migration of peripheral immune cells into the brain. The nucleotide-binding domain and leucine-rich repeat (NLR) family pyrin domain–containing 3 protein (NLRP3) is a key component of secondary injury. Pioglitazone regulates NLRP3 and other inflammatory cytokines. In the present study, the role of NLRP3 and the pharmacological effects of pioglitazone were investigated in animal TBI models.
Brain contusion was induced in a weight drop model involving 3 groups of mice: C57 BL/6 (sham group), NLRP3 knockout (K/O group), and pioglitazone-treated mice (treatment group). The percentage of brain water content of the 3 groups of mice was compared over a period of time. Western blot, immunohistochemistry, and immunofluorescence analyses were conducted to investigate NLRP3-related inflammasomes and the effects of pioglitazone in the TBI models.
Brain edema was the highest on day 3 after TBI in the sham group. Brain edema in both the K/O and the treatment groups was lower than in the sham group. In Western blot, the expression of inflammasomes was higher after TBI in the sham group, but the expression of interleukin-1β, caspase-1, and NLRP3 was decreased significantly following treatment with pioglitazone. The expression of GFAP (glial fibrillary acidic protein) and Iba1 was decreased in both the K/O and treatment groups. In addition, confocal microscopy revealed a decrease in microglial cell and astrocyte activation following pioglitazone therapy.
The inflammasome NLRP3 plays a pivotal role in regulating cerebral edema and secondary inflammation. Interestingly, pioglitazone reduced cerebral edema and immune response after TBI by downregulating the effects of NLRP3. These results suggest that the clinical application of pioglitazone may be a neuroprotective strategy in TBI.
Hyoung-Sub Kim, Jong Beom Lee, Jong Hyeok Park, Ho Jin Lee, Jung Jae Lee, Shumayou Dutta, Il Sup Kim, and Jae Taek Hong
Little is known about the risk factors for postoperative subaxial cervical kyphosis following craniovertebral junction (CVJ) fixation. The object of this study was to evaluate postoperative changes in cervical alignment and to identify the risk factors for postoperative kyphotic change in the subaxial cervical spine after CVJ fixation.
One hundred fifteen patients were retrospectively analyzed for postoperative subaxial kyphosis after CVJ fixation. Relations between subaxial kyphosis and radiological risk factors, including segmental angles and ranges of motion (ROMs) at C0–1, C1–2, and C2–7, and clinical factors, such as age, sex, etiology, occipital fixation, extensor muscle resection at C2, additional C1–2 posterior wiring, and subaxial laminoplasty, were investigated. Univariate and multivariate logistic regression analyses were conducted to identify the risk factors for postoperative kyphotic changes in the subaxial cervical spine.
The C2–7 angle change was more than −10° in 30 (26.1%) of the 115 patients. Risk factor analysis showed CVJ fixation combined with subaxial laminoplasty (OR 9.336, 95% CI 1.484–58.734, p = 0.017) and a small ROM at the C0–1 segment (OR 0.836, 95% CI 0.757–0.923, p < 0.01) were related to postoperative subaxial kyphotic change. On the other hand, age, sex, resection of the C2 extensor muscle, rheumatoid arthritis, additional C1–2 posterior wiring, and postoperative segmental angles were not risk factors for postoperative subaxial kyphosis
Subaxial alignment change is not uncommon after CVJ fixation. Muscle detachment at the C2 spinous process was not a risk factor of kyphotic change. The study findings suggest that a small ROM at the C0–1 segment with or without occipital fixation and combined subaxial laminoplasty are risk factors for subaxial kyphotic change.