Nakamasa Hayashi

Chordomas of the skull base: surgical management and outcome.

OBJECTnThe goal of this study was to report on the surgical management of skull base chordomas and to evaluate both the short- and long-term treatment outcomes.nnnMETHODSnThe authors retrospectively studied data from 49 patients who had undergone consecutive surgeries at a single institution. They also analyzed patterns of chordoma extension. Complications and surgery-related morbidity were recorded. A Kaplan-Meier analysis was performed to determine survival rates in patients 5 and 10 years after their first surgery. Operative approaches were selected on the basis of the predominant tumor extension.nnnRESULTSnThe approach used most frequently was the transethmoidal in 36.3%, followed by the pterional in 23.4% and the retrosigmoid in 23.4%. The tumor was totally removed in 49.4% and subtotally in 50.6%. The rate of total removal was highest at initial surgery (78%) and progressively declined thereafter. In 11.8% of cases a new neurological deficit developed, while the preoperative deficit remained unchanged. In 20% of cases the preoperative deficits improved, but new deficits also appeared. The 5- and 10-year survival rates are 65 and 39%, respectively.nnnCONCLUSIONSnWith an individually tailored surgical approach, total tumor removal in 78% of the cases was achieved at the initial surgery. Radical surgery appears to increase slightly the surgical morbidity, but at the same time prolongs the recurrence-free interval. Chordomas cannot be regarded as surgically curable tumors given the 5- and 10-year survival rates in patients harboring such lesions.

Surgical treatment of skull base chondrosarcomas

Skull base chondrosarcomas are rare tumors and individual experience with their management is limited. We present a series of such tumors treated at our institution. Particular attention was paid to their extension pattern, choice of surgical approach, and outcome. Twenty-five patients were operated consecutively over a period of 19xa0years. Their clinical presentation, radiological features, surgical treatment, early and late treatment outcome, as well as survival rate were analyzed. The most frequent initial symptom was abducent palsy. The typical bone destruction of the petrous apex was found in 83%. Chondrosarcomas extended in 92% to the posterior cranial fossa. Total number of surgeries was 39. The operative approach was tailored to each case. The retrosigmoid approach was used in 30.8%, the pterional in 23%, and the transethmoid in 15.4%. Total tumor removal was achieved in 19 of the surgeries. New neurological deficits immediately after surgery appeared in 33.3%. The perioperative mortality was 0%. The average Karnofsky performance score at last follow-up was 91%, and 5- and 10-year survival rates were 95%. Individually tailored approach in skull base chondrosarcomas allows radical removal with low morbidity rates and without mortality. Given the good long-term prognosis, surgical treatment should not deteriorate significantly patients’ quality of life.

Postpartum dissecting aneurysm of the posterior cerebral artery

Intracranial dissecting aneurysm may cause subarachnoid hemorrhage (SAH) or infarction, and postpartum dissecting aneurysm is rare. A 30-year-old 6 days postpartum woman presented with posterior cerebral artery (PCA) dissection evolving dramatically over a short period. She had been well until 6 days after delivery when she suffered sudden onset of headache, vomiting, and unconsciousness. CT scan demonstrated SAH and digital subtraction angiography (DSA) revealed a fusiform dilatation of the left PCA (P3/P4 segment). The initial diagnosis was ruptured dissecting aneurysm, and conservative management was recommended in the acute period. DSA showed smoothening of the vascular wall 6 days after onset, and obliteration of the left P3/P4 segment was observed 13 days after onset. She was discharged without neurological deficits 26 days after onset. Postpartum SAH due to dissecting aneurysm of the PCA is rare, but should be considered in the differential diagnosis of postpartum headache.

Chronologic Changes of Cerebral Ventricular Size in a Transgenic Model of Hydrocephalus

We have maintained a transgenic mouse model of hydrocephalus created to overproduce the cytokine, transforming growth factor-β1 (TGF-β1) in the central nervous system (CNS). The aim of the present study was to estimate the embryonic period when the transgenic mice would develop hydrocephalus, by investigating the chronological developmental changes of the cerebral ventricles. Qualitative analysis of ventricular size was performed on sections cut in the coronal plane of embryos at the 15th (E15) and 18th (E18) embryonic days, and postnatal mice aged 4 days (P4). The presence of the TGF-β1 transgene was determined by performing polymerase chain reaction (PCR) analysis. We have examined 24 embryos and 14 postnatal mice. By performing PCR analysis, the TGF-β1 transgene was determined to be present in 16 (42.1%). Five of 16 embryos at E15 carried the transgene, and showed a slight enlargement of the lateral ventricles. Three of 8 embryos at E18 carried the transgene, and had remarkable enlargement of the lateral ventricles. Eight of 14 pups at P4 carried the transgene, and 7 of 8 pups with the transgene developed hydrocephalus. In pups that were positive for the transgene, massive enlargement of the lateral ventricles was observed and there was an associated thinning of the overlying cerebral cortex. These results suggest that congenital hydrocephalus may develop at an important embryonic time period, which coincides with the stage of neural stem cell proliferation and differentiation in the CNS.

Thrombin-induced cell proliferation and platelet-derived growth factor-AB release from A172 human glioblastoma cells

Background:u2002In a previous study, we found that thrombin induced proliferation of TM‐1 and T98G human glioma cells and that the mitogenic effect was abolished by hirudin. Objectives:u2002We investigated thrombin’s effects on the proliferation of A172 human glioblastoma cells and the induction of growth factors. Furthermore, we examined whether or not the expression of heparin cofactor II (HCII) in A172 cells using adenovirus vector could suppress thrombin’s effects. Methods:u2002The effect of thrombin on cell proliferation was assessed using a 3‐(4,5‐dimethylthiazol‐2‐yl)‐2,5‐diphenyl‐tetrazolium bromide assay. The amount of growth factors in the conditioned medium was measured by enzyme‐linked immunosorbent assay. The level of platelet‐derived growth factor (PDGF)‐B mRNA was assessed by reverse transcriptase‐polymerase chain reaction analysis. Results:u2002Thrombin‐induced proliferation of A172 cells primarily depended on the enhanced secretion of PDGF‐AB by thrombin. The action of thrombin depended on its proteolytic activity. However, thrombin‐induced PDGF‐AB secretion was not abolished by anti‐protease‐activated receptor (PAR) antibody. The PAR‐1 agonist peptide had no effect on cell growth and PDGF‐AB levels. Thrombin did not increase PDGF‐B gene expression. Expression of HCII effectively suppressed thrombin‐induced PDGF‐AB release. Conclusions:u2002These results indicate that thrombin may play an important role in the proliferation of A172 cells by inducing PDGF‐AB secretion and that thrombin’s action is mediated by its proteolytic activity. Inhibition of thrombin’s proteolytic activity may be a new therapeutic method for gliomas.