Acute aggravation of subdural fluid collection associated with dural metastasis of malignant neoplasms: case report and review of the literature.

A 63-year-old woman was admitted to our hospital with serious headache and vomiting. Five months before admission, she had undergone surgery for a primary advanced gastric cancer. Neuroradiological examinations revealed subdural fluid collection. We twice performed evacuation of the subdural fluid collection. However, aggravation of her state of consciousness progressed and she passed away. Histological examinations demonstrated that the dural veins were infiltrated by numerous tumor cells that produced mucus; however, ruptured vessels were not found. Furthermore, the subdural fluid collection increased shortly after the initial operation. We infer that the cause of the collection, which was associated with the dural metastasis of malignant tumors, was not only mucin secretion by tumor cells but also a rapid increase in perfusion pressure in the vessels of the dura mater, resulting in extravasation of plasma components into the subdural space. Our case demonstrates that the pathogenetic mechanism that is specific for subdural fluid collection caused by dural metastasis of malignant tumors differs from the mechanism of production of subdural hematoma associated with dural metastasis.

[Metastatic brain tumors with simultaneous multiple cerebral hemorrhages: a case report].

We encountered a case of multiple metastatic brain tumors with simultaneous multiple cerebral hemorrhages. A 45-year-old male suffered from sudden left hemiplegia and was admitted to our hospital. CT scans on admission revealed multiple cerebral hemorrhages with surrounding brain edema in the right frontal lobe, left frontal lobe, right occipital lobe and right basal ganglia. On full-body examination, renal cell carcinoma of the left kidney and multiple metastatic tumors in the lung, liver and vertebral body were identified. We continued conservative therapy, but the patient's condition worsened and he died 36 days later. The autopsy findings indicated that all hemorrhages had occurred in the necrotic tissue associated with the metastatic brain tumors. Simultaneous multiple cerebral hemorrhages caused by metastatic brain tumors are very rare, and the differential diagnosis of cerebral hemorrhage due to metastatic brain tumor and hypertensive cerebral hemorrhage is difficult. The present case indicates that metastatic brain tumor should be taken into consideration in cases with simultaneous multiple intracerebral hemorrhages.

[Nontraumatic arterial dissection of the anterior cerebral artery with simultaneous cerebral infarction and subarachnoid hemorrhage: a case report].

We encountered a case of nontraumatic arterial dissection of the anterior cerebral artery (ACA) which exhibited cerebral infarction and subarachnoid hemorrhage (SAH) simultaneously, and whose symptoms were improved by conservative treatment. A 55-year-old female presenting with headache and weakness in her left leg was admitted to our hospital. CT scans on admission revealed SAH in the interhemispheric fissure and surface of the right frontal lobe, but CT scans at 3 days after onset demonstrated cerebral infarction in the medial part of the right frontal lobe. Cerebral angiography on day 6 disclosed an aneurysmal dilatation and narrowing at the right A2-A3 segment. We continued conservative therapy including blood pressure control, since there was no symptomatic deterioration. The aneurysmal dilatation disappeared and the weakness of the left leg also improved. This case indicates that conservative treatment could be an option for the management of nontraumatic arterial dissection of the ACA with simultaneous cerebral infarction and SAH.

[A case of cerebral arteriovenous malformation revealing repeated intranidal hemorrhage accompanying neovascularization after stereotactic radiosurgery].

We report a patient with cerebral arteriovenous malformation (AVM) revealing growing mass lesion after stereotactic radiosurgery. This 12-year-old female presented headache. CT scan showed hematoma at the head of the right caudate nucleus and angiography showed AVM at the site. LINAC-based stereotactic radiosurgery was performed with the patient. Twenty-three months after the radiosurgery the patient complained headache and CT scan showed hematoma again at the same site, although angiography did not show AVM. Thirty-five months after the radiosurgery mass lesion with enhancement effect was observed at the site and the mass lesion grew gradually thereafter. Thirty-nine months after the radiosurgery the mass lesion was evacuated. Histological examination revealed fibrotic core and surrounding neovascularized area with hemorrhage. The histology shows a new etiology of growing mass lesion after radiosurgery for AVM.

[Hyperkalemia caused by intravenous administration of mannitol in a patient with arteriovenous malformation: case report].

We experienced a case in which hyperkalemia was induced by mannitol administration. The medication with mannitol was given to a 15-year-old male patient who underwent a removal operation for arteriovenous malformation under general anesthesia. Following the mannitol infusion, his arterial blood gas and electrolyte analysis revealed severe metabolic acidosis and an increase in serum potassium. Furthermore, a change in his electrocardiogram was observed. The hyperkalemia was quickly normalized by medication with calcium gluconate and sodium bicarbonate. We stopped the removal operation with the aim of giving priority to the patient's safety. It is speculated that the hyperkalemia was caused by the administration of mannitol. Checks of electrolyte levels, arterial blood gas analysis and electrocardiogram monitoring should therefore be carried out when using mannitol, especially in an emergency situation such as intracranial hemorrhage.

Growth control of C6 glioma in vivo by nerve growth factor.

Treatment with nerve growth factor (NGF) causes differentiation of rat C6 glioma cells and strongly inhibits their proliferation in vitro. This suggests that induction of NGF-mediated differentiation may provide a novel therapeutic approach to growth control of glial tumors. We examined the effects of NGF treatment on the growth potential of C6 glioma, which expressed NGF receptor in vivo. C6 glioma cells (1 x 10(6) cells/10 microl) were transplanted into the rat striatum. After 4 days, the animals were given successive injections of 100 ng NGF into the growing tumor at every 4 days (n = 10 rats). Controls were subjected to identical procedures with vehicle which did not contain NGF (n = 10 rats). At 14 days after transplantation, we evaluated the tumor volume, proliferative cell index (PCI) based on the MIB-1 immunoreactivity and enzyme activities related to energy metabolism by enzyme histochemistry. We found that the NGF treatment markedly reduced the tumor volume of the C6 glioma (34.00 +/- 8.47 mm3 to 7.22 +/- 4.92 mm3, p < 0.01). NGF treatment also decreased the PCI (33.34 +/- 9.57% to 3.85 +/- 3.56%, p < 0.01) with a negative correlation with tumor volume (r = 0.972, p < 0.01), and the hexokinase (HK) and glucose-6-phosphate dehydrogenase (G6PDH) activities (p < 0.01 and p < 0.01, respectively) which reflect the demand for nucleic acid synthesis for proliferation through the glycolytic and pentose phosphate pathways. The present results demonstrate for the first time that inhibition of tumor cell proliferation of C6 glioma by NGF occurs in vivo, probably through the NGF-mediated differentiation of C6 glioma cells which has been observed in in vitro studies.