A 69-year-old female presented with sudden onset of truncal ataxia, urinary incontinence , mental confu sion, and Parinaud's sign. With conservative treatment, her ataxia and urinary incontinence resolved . Magnetic resonance (MR) imaging disclosed a round mass with laminated intramural hemorrhage in the third ventricle. Right vertebral angiography demonstrated a giant aneurysm in the distal basilar ar tery. Xenon-enhanced computed tomography showed that cerebral blood flow (CBF) was reduced in the thalamus bilaterally and was paradoxically decreased by acetazolamide. Two months later , MR imag ing showed that the intramural hemorrhage had shrunk, and the edema in the thalamus was resolving . The CBF reduction and vascular response to acetazolamide had reversed to some extent . A partially thrombosed giant aneurysm can grow acutely as the result of fresh intramural hemorrhage . The edema is secondary to ischemia and loss of vasoresponsivity.
An adult autopsy case of the persistent primitive trigeminal artery (PTA) is reported. At the origin of the PTA in the cavernous portion of the internal carotid artery, the PTA branched into the meningohypophyseal trunk and the artery of the inferior cavernous sinus. This might indicate that these arteries were formed at the same embryonic stage. At the cisternal portion of the PTA in the posterior fossa, it also branched into the trigeminal nerve root and pons on the way to the basilar artery. The PTA might have functions for the normal structures even in the case of adults. The PTA passed through the dural foramen, which was located medial to Meckel's cave, and connected with the basilar artery. The diameter of the PTA decreased markedly at the foramen. The dural foramen might be the site of regression of the PTA during the embryonic stage.
We earlier reported that endogenous TNF could be induced in mice as well as in patients by successive administration of exogenous TNF as a primer and OK-432 as a trigger, and we termed this exogenous/endogenous TNF (EET) therapy. We studied the effect of EET therapy with cyclophosphamide (CY) on tumor-transplanted rats. In order to induce endogenous TNF, 5 x 10(5) U/kg of recombinant human TNF-S(AM2) (rTNF; 5.6x10(6) U/mg protein) was injected intravenously (iv) as a primer followed by injection of 25 KE/kg of OK-432 as a trigger. TNF activity induced in serum was about 500 U/ml. Only 1 U/g of TNF was detected in the brain. To evaluate the antitumor effect, C6 glioma cells (1.6 x 10(4) cell/5 microliters) was transplanted into the brain. On day 7 of the transplantation, the rats were administered iv with CY (75 mg/kg), treated with EET therapy 7 days thereafter, and survival days were checked. No clear difference in survival days was observed between the rats treated with the EET and the control group. Three rats out of 6 treated with CY survived for more than 40 days, and all the rats treated with the combination of CY and EET continued to survive. The histological examination on day 44 revealed necrotic changes at the tumor lesions in all of the surviving rats, and the animals were evaluated as completely cured. These results suggest that applied treatment based on the EET therapy will be also effective against malignant brain tumors.
scite is a Brooklyn-based organization that helps researchers better discover and understand research articles through Smart Citations–citations that display the context of the citation and describe whether the article provides supporting or contrasting evidence. scite is used by students and researchers from around the world and is funded in part by the National Science Foundation and the National Institute on Drug Abuse of the National Institutes of Health.