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Introduction. The purpose of this paper is to clarify the clinical course, with the dural carotid cavernous fistula (CCF), featuring a pallet of symptoms, paying special attention to radiological findings. Methods. Seventy-six consecutive patients with dural CCFs were investigated in detail, all of whom were defined by angiography. Results. The most common initial symptom was diplopia in 47 patients (62%) and the most frequently observed on arrival were type II, featuring cranial nerve palsies followed by the classical triad in 27, and then type I only with cranial nerve palsies. The time until admission with type I (mean: ) was significantly shorter than that with type II (mean: ). Branches from bilateral carotid arteries widely inflowing into bilateral carotid cavernous sinus were present in 30 (39%), 20 (26%) of which also demonstrated direct inflow into the intercavernous sinus. type I and II had more multiple venous drainage routes as compared with type III (classical triad only on arrival) and IV (initial development of the classical triad followed by cranial nerve palsy). Conclusion. In our series of dural CCF patients, the most common initial symptom was cranial nerve palsy, mostly featuring multiple venous drainage including cortical drainage. Such palsies should be added to the classical triad as indicative symptoms. Bilateral carotid arteries often inflow into cavernous and intercavernous sinuses, which should be taken into account in choice of therapeutic strategy.

Nonsteroidal anti-inflammatory drugs are known to suppress the occurrence and progression of malignancies such as colorectal cancers. However, the precise mechanism of these actions remains unknown. We have evaluated the role of an inducible cyclo-oxygenase (COX-2) in tumor-associated angiogenesis and tumor growth, and identified the downstream molecules involved using a ddy mouse model of sponge angiogenesis, which mimics tumor angiogenesis and is COX-2 and vascular endothelial growth factor (VEGF) dependent. In this model, VEGF expression was down-regulated by selective COX-2 inhibition with NS-398. To find out the involvement of COX-2/VEGF pathway in tumor-associated angiogenesis, we estimated angiogenesis occurring around implanted Millipore chambers containing sarcoma-180 (S-180) cells or Lewis lung carcinoma cells. Daily oral administration of NS-398 or of aspirin, a nonselective COX inhibitor, suppressed angiogenesis seen around the Millipore chambers. S-180 cells implanted in ddy mice formed substantial tumors with extensive angiogenesis markedly suppressed by aspirin and COX-2 inhibitors NS-398 and JTE522, but not by mofezolac, an inhibitor of constitutive COX-1. Tumor-associated angiogenesis was also significantly suppressed by a neutralizing antibody against VEGF. S-180 tumor growth in the subcutaneous tissues was also suppressed by aspirin, COX-2 selective inhibitors, and the VEGF antibody, but not by the COX-1 inhibitor. These results demonstrate that the inhibition of the COX-2/VEGF-dependent pathway was effective in tumor-associated angiogenesis, tumor growth, and tumor metastasis.

We investigated whether the kinin-generating system enhanced angiogenesis in chronic and proliferative granuloma and in tumor-surrounding stroma. In rat sponge implants, angiogenesis was gradually developed in normal Brown Norway Kitasato rats (BN-Ki). The development of angiogenesis was significantly suppressed in kininogen-deficient Brown Norway Katholiek rats (BN-Ka). The angiogenesis enhanced by basic fibroblast growth factor was also significantly less marked in BN-Ka than in BN-Ki. Naturally occurring angiogenesis was significantly suppressed by B(1) or B(2) antagonist. mRNA of vascular endothelial growth factor was more highly expressed in the granulation tissues in BN-Ki than in BN-Ka. Daily topical injections of aprotinin, but not of soy bean trypsin inhibitor, suppressed angiogenesis. Daily topical injections of low-molecular weight kininogen enhanced angiogenesis in BN-Ka. Topical injections of serum from BN-Ki, but not from BN-Ka, also facilitated angiogenesis in BN-Ka. FR190997, a nonpeptide mimic of bradykinin, promoted angiogenesis markedly, with concomitant increases in vascular endothelial growth factor mRNA. Angiogenesis in the granulation tissues around the implanted Millipore chambers containing Walker-256 cells was markedly more suppressed in BN-Ka than in BN-Ki. Our results suggest that endogenous kinin generated from the tissue kallikrein-kinin system enhances angiogenesis in chronic and proliferative granuloma and in the stroma surrounding a tumor. Thus, the agents for the kinin-generating system and/or kinin receptor signaling may become useful tools for controlling angiogenesis.

In this case, a ruptured anterior wall aneurysm of the internal carotid artery disappeared on angiography immediately after stent placement. We focus on the underlying nature of the lesion and this possible alternative treatment.