This is the first study to demonstrate the in vivo mechanisms of intracranial aneurysm formation. The inflammatory response that follows endothelial injury is the basic step in the pathogenesis of these lesions. In this study the investigators have expanded the understanding of the origin of intracranial aneurysms and have contributed to the further development of measures to prevent and treat aneurysms.

In some cavernous sinus dAVFs with palliative transarterial embolization or observational management, there was a change in the venous drainage patterns, consisting of a decrease in the number of venous drainage routes. There was a trend for the posterior route to close before the anterior drainage or cortical drainage route. This suggests the occurrence of a staged progression in a regular direction in cavernous sinus dAVFs. Without treatment aiming at a complete cure, most cavernous sinus dAVFs can behave benignly, with a low possibility of development of cortical venous reflux during follow-up.

The incidence of hypoglossal canal DAVF was not very low in our series. Contralateral carotid injection is an essential examination to provide an accurate diagnosis. TVE should be considered when access is available, although TAE is also appropriate for shunt reduction.

The zeta potentials of 1,2-dipalmitoyl-sn-glycero-3-phosphatidylcholine (DPPC) liposomes were measured at a gel phase as a function of CaCl2 concentration (0-200 mM) in a solution containing different NaCl concentrations (0-200 mM). The data obtained were analyzed with the diffuse double layer theory including the Graham theory. The intrinsic binding constants of ions to DPPC membranes and the distance of the shear plane have been determined independent of both the concentration of CaCl2 and that of NaCl. The values of the constants were 37 M-1 for Ca2+, 0.28 M-1 for Cl, and 0.25 M-1 for Na+; the distance was 0.24 nm under the assumption of binding stoichiometry of Ca2+/DPPC = 1:1.

We used immunohistochemical methods to analyze the phenotypes of smooth muscle cells (SMCs) in human cerebral arteries and aneurysmal walls. Thirty-two aneurysmal walls were studied; 31 aneurysmal walls were resected at operation and 1 aneurysm was obtained at autopsy. Seven control arteries were obtained at autopsy. Semiserial sections were subjected to immunohistochemical staining with antibodies to alpha-smooth muscle actin (alpha-SMA), desmin and smooth muscle myosin heavy chain isoforms: SM1, SM2 and SMemb. In control cerebral arteries, SMCs in the media were strongly immunostained for alpha-SMA, desmin, SM1 and SM2; immunoreactivity for SMemb was faint or weakly positive. SMCs in both non-ruptured and ruptured aneurysmal walls showed no staining for desmin; the expression of alpha-SMA was well preserved. Compared with control cerebral arteries, in 4 of 11 non-ruptured aneurysmal walls, the staining intensity of SMCs for SMemb was clearly increased. In ruptured aneurysmal walls, the expression of SM2 was lower than in control cerebral arteries and non-ruptured aneurysmal walls. Our study suggests that the phenotype of SMCs in aneurysmal walls is different from the contractile type in the media of normal cerebral arteries, at least partially changing to the synthetic type in some non-ruptured aneurysms. SMCs in ruptured aneurysmal walls may have lost both phenotypes before rupture. Phenotypic modulation of SMCs in the aneurysmal walls appears to be related to a remodeling of the aneurysmal wall and to a rupture mechanism.