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Notes: Summary Sinus thrombosis has been regarded as an aetiological factor in DAVFs. However, this claim has been disputed in the literature, because it is not possible to prove that DAVFs arise as a result of sinus thrombosis in all cases, and there is evidence that venous thrombosis can be acquired from a DAVF. The purpose of this study is to examine the hypothesis that the different angiomorphologies of DAVFs depend on the location of their venous outflow, and that a territorial classification of spontaneous DAVFs can be created which is based on their acquired development as a consequence of the breakdown of autoregulation of dural microvascularisation after venous thrombosis. The clinical and radiographic findings of 96 patients with DAVFs were reviewed. The angiomorphology of these lesions was examined using extensive prospective and retrospective angiographic studies, especially with regard to their venous characteristics. The associated phlebothrombosis of the venous outflow was determined in all cases by angiography, and in 8 cases by CT or MRI. We also applied the Venturi effect, a well-confirmed engineering principle, to propose a new hypothesis concerning the development of acquired DAVFs: namely, that there is an acceleration of the shunt volume of the physiological dural AVshunts after a breakdown of their autoregulation occurs. This acceleration seems to be proportional to the flow volume of the venous outflow. The imaging examination showed venous thrombosis in 51 cases. In 98% (44) of the non-thrombotic cases, predisposing histories for phlebothrombosis were documented — for example, hypercoagulable states (venous embolism, phlebothrombosis of the leg, cardiac disease), diabetes mellitus, chronic otitis media, or various low-grade infections. In addition, in 78% of the non-thrombotic cases (excluding the DAVFs of the venous plexus at the base of the skull) there were also angiographically documented deformations of the sinus wall, including hypoplasia of the sigmoid or transverse sinus (20 cases), segmental narrowing of the sinus (8 cases), septation of the sinus lumen (2 cases), and cavernous nodules projecting into the lumen of the transverse (6 cases), sigmoid (4 cases), or sagittal (3 cases) sinuses. The clinical presentation suggested that DAVFs probably develop after a breakdown of the autoregulation of the physiological AV shunts resulting from a venous thrombosis, when there are suitable arteriovenous pressure gradients in the venous recipient. This development would depend on the haemodynamic action of the Venturi effect. The causal phlebothrombosis prior to DAVF may arise in the region of the sinus lumen, the intradural segments of afferent veins, the emissary veins, the venous plexus at the base of the skull, or the residual lumen of an aberrant dural sinus (falciform sinus). In terms of their location and pathogenesis, DAVFs are subdivided into five groups: Type 1 — DAVFs of the dural sinuses (39); Type 2 — DAVFs of the cavernous sinus (29); Type 3 — DAVFs of Galen's system (10); Type 4 — DAVFs of the venous plexus at the base of the skull (9); Type 5 — DAVFs of the cortical veins situated near the dural sinuses (9). The documentation of a sinus thrombosis depends on the location of the DAVM: in 72% of the cases with type 1 DAVFs there was a thrombosis at the time of the investigation, but no thrombosis could be proved in cases with type 4 DAVFs. The reason for the impossibility of identifying a previous causal probably venous sinus thrombosis in cases with DAVFs appears to be either the generally subclinical symptoms of these lesions or their bland clinical course. Moreover, even if a thrombosis precedes the development of type 4 and type 5 DAVFs, its clinical and imaging documentation is not feasible in practice. The morphological development of an actual DAVF begins with the activation of the Venturi effect. A pronounced development of pathological AV shunts simultaneous with a general rise in shunt volume takes place at the level of the large basal dural sinuses (type 1) or of the straight sinus (type 3). On the other hand, a delayed development of pathological AV shunts with a mainly low shunt volume occurs in a venous channel with a low arteriovenous pressure gradient — as, for example, in the region of the cortical veins situated near the dural sinuses (type 5), the venous plexuses at the base of the skull (type 4), the tentorial sinuses (type 3 or type 5), some cavernous sinuses (type 2), or in cases with morphological stenosis or hypoplasia of the sinus.

Notes: Interaction of slightly crosslinked hydrogels of poly(diallyldimethylammonium chloride) (PDADMACI) and of copolymer DADMACI/acrylamide (AAm) with sodium dodecylsulfate (SDS) and sodium dodecylbenzenesulfate (SDBS) results in significant shrinking of the gels due to the formation of polymer-surfactant complexes. Jump-wise transitions in the collapsed state were observed for the networks with the content of cationic groups 100 and 75 mol %. The structure of complexes was studied by means of X-ray scattering method. The scattering curves for collapsed gels, where most chloride anions were replaced by anions of SDS, show a set of well-pronounced narrow diffraction maxima. Fully charged “wet” complexes studied at the equilibrium swelling conditions exhibit high degree of ordering, which diminishes upon drying with the simultaneous transition from hexagonal to lamellar type of ordering. In contrast to this, for DADMACl/AAm copolymer gels (75 mol % of DADMACl monomers in the initial polymerization mixture) the ordering is less pronounced in the “wet” state and becomes more perfect upon drying. The SDS aqueous solutions of the same concentration in the absence of gel do not show such high degree of ordering, while the system of SDS/neutral AAm gel exhibits lamellar ordering typical for low-temperature phases of SDS solutions. © 1996 John Wiley & Sons, Inc.