Sandro Rossitti

MR Imaging of Experimentally Induced Intracranial Hemorrhage in Rabbits during the First 6 Hours

Purpose: To evaluate the MR appearance of intracranial, especially intraparenchymal, hemorrhage during the first 6 hours after bleeding with various pulse sequences in an animal model. Material and Methods: Intracerebral hematomas and subarachnoid hemorrhage were created by injecting autologous blood in 9 rabbits. MR studies were performed using a 1.5 T scanner with pixel size and slice thickness comparable to those used in clinical practice before blood injection, immediately after injection, and at regular intervals during 6 hours. The images were compared with the hematoma sizes on formalin-fixed brain slices. Results: In every animal, susceptibility-weighted gradient-echo (GRE) pulse sequences depicted the intraparenchymal hematomas and blood escape in the ventricles or subarachnoid space best as areas of sharply defined, strong hypointensity. The findings remained essentially unchanged during follow-up. The sizes corresponded well to the post-mortem findings. Gradient- and spin-echo (GRASE) imaging revealed some hypointensities, but these were smaller and less well defined. Spin-echo (SE) sequences (proton density-, T1- and T2-weighted) as well as a fluid-attenuated inversion recovery turbo spin-echo sequence (fast FLAIR) depicted the hemorrhage sites as mostly isointense to brain. Conclusion: Susceptibility-weighted GRE imaging at 1.5 T is highly sensitive to both hyperacute hemorrhage in the brain parenchyma and to subarachnoid and intraventricular hemorrhage.

Endovascular coiling of intracranial aneurysms using bioactive coils: a single-center study

Background: Some degree of recanalization is reported in up to one-third of intracranial aneurysms treated with endovascular coiling. A technical development potentially effective in avoiding recanalization is the Matrix Detachable Coil (MDC), which is covered with a biodegradable polymeric material that enhances intra-aneurysmal clot organization and fibrosis. Purpose: To report the initial clinical experience of MDC for endovascular aneurysm coiling in a single-center, single-operator, and well-defined population setting. Material and Methods: 118 aneurysms in 104 patients (73 with subarachnoid hemorrhage, SAH) were embolized with MDC alone (n = 52) or combined with bare platinum coils (n = 66). Results: Initial aneurysm obliteration was class 1 (complete obliteration) in 45 aneurysms (38.1%), class 2 (residual neck) in 44 (37.3%), and class 3 (residual aneurysm) in 29 (24.6%). Procedure-related morbidity was 4.8%, and mortality 0.96%. Clinical follow-up of 61 patients with SAH (mean 5.9 months, range 1–17 months) showed good outcome (Glasgow Outcome Scale, GOS 4–5) in 39 (63.9%), and poor outcome or death (GOS 1–3) in 22 (36.1%). Imaging follow-up of 73 aneurysms (average 6.5 months, range 1–17 months) showed class 1 in 47 (64.4%), class 2 in 18 (24.7%), and class 3 in eight (10.9%). Recanalization occurred in 11 aneurysms (15%), of which four (5.5%) required re-treatment. Conclusion: This study confirms that aneurysm coiling with MDC is feasible, effective, and safe.

Shear Stress in Cerebral Arteries Carrying Saccular Aneurysms A preliminary study

Purpose: To investigate whether the branching geometry determines an underlying increase of shear stress (SS) on the vessel wall in cerebral arteries of patients with aneurysms located distally to the circle of Willis. Increased SS is regarded as a major factor in the etiology of intracranial saccular aneurysm. Aneurysms occur commonly in the Willisian arteries, where the role of hemodynamic forces are evident, but they occur also in more peripheral arteries. Material and Methods: the ratio between SS in the branches and SS in the parent vessel at bifurcations was estimated using exponential relations of vessel caliber. the absolute difference of SS branch ratios in every bifurcation represents the SS gradient at the apex. Cerebral angiograms of 10 patients with aneurysm of the distal anterior cerebral artery were analyzed and compared with normal values from an earlier study. Results: the branching geometry determines a relatively small but significant increase of SS in branches and of SS gradients at bifurcation apices in cerebral arteries of patients with aneurysm. Conclusion: the results may reflect increased cerebral vessel tone after sub-arachnoidal hemorrhage, or alternatively an underlying derangement of the regulation of cerebral arterial caliber and SS in these patients.

Preoperative embolization of lower-falx meningiomas with ethylene vinyl alcohol copolymer: technical and anatomical aspects

Purpose: To report the feasibility of using ethylene vinyl alcohol copolymer (EVAC) for embolization of lower-falx meningiomas. Material and Methods: Three patients were treated. The procedures were done under general anesthesia. A terminal branch of the middle cerebral artery in the proximity of the tumor was catheterized as near as possible or into the pre-falcine arterial anastomotic network around the superior sagittal sinus, and embolization with EVAC was performed with a standard injection technique. Results: This technique resulted in filling of the tumor-supplying dural arteries including all collaterals from both sides, filling of the dural territory of the tumor circulation, and some obliteration of the tumors pial supply. On later operation, the tumors could be removed from the inside out with minimal brain retraction. Conclusion: Effective preoperative embolization of lower-falx meningiomas using EVAC is feasible. This technique has a sound anatomical basis, and it can be used with benefit even in falx meningiomas with predominantly pial vascular supply.

Hidden compartments in intracranial arteriovenous malformation

PELLETTIERI et al. (10) have presented the hypothesis that intracranial arteriovenous malformations (AVMs) may contain angiographically occult regions which they have called hidden compartments (HCs). This anatomical entity was said to occur in a minority of cases, and to be located within, contiguous to or relatively far from the angiographically demonstrated AVM nidus. In these cases, it might be responsible for the increase in size over time of the AVM, for the size-dependent risk of AVM bleeding, and for the risk of AVM recurrence after an initially successful treatment. Besides other controversial issues, the HC theory was said to challenge the normal perfusion pressure breakthrough (NPPB) theory in the pathogenesis of brain edema and hemorrhage that may occur after removal of highflow AVMs. We should like to discuss some aspects of this very interesting hypothesis, and we start by considering the evidence provided by the authors to support the HC theory. In spite of the wide experience of the authors in the management of cerebral AVMs, the clinical material presented as support for their theory is limited to only three case reports of recurrent AVMs after complete removal of the lesion (as verified in angiograms). We agree with the editorial note accompanying the original article (8) that this fact should not detract from the relevance of the HC theory in explaining several controversies in AVM dynamics. Further evidence of the same kind can be found in the literature. Reports have recently been published on recurrent AVMs after surgical excision and negative postoperative angiograms (3, 5), as well as on intra-operative sonographic evidence of persistent feeding arteries to an active residual nidus after embolization (4). Even in the authors’ own material, reported elsewhere (13), there were two cases of recanalization of embolized niduses, one of which might be attributed to HCs. The crux is that the presence of HCs was not demonstrated in these patients. Such compartments are, by definition, hidden. The hypothesis that intracerebral AVMs can have angiographic HCs could as well be considered alone, with reference to the actual clinical problems. The concept of HCs in AVMs is perfectly compatible with basic and relatively noncontroversial concepts of normal and abnormal cerebrovascular anatomy found even in relatively old literature (2,6,7,9). The underlying lesion resulting in an AVM was said to be a capillary malformation, i.e. the perpetuation of a primitive AV shunt which normally would be replaced by an intervening capillary network. It is also interesting to bear in mind that feeding and draining vessels in an AVM are separated by brain parenchyma. Capillaries develop from a primordial plexus of solid cords of angioblasts, and the embryonal cerebral arteries and veins originate from these pre-existing nets rather than from single trunk-like formations. AVMs are fed both by the main vessel to the specific region of the brain and also through the collateral connections to them from the other large branches from the carotid and vertebrobasilar artery systems. The site of the AVM in the brain would determine whether one, two or more main channels were potentially involved. The watershed areas thus offer exceptionally favorable anatomical and hemodynamic preconditions for HCs, a fact that was pointed out by PELLETTIERI et al. (10). Another issue is the speculative role of HCs in the development of edema or hemorrhage in the normal brain parenchyma surrounding the AVM nidus, which may occur after complete embolization or surgical removal of high-flow AVMs. The HC theory suggests that the sudden redistribution of blood flow and pressure gradients due to closure of the AV shunt might increase the hemodynamic stresses in the HC vessels, thus causing edema and hemorrhage. There are three other theories that explain this phenomenon. The NPPB theory (12) suggests that the cerebral hemisphere on the side of the AVM is made chronically ischemic by the AV shunt, resulting in a chronically dilated arterial network with impaired autoregulation. The inability to regulate tissue perfusion following AVM removal, when a normal perfusion pressure is usually re-established, would lead to capillary breakthrough resulting in brain edema and hemorrhage. The occlusive hyperemia theory (1) suggests that it is the obstruction of the venous outflow system of the brain adjacent to the AVM and associated with stagnant arterial flow in former AVM feeders that results in swelling and hemorrhage into these areas. The NPPB and the venous occlusion theories neither exclude each other nor are incompatible with the HC theory (which in both cases provides a rational locus minor resistentiae). A more recent theory, supported by experiments in rats (1 l), suggests that capillary proliferation occurs in regions made chronically ischemic by the AV shunt, resulting in areas of increased capillary fragility that are unable to bear the increase in perfusion pressure to otherwise normal levels following AVM removal. Note that neo-angiogenesis mediated by humoral factors has also been suggested as the cause of recurrent AVMs (5). Thus neo-angiogenesis represents an alternative to the HC hypothesis to explain regrowth of AVMs as well as NPPB-related phenomena. Conclusion: The concept of HCs in intracranial AVMs is sound and largely compatible with current concepts of AVM anatomy and hemodynamics. It is important to emphasize the clinical challenge behind the considerations above, i.e. that patients who have no residual nidus or early draining veins on early postoperative or post-embolization angiograms should still not be considered cured, and that the risk of hemorrhage is