Basilar artery dissection: series of 12 consecutive cases and review of the literature.

BACKGROUND: Current knowledge on primary or isolated basilar artery dissection (IBAD) is limited to case vignettes and small patient series. OBJECTIVE: To delineate the frequency and clinical presentations of IBAD along with short-term outcome, specific prognosis and targeted management. METHODS: Data were derived from a series of 12 consecutive patients and a review of 88 cases reported in the literature. In all the cases, the dissection was confined to the basilar artery. RESULTS: Disease incidence was estimated at 0.25 per 100,000 person-years. IBAD accounted for roughly 1.0% of all subarachnoid hemorrhage events and for no less than 10.5 and 4.5% of posterior circulation and brain-supplying artery dissections, respectively. The main clinical presentations were subarachnoid hemorrhage (46%) and posterior circulation brain ischemia (42%). Subarachnoid hemorrhage typically manifested at a higher age than brain ischemia (mean age, 48.9 vs. 41.4 years) and was more prevalent among women. Rebleedings related to pseudoaneurysm formation in patients with subarachnoid hemorrhage and recurrent ischemia in stroke patients were common in the acute phase (26.1 and 33.3%, respectively) but were rare in the long term. The outcome was generally favorable in stroke patients but variable in subarachnoid hemorrhage (case fatality rate, 21.7%). The mainstay of therapy for subarachnoid hemorrhage related to IBAD was endovascular occlusion of the aneurysm pouch whereas stroke patients were usually put on anticoagulants. CONCLUSIONS: IBAD is probably an underrecognized disease with heterogeneous clinical presentation and prognosis. It should be considered as a differential diagnosis in peritruncal subarachnoid hemorrhage, classic subarachnoid hemorrhage and posterior circulation stroke, especially in young individuals. Case management is challenging and has to be tailored to each patient.

Comparison of computed tomography and microradiography for graft evaluation after reconstruction of critical size bone defects using beta-tricalcium phosphate.

INTRODUCTION: The aim of the study was to evaluate the accuracy of computed tomography (CT) for in vivo follow up after mandibular reconstruction. MATERIAL AND METHODS: Unilateral mandibular defects were surgically created in ten sheep and either reconstructed using blood soaked beta-tricalcium phosphate (beta-TCP) cylinders (group A, n=5) or blood soaked beta-TCP cylinders that were additionally loaded with autologous bone marrow (group B, n=5). The two graft designs resulted in different stages of graft ossification representative of different stages of healing. CT datasets were fused with microradiographs and measurements of ceramic area based on both methods were compared. RESULTS: Two animals (groups A (n=1) and B (n=1)) presented infection and graft dislocation that was visible on CT and were excluded from statistical evaluation. Group A grafts underwent moderate degradation (53.55%+/-9.7) and incomplete bony incorporation representing an intermediate state of healing while ceramic grafts within group B developed a high grade of osseointegration and degradation (94.2%+/-3.3) consistent with progressive healing. Statistical comparison of measurements based on both methods revealed a significant bias (p<0.05) and a non-significant variance for group A and a significant variance (p<0.05) and non-significant bias for group B. CONCLUSION: Our results indicate that conventional CT is not suitable to objectively evaluate ossification and degradation of a beta-TCP graft in vivo and further attempts to improve clinical visualization of beta-TCP need to be undertaken.

A new model for quantitative in vivo microscopic analysis of thrombus formation and vascular recanalisation: the ear of the hairless (hr/hr) mouse.

The alteration of rheological blood properties as well as deterioration of vascular perfusion conditions and cell-cell interactions are major determinants of thrombus formation. Herein, we present an experimental model which allows for quantitative in vivo microscopic analysis of these determinants during both thrombus formation and vascular recanalisation. The model does not require surgical preparation procedures, and enables for repeated analysis of identical microvessels over time periods of days or months, respectively. After i.v. administration of FITC-dextran thrombus formation was induced photochemically by light exposure to individual arterioles and venules of the ear of ten anaesthetised hairless mice. In venules, epi-illumination induced rapid thrombus formation with first platelet deposition after 0.59 +/- 0.04 min and complete vessel occlusion within 7.48 +/- 1.31 min. After a 24-h time period, 75% of the thrombosed venules were found recanalised. Marked leukocyte-endothelial cell interaction in those venules indicated persistent endothelial cell activation and/or injury, even after an observation period of 7 days. In arterioles, epi-illumination provoked vasomotion, while thrombus formation was significantly (p <0.05) delayed with first platelet deposition after 2.32 +/- 0.22 min and complete vessel occlusion within 20.07 +/- 3.84 min. Strikingly, only one of the investigated arterioles was found recanalised after 24 h, which, however, did not show leukocyte-endothelial cell interaction. Heparin (300 U/kg, i.v.) effectively counteracted the process of thrombus formation in this model, including both first platelet deposition and vessel occlusion. We conclude that the model of the ear of the hairless mouse allows for distinct in vivo analysis of arteriolar and venular thrombus formation/recanalisation, and, thus, represents an interesting tool for the study of novel antithrombotic and thrombolytic strategies, respectively.