Vessel territory mapping after cerebral revascularization surgery using selective angiographic flat detector perfusion imaging.

The technical feasibility and diagnostic potential of angiographic flat-detector perfusion imaging technique, combining digital subtraction angiography with a flat-detector computed tomography steady-state perfusion imaging, was explored in patients treated with direct or indirect revascularization surgery. This short communication is about an imaging modality with great potential for evaluation, comparison and grading of vascular perfusion territory areas and anatomical location selectively perfused by direct and indirect cerebral bypasses.

Cerebral venous thrombosis in women of childbearing age: diagnosis, treatment, and prophylaxis during a future pregnancy.

Sex-specific risk factors for cerebral venous thrombosis (CVT) in women include oral contraceptives, pregnancy, puerperium, and hormone replacement therapy. The acute treatment of CVT is anticoagulation using therapeutic doses of low molecular weight heparin, which is also the preferred treatment in the post-acute phase in pregnancy and during breastfeeding. In patients with imminent brain herniation decompressive surgery is probably life-saving. A medical history of CVT alone is not a contraindication for future pregnancies. The optimal dosage of low molecular weight heparin as thrombosis prophylaxis during future pregnancies after a history of venous thrombosis including CVT is the topic of an ongoing trial.

Complete Transection of Optic Nerve After Endovascular Coiling of a Large Ophthalmic Artery Aneurysm.

BACKGROUND: We describe a patient who developed delayed blindness of the left eye at 5 weeks after endovascular coiling of a large ophthalmic aneurysm. CASE DESCRIPTION: A 44-year-old male was admitted with visual decline due to compression of the optic nerve by a large ophthalmic aneurysm. The aneurysm was treated by endovascular coiling, but visual function was unchanged. One month and 7 days later, the patient developed sudden blindness of the affected eye, despite complete angiographical occlusion of the aneurysm. Surgical exploration in an attempt to restore vision showed a fully thrombosed aneurysm but, surprisingly, complete transection of the optic nerve just proximal to its entry into the optic canal. CONCLUSIONS: This report describes a rare complication of a sudden increase in size of a large ophthalmic aneurysm despite successful endovascular occlusion.

CD8 signaling in microglia/macrophage M1 polarization in a rat model of cerebral ischemia.

Classical or M1 activity of microglia/macrophages has been described in several neurodegenerative and brain inflammatory conditions and has also been linked to expansion of ischemic injury in post-stroke brain. While different pathways of M1 polarization have been suggested to occur in the post-stroke brain, the precise underlying mechanisms remain undefined. Using a transient middle cerebral artery occlusion (MCAO) rat model, we showed a progressive M2 to M1 polarization in the perilesional brain region with M1 cells becoming one of the dominant subsets by day 4 post-stroke. Comparing key receptors involved in M1 polarization (CD8, IFNγR, Clec4, FcγR, TLR3 and TLR4) and their signal transducers (Syk, Stat1, Irf3, and Traf6) at the day 4 time point, we showed a strong upregulation of CD8 along with SYK transducer in dissected perilesional brain tissue. We further showed that CD8 expression in the post-stroke brain was associated with activated (CD68+) macrophages and that progressive accumulation of CD8+CD68+ cells in the post-stroke brain coincided with increased iNOS (M1 marker) and reduced Arg1 (M2 marker) expression on these cells. In vitro ligand-based stimulation of the CD8 receptor caused increased iNOS expression and an enhanced capacity to phagocytose E. coli particles; and interestingly, CD8 stimulation was also able to repolarize IL4-treated M2 cells to an M1 phenotype. Our data suggest that increased CD8 signaling in the post-stroke brain is primarily associated with microglia/macrophages and can independently drive M1 polarization, and that modulation of CD8 signaling could be a potential target to limit secondary post-stroke brain damage.

Phenotypical characterization of α-galactosidase A gene mutations identified in a large Fabry disease screening program in stroke in the young.

OBJECTIVE: In the Belgian Fabry Study (BeFaS), the prevalence of Fabry disease was assessed in 1000 young patients presenting with stroke, unexplained white matter lesions or vertebrobasilar dolichoectasia. The results of the BeFaS suggested that Fabry disease may play a role in up to 1% of young patients presenting with cerebrovascular disease. However, the clinical relevance was unclear in all cases. We report on detailed phenotyping in subjects identified with α-galactosidase A (α-Gal A) enzyme deficiency or GLA mutations identified in the BeFaS (n=10), and on the results of family screening in this population. METHODS: Family screening was performed to identify additional mutation carriers. Biochemical and/or clinical evaluation of all subjects (BeFaS index patients and relatives carrying a GLA mutation) was performed. RESULTS: Genetic family screening revealed 18 additional GLA mutation carriers. Bloodspot α-Gal A enzyme activity was normal in all GLA mutation carriers, even in 2 males with the p.A143T mutation. Plasma Gb3 and lyso-Gb3 levels were normal in all subjects. Elevated Gb3 in urine was detected in 2 subjects. Some classic clinical signs of Fabry disease, like angiokeratoma or cornea verticillata, could not be detected in our population. Cardiac symptoms of Fabry disease were found in 6 out of 10 p.A143T carriers. No signs of cerebrovascular disease were found in the relatives with a GLA mutation. CONCLUSIONS: We could not identify mutations causing the classical clinical phenotype of Fabry disease in our cerebrovascular disease population. Enzyme activity analysis in bloodspots and plasma may fail to identify late-onset variants of Fabry disease. We recommend genetic testing when an atypical, late-onset variant of Fabry disease is suspected in a male cerebrovascular disease patient. However, this may lead to the identification of non-disease causing or controversial genetic variants.