High-Flow Vascular Malformations in Children.

Children can have a variety of intracranial vascular anomalies ranging from small and incidental with no clinical consequences to complex lesions that can cause substantial neurologic deficits, heart failure, or profoundly affect development. In contrast to high-flow lesions with direct arterial-to-venous shunts, low-flow lesions such as cavernous malformations are associated with a lower likelihood of substantial hemorrhage, and a more benign course. Management of vascular anomalies in children has to incorporate an understanding of how treatment strategies may affect the normal development of the central nervous system. In this review, we discuss the etiologies, epidemiology, natural history, and genetic risk factors of three high-flow vascular malformations seen in children: brain arteriovenous malformations, intracranial dural arteriovenous fistulas, and vein of Galen malformations

Bringing high-grade arteriovenous malformations under control: clinical outcomes following multimodality treatment in children.

OBJECTIVE:Brain arteriovenous malformations (AVMs) consist of dysplastic blood vessels with direct arteriovenous shunts that can hemorrhage spontaneously. In children, a higher lifetime hemorrhage risk must be balanced with treatment-related morbidity. The authors describe a collaborative, multimodal strategy resulting in effective and safe treatment of pediatric AVMs. METHODS:A retrospective analysis of a prospectively maintained database was performed in children with treated and nontreated pediatric AVMs at the University of California, San Francisco, from 1998 to 2017. Inclusion criteria were age ≤ 18 years at time of diagnosis and an AVM confirmed by a catheter angiogram. RESULTS:The authors evaluated 189 pediatric patients with AVMs over the study period, including 119 ruptured (63%) and 70 unruptured (37%) AVMs. The mean age at diagnosis was 11.6 ± 4.3 years. With respect to Spetzler-Martin (SM) grade, there were 38 (20.1%) grade I, 40 (21.2%) grade II, 62 (32.8%) grade III, 40 (21.2%) grade IV, and 9 (4.8%) grade V lesions. Six patients were managed conservatively, and 183 patients underwent treatment, including 120 resections, 82 stereotactic radiosurgery (SRS), and 37 endovascular embolizations. Forty-four of 49 (89.8%) high-grade AVMs (SM grade IV or V) were treated. Multiple treatment modalities were used in 29.5% of low-grade and 27.3% of high-grade AVMs. Complete angiographic obliteration was obtained in 73.4% of low-grade lesions (SM grade I-III) and in 45.2% of high-grade lesions. A periprocedural stroke occurred in a single patient (0.5%), and there was 1 treatment-related death. The mean clinical follow-up for the cohort was 4.1 ± 4.6 years, and 96.6% and 84.3% of patients neurologically improved or remained unchanged in the ruptured and unruptured AVM groups following treatment, respectively. There were 16 bleeding events following initiation of AVM treatment (annual rate: 0.02 events per person-year). CONCLUSIONS:Coordinated multidisciplinary evaluation and individualized planning can result in safe and effective treatment of children with AVMs. In particular, it is possible to treat the majority of high-grade AVMs with an acceptable safety profile. Judicious use of multimodality therapy should be limited to appropriately selected patients after thorough team-based discussions to avoid additive morbidity. Future multicenter studies are required to better design predictive models to aid with patient selection for multimodal pediatric care, especially with high-grade AVMs

Redox stress defines the small artery vasculopathy of hypertension: how do we bridge the bench-to-bedside gap?

Although convincing experimental evidence demonstrates the importance of vascular reactive oxygen and nitrogen species (RONS), oxidative stress, and perturbed redox signaling as causative processes in the vasculopathy of hypertension, this has not translated to the clinic. We discuss this bench-to-bedside disparity and the urgency to progress vascular redox pathobiology from experimental models to patients by studying disease-relevant human tissues. It is only through such approaches that the unambiguous role of vascular redox stress will be defined so that mechanism-based therapies in a personalized and precise manner can be developed to prevent, slow, or reverse progression of small-vessel disorders and consequent hypertension

Combination of high-resolution cone beam computed tomography and metal artefact reduction software: a new image fusion technique for evaluating intracranial stent apposition after aneurysm treatment.

We introduce a new imaging technique to improve visualisation of stent apposition after endovascular treatment of brain aneurysms employing high-resolution cone beam CT and three-dimensional digital subtraction angiography. After performing a stent-assisted coil embolisation of brain aneurysm, the image datasets were processed with a metal artefact reduction software followed by the automated image fusion programmes. Two patients who underwent aneurysm coiling using a Neuroform stent were evaluated. The reconstructed 3D images showed a detailed structure of the stent struts and identified malappositions of the deployed stents. Case 1 showed good apposition on the outer curvature side of the carotid siphon, while the inner curvature side showed prominent malapposition. Case 2, with multiple aneurysms, showed good apposition on both outer and inner curvature sides, although inward prolapse of the struts was observed. This new imaging technique may help evaluate stent apposition after the endovascular aneurysm treatment

Identification of Plasmodium falciparum var1CSA and var2CSA domains that bind IgM natural antibodies

Malaria in pregnancy is responsible for maternal anaemia, low-birth-weight babies and infant deaths. Plasmodium falciparum infected erythrocytes are thought to cause placental pathology by adhering to host receptors such as chondroitin sulphate A (CSA). CSA binding infected erythrocytes also bind IgM natural antibodies from normal human serum, a process that may facilitate placental adhesion or promote immune evasion. The parasite ligands that mediate placental adhesion are thought to be members of the variant erythrocyte surface antigen family P. falciparum erythrocyte membrane protein 1 (PfEMP1), encoded by the var genes. Two var gene sub-families, var1CSA and var2CSA, have been identified as parasite CSA binding ligands and are leading candidates for a vaccine to prevent pregnancy-associated malaria. We investigated whether these two var gene subfamilies implicated in CSA binding are also the molecules responsible for IgM natural antibody binding. By heterologous expression of domains in COS-7 cells, we found that both var1CSA and var2CSA PfEMP1 variants bound IgM, and in both cases the binding region was a DBL epsilon domain occurring proximal to the membrane. None of the domains from a control non-IgM-binding parasite (R29) bound IgM when expressed in COS-7 cells. These results show that PfEMP1 is a parasite ligand for non-immune IgM and are the first demonstration of a specific adhesive function for PfEMP1 epsilon type domains

A system analysis of a suboptimal surgical experience

© 2009 Lee et al; licensee BioMed Central Ltd. This is an Open Access article distributed under the terms of the Creative Commons Attribution Licens

Pseudophakic Dysphotopsia

Pseudophakic dysphotopsia is an unwanted entoptic phenomenon caused by intraocular lenses. Dysphotopsias have been classified as positive (brightness, streaks, haze, or glare) and negative (temporal arc or half-moon crescent) in the visual field. These visual phenomena seem to be well tolerated cause in the case of positive dysphotopsia, but not as well in the negative cases that sometimes discomfort to the patient. The incidence of dysphotopsia ranges from 20% to 77.7%, and the prevalence seems not to be altered by the type of intraocular lens. Pseudophakic dysphotopsia continues to be enigmatic over time; however, many efforts are being made in order to resolve the mystery. In this chapter, the evolution of the dysphotopsia, possible causes, and proposed treatments will be described

Comparison of safety of loteprednol 0.5%/difluprednate 0.05%/prednisolone 1% eye drops in the post cataract surgery patients

Background: Post surgical ocular inflammation is a common happening after the cataract surgery. Topical steroids are the main stay of the treatment. Although it is quite effective in controlling it but it produces severe adverse drug reactions i.e. rise in intraocular pressure and dryness in the eyes. In present study we have compared the two newer topical steroids i.e. loteprednol and difluprednate with prednisolone for the safety issue.Methods: Total n=150 patients of cataract were enrolled in the study. Institutional ethics committee approval was taken. After randomization, patients were allocated into three groups of 50 each. Baseline reading of intraocular pressure and tear film breakup time was recorded. Post operatively examination was done on day 7, 15 and 30 day. The results were compared as prednisolone versus loteprednol, prednisolone versus difluprednate.Results: A. On intraocular pressure 1.prednisolone versus difluprednate statistically significant effect at day 7 (p=0.043), day15 (p=0.010) and at day 30(p=0.036) were there. 2. Prednisolone versus loteprednol- The difference was statistically highly significant at day 7 (0.00), day 15 (p=0.009) and at day 30th (p=0.00).  B. On tear film breakup time-No significant effect on tear film breakup time is observed.Conclusions: Both the newer drugs are much safer as compared to prednisolone for intraocular pressure. As they are equiefficacious to prednisolone their use in post cataract surgery inflammation is recommended

Correction of negative dysphotopsia in Crystalens “Z syndrome”

We report a case of negative dysphotopsia in the left eye of a 56-year-old patient three months after uneventful bilateral phacoemulsification and implantation of a Crystalens® intraocular lens (Bausch and Lomb®) placed in the capsular bag. Three months postoperatively, the patient described visual field loss in the inferior temporal quadrant in the left eye under low light conditions. Anterior capsulorhexis was eccentric, allowing the inferior temporal optic edge to move forward, producing late asymmetric vault of the lens. One month later, when the equatorial diameter of the capsular bag decreased, we pushed the inferior temporary hinge backwards so that the lens moved back into the correct position. Six months after relocation, the lens position remained stable and negative dysphotopsia was absent. This case shows Crystalens Z syndrome as a new etiology of negative dysphotopsia, and a successful novel treatment in a patient without capsular fibrosis