Acute Stenting and Concomitant Tirofiban Administration for the Endovascular Treatment of Acute Ischemic Stroke Related to Intracranial Artery Dissections: A Single Center Experience and Systematic Review of the Literature

BackgroundIntracranial artery dissection is an uncommon cause of acute ischemic stroke. Although acute stenting of the dissected arterial segment is a therapeutic option, the associated antiplatelet regimen remains a matter of debate.ObjectivesTo evaluate the efficacy and safety of acute intracranial stenting together with concomitant intravenous administration of tirofiban and to perform a systematic review of the literature.Materials and methodsA single-center, retrospective study of the clinical and radiological records of all patients treated at our center by intracranial stenting in the setting of acute ischemic stroke between January 2010 and December 2020. A systematic review of the literature was conducted according to the PRISMA-P guidelines for relevant publications from January 1976 to December 2020 on intracranial artery dissection treated by stent.ResultsSeven patients with intracranial artery dissections underwent acute stenting with concomitant tirofiban during the study period. Mid-term follow-up showed parent artery patency in 6/7 cases (85.7%). The modified Rankin Score was ≤ 0-2 at 3 months in 5/7 cases (71.4%). The literature review identified 22 patients with intracranial artery dissection treated with acute stenting in association with different antithrombotic therapies. Complete revascularization was obtained in 86.3% of cases with a modified Rankin Score of ≤ 0-2 in 68% of patients at 3-month follow-up.ConclusionsAcute intracranial stenting together with intravenous tirofiban administration could be a therapeutic option in patients with intracranial artery dissection and a small ischemic core.     

Latanoprost and brimonidine: therapeutic and physiologic assessment before and after oral nonsteroidal anti-inflammatory therapy.

PURPOSE: To assess, before and during oral nonsteroidal anti-inflammatory drug coadministration, latanoprost's and brimonidine's hypotensive action in eyes at risk of glaucomatous progression, assessing the effect of each drug on ocular perfusion and visual function. METHODS: Twenty consenting adults with open-angle glaucoma or ocular hypertension underwent a double-masked, bilateral, randomized prospective study. Treatment started with either latanoprost 0.005% in the morning and placebo in the evening, or brimonidine 0.2% twice daily in one eye; after 1 week starting the other in the fellow eye. After another week, oral indomethacin 25 mg four times a day, commenced for 2 more weeks. Intraocular pressure, ocular circulation, and visual function were monitored pretreatment, after unilateral monotherapy (day 7), bilateral ocular therapy (day 14), and coadministered oral indomethacin (day 28). Intrasubject differences (interocular and intraocular relative to baseline) were determined by two-tailed paired t test. RESULTS: A loss of the significance of intraocular pressure reduction with brimonidine was noted after oral indomethacin coadministration (-14%; P =.004 for brimonidine alone versus -11%; P =.3 with indomethacin). Significant intraocular pressure reduction with latanoprost persisted despite indomethacin (-25%; P <.0001 for latanoprost alone versus -30%; P <.0001 with indomethacin). Pulsatile ocular blood flow increased 40% with latanoprost, but was unchanged with brimonidine (interdrug difference, P =.004). Midperipheral retinal microcirculation increased 23% (P =.03) with latanoprost. Humphrey perimetry and contrast sensitivity remained consistently at or above baseline with both latanoprost and brimonidine. Indomethacin had no significant effect on ocular perfusion or visual function measures. CONCLUSIONS: Circulatory and hydrodynamic findings differed substantially for the two drugs. The loss of significance of intraocular pressure reduction with brimonidine during indomethacin treatment may be clinically important.     

Brief report: Self-blame and PTSD symptoms in adolescents exposed to terrorism: Is school connectedness a mediator?

Previous research has shown that self-blame predicts increased risk of posttraumatic stress disorder (PTSD) in youth exposed to terrorism, but little is known about the factors mediating such relationship. This study aimed to explore whether school connectedness (SC) mediates the effect of self-blame on PTSD in 60 adolescents (aged 14–18 years) who survived the 2004 terrorist attack against school no. 1 in Beslan, Russia. Participants completed measures of coping, SC, and PTSD three years after the traumatic event. Endorsement of self-blaming behaviors was found to be significantly positively related to the presence of PTSD; self-blame was negatively associated with SC, which in turn was negatively related to PTSD. The mediation hypothesis was supported, with SC partially mediating the link between self-blame and PTSD. Adolescents affected by terrorism may benefit from school-based interventions aimed at fostering students' sense of belonging and emotional bonding to teachers, peers, and the school environment.     

Experimental evaluation of the NeVa™ thrombectomy device a novel stent retriever conceived to improve efficacy of organized clot removal

Background and purpose

Stent retrievers are recognized as the most effective devices for intracranial thrombectomy. Although highly effective, such devices fail in clot removal when the brain vessel occlusion is due to organized, firm clots. The mechanism of failure is that during the retrieval, devices remain compressed by the organized clot and slide between it and the vessel wall without any removal effect. The aim of the current study is to present the preclinical evaluation of the Neva? device, a novel stent retriever designed to improve the incorporation and removal of organized thrombi.

Decreased Vascular Patterning in the Retinas of Astronaut Crew Members as New Measure of Ocular Damage in Spaceflight-Associated Neuro-ocular Syndrome

PurposeOcular structural and functional changes, collectively termed spaceflight-associated neuro-ocular syndrome (SANS), have been described in astronauts undergoing long-duration missions in the microgravity environment of the International Space Station. We tested the hypothesis that retinal vascular remodeling, particularly by smaller vessels, mediates the chronic headward fluid shifts associated with SANS.MethodsAs a retrospective study, arterial and venous patterns extracted from 30° infrared Heidelberg Spectralis retinal images of eight crew members acquired before and after six-month missions were analyzed with NASA''s recently released VESsel GENeration Analysis (VESGEN) software. Output parameters included the fractal dimension and overall vessel length density that was further classified into large and small vascular branching generations. Vascular results were compared with SANS-associated clinical ocular measures.ResultsSignificant postflight decreases in D_f, L_v, and in smaller but not larger vessels were quantified in 11 of 16 retinas for arteries and veins (P value for D_f, L_v, and smaller vessels in all 16 retinas were ≤0.033). The greatest vascular decreases occurred in the only retina displaying clinical evidence of SANS by choroidal folds and optic disc edema. In the remaining 15 retinas, decreases in vascular density from D_f and L_v ranged from minimal to high by a custom Subclinical Vascular Pathology Index.ConclusionsTogether with VESGEN, the Subclinical Vascular Pathology Index may represent a new, useful SANS biomarker for advancing the understanding of SANS etiology and developing successful countermeasures for long duration space exploration in microgravity, although further research is required to better characterize retinal microvascular adaptations.