Compared with ETV, VPS is a superior method because it had better functional neurological outcomes 12 months after surgery.

Patients with hydrocephalus and risk factors for overdrainage may be submitted to ventricular shunt (VS) implant with antisiphon device. The objective of this study was to prospectively evaluate for two years the clinical and tomographic results of the implant of fixed-pressure valves with antisiphon device SPHERA® in 35 adult patients, with hydrocephalus and risk factors for overdrainage. Of these, 3 had congenital hydrocephalus in adult patients with very dilated ventricles (Evans index >50%), 3 had symptomatic overdrainage after previous VS implant (subdural hematoma, hygroma or slit ventricle syndrome), 1 had previous chronic subdural hematoma, 15 had normal pressure hydrocephalus with final lumbar pressure <5 cm H2O after tap test (40 mL), 6 had pseudotumor cerebri, and 7 had hydrocephalus due to other causes. Clinical improvement was observed and sustained in 94.3% of the patients during the two-year period with no computed tomography (CT) evidence of hypo or overdrainage, and no immediate early or late significant complications.

Normal pressure hydrocephalus (NPH) is characterized by the triad of gait apraxia, dementia and urinary incontinence associated with ventriculomegaly and normal pressure of cerebrospinal fluid. Treatment is accomplished through the implantation of a ventricular shunt (VPS), however some complications are still frequent, like overdrainage due to siphon effect. This study analyses the performance of a valve with anti-siphon device (SPHERA®) in the treatment of patients with NPH and compares it with another group of patients with NPH who underwent the same procedure without anti-siphon mechanism (PS Medical® valve). 30 patients were consecutively enrolled in two groups with 15 patients each and followed clinically and radiologically for 1 year. Patients submitted to VPS with SPHERA® valve had the same clinical improvement as patients submitted to VPS with PS Medical®. However, complications and symptomatology due to overdrainage were significantly lower in SPHERA® group, suggesting it as a safe tool to treat NPH.

Background The illicit use of anabolic androgenic steroids (AAS) has been associated with diminished cholesterol efflux mediated by HDL, remarkable decrease in high-density lipoprotein (HDL) plasma concentration and subclinical coronary artery disease (CAD). Inflammation is the key to the atherogenic process associated with atherosclerotic plaque vulnerability. The pericoronary mean fat attenuation (pFAM) has emerged as a marker of coronary inflammation and can predict future cardiovascular events, which is measurable from standard coronary computed tomography angiography (CCTA). However, whether AAS abuse has a role in pFAM in young male AAS users is unknown. Purpose The aim of this study was to evaluate whether AAS abuse could leads to higher pFAM and premature coronary inflammation in young male AAS users. Methods Twenty strength-trained AAS users (AASU) age 29±5 yr, 20 age-matched strength-trained AAS nonusers (AASNU), and 10 sedentary controls (SC) were enrolled in this study. Coronary inflammation was assessed by pFAM-CCTA in the right coronary artery (RCA), left anterior descending artery (LDA) and left circumflex coronary artery (Cx). Results pFAM in the RCA was significantly higher in AASU compared with AASNU and SC (−64.59±9.45 vs. −79.21±6.67 vs. −80.97±7,91 Hounsfield Units (HU), respectively, p&lt;0.001]. Also, the pFAM in the LAD was higher in AASU compared with AASNU and SC (−72.83±7.21 vs. −79.41±6.72 vs. −80.97±7.72 HU, p=0.006). However, no difference to pFAM in the Cx between AASU, AASNU and SC (−74.30±5.85 vs. −79.77±7.13 vs. −78.19±5.82 HU, respectively, p=0.069) was found. Conclusion This study indicates that AAS abuse may be associated with higher pFAM and premature coronary inflammation in the RCA and LAD. The higher pFAM may be linked to early development of CAD in young AAS users. Funding Acknowledgement Type of funding sources: Other. Main funding source(s): Fundação Zerbini