Introduction: Myelomeningocele is one of the most complex birth defects that cause physical disability, with consequent fecal incontinence and therefore difficulty in social integration of these patients. Objective: To improve the quality of life and manometric values after biofeedback therapy. Method: Longitudinal, prospective, analytical and experimental study. Patients with myelomeningocele and fecal incontinence who were between 5 to 15 years old and their parents were included in the study. Child and parent reports of PedsQMtm generic questionnaire were collected after obtaining informed consent and assent. Anorectal manometry and first biofeedback sessions were held with each child. Following treatment completion, the PedsQMtm was applied again. Results: 17 children and their parents were included in the study. All the patients presented fecal incontinence and an inability to voluntarily evacuate rectal contents. After biofeedback, the totality of patients improved their fecal incontinence. Nine of them stop using diaper. All reported successful use of the toilet. Statistically significant differences were observed when comparing the quality of life of children and parents at the beginning and at the end of treatment. There was an improvement in quality of life after the treatment with biofeedback for both children and parents, which was more perceived by these. Conclusions: It is highly significant for the improvement both in clinic and manometric values. The improvement in quality of life is more evident in the parents.

Background: Impaired gut barrier function has been reported in some functional gastrointestinal (GI) disorders. Evidences suggest that gut microbiota affects GI motility in particular Lactobacillus species elicits anti-inflammatory activity and exerts protective effects on damage induced by pathogen Gram negative-derived lipopolysaccharide (LPS). LPS produced an oxidative imbalance in human colonic smooth muscle cells (SMC) that persists after LPS-washout and contributes to SMC morphofunctional alterations. The aim was to evaluate if supernatants harvested from LGG cultures protect SMC from LPS-induced myogenic damage. Methods: L. rhamnosus GG (ATCC 53103 strain) was grown in MRS medium and samples were collected from bacterial cultures in middle exponential phase, in early, in middle and late stationary phase (overnight). Supernatants were recovered, filtered and stored at -20 8C. Highly pure human SMC culture was then exposed for 24 h to highly purified LPS (1 mg/ml) of E. coli (O111:B4) in the absence and presence of the supernatants. Their effects were evaluated on LPS-induced SMC morphofunctional alterations and pro-inflammatory IL-6 production. Data are expressed as mean AE SE (P < 0.05 significant). Results: LPS induced persistent significant 20.7% AE 1.2 cell shortening and 35.2% AE 2.6 decrease in contraction of human colonic SMC. These alterations were paralleled to a 238.5% AE 82.5% increase in IL-6 production. These effects disappeared in the presence of LGG-supernatants, following a progression related to LGG growth curve phases. Supernatants collected in the middle exponential phase already significantly partially restored LPS-induced cell shortening by 43.4% AE 10.2% and IL-6 increase by 47.6% AE 13.1%, but had no effect on LPS-induced inhibition of contraction. Supernatants collected later, in the early and middle stationary phase, further counteract LPS-induced damage, including inhibition of contraction. Maximal protective effects were observed with supernatants of the late stationary phase where LPS-induced cell shortening was reversed by 86% AE 4.7%, inhibition of contraction by 98.2% AE 1.8%, and IL-6 basal production by 91.3% AE 0.6%. Conclusions: LGG-secreted products are substances/byproducts able to directly protect human SMC from LPS-induced myogenic damage. Novel insights are then provided about the possibility that LGG-derived products could reduce the risk of progression to a post-infective motor disorder.