A reforma psiquiátrica em relatos de cuidadores de residências terapêuticas / Psychiatry reform in reports of therapeutic residence care providers

Resumo A Reforma Psiquiátrica brasileira criou uma série de dispositivos para substituir o sistema asilar, entre eles o Serviço Residencial Terapêutico (SRT). Com o objetivo de ampliar as reflexões sobre os desafios enfrentados pela proposta reformista, este estudo analisa os discursos construídos pelos cuidadores das residências terapêuticas de Campina Grande (PB), visando detectar estratégias argumentativas favoráveis ou contrárias à Reforma, identificar as identidades que constroem para si próprios, para os demais profissionais da rede de saúde mental e para os usuários do serviço, além de analisar como nomeiam e descrevem o sofrimento psíquico. A pesquisa, de cunho qualitativo, baseou-se na perspectiva teórico-metodológica da psicologia social discursiva. Obtiveram-se 18 depoimentos orais que foram submetidos à análise de discurso. Apesar dos cuidadores se posicionarem a favor da reforma psiquiátrica, apresentam relatos que reforçam a necessidade dos hospitais psiquiátricos, sobretudo, nos momentos de crise dos usuários. Ademais, os profissionais dos hospitais são posicionados, em alguns relatos, como mais capacitados do que os da rede substitutiva. Esses relatos ainda associam o sofrimento psíquico à doença, à periculosidade e à alienação, e caracterizam os usuários como agressivos, perigosos e instáveis. De modo geral, os entrevistados justificam algumas práticas hospitalocêntricas, valorizam o saber médico e reproduzem discursos asilares.

Abstract The Brazilian Psychiatry Reform has created a number of alternatives to substitute the asylum internment system, among them, the Therapeutic Residential Service (SRT). Aiming at deepening the reflections over the challenges the reformist proposal faces, this study analyzes the discourses constructed by care providers of therapeutic residences in Campina Grande (state of Paraíba), to identify argumentative strategies either in favor or against the Reform, identify the identities they build for themselves and for other mental health network professionals and for the service users, in addition to analyzing how they name and describe psychic suffering. The research has a qualitative character, based on the theoretical-methodological perspective of discursive social psychology. A total of 18 oral reports were obtained and submitted to discourse analysis. Although the care providers revealed their approval of the psychiatric reform, their reports stress the need for psychiatric hospitals, mainly for those users undergoing crises. Besides, hospital professionals are seen, in some of those reports, as more capable than those in the substitutive network. Moreover, these reports associate psychiatric suffering to disease, to dangerousness, and to alienation and characterize the users as aggressive, dangerous, and unstable. On the whole, those interviewed justify some practices typical of hospitals, value medical knowledge and reproduce asylum discourses.

Peripheral lymph nodes contain migratory and resident innate lymphoid cell populations.

Tissue residency is considered a defining feature of the innate lymphoid cell (ILC) populations located within mucosal and adipose tissues. ILCs are also present within all lymphoid tissues, but whether ILCs migrate between lymphoid and nonlymphoid sites and in what context is poorly understood. To determine whether migratory ILCs exist within peripheral lymph nodes (LNs), we labeled all cells within the brachial LN (bLN) of transgenic mice expressing a photoconvertible fluorescent protein by direct exposure to light. Tracking of cellular changes in the labeled LN revealed the gradual migration of new ILCs into the tissue, balanced by egress of ILCs dependent on sphingosine-1-phosphate receptors. Most of the migratory ILCs were ILC1s, entering LNs directly from the circulation in a CD62L- and CCR7-dependent manner and thus behaving like conventional natural killer (cNK) cells. Upon egress, both ILC1s and cNK cells were found to recirculate through peripheral LNs. A distinct population of migratory ILC2s were detected in the LN, but most of the ILC3s were tissue resident. Functionally, both migratory and resident ILC1s within LNs were able to rapidly produce IFN-γ to support the generation of robust TH1 T cell responses after immunization. Thus, migratory and resident ILC populations exist within peripheral LNs, with ILC1s, akin to cNK cells, able to traffic into these tissues where they can contribute to the initiation of adaptive immunity.

Divergent roles for Clusterin in Lung Injury and Repair.

Lung fibrosis is an unabated wound healing response characterized by the loss and aberrant function of lung epithelial cells. Herein, we report that extracellular Clusterin promoted epithelial cell apoptosis whereas intracellular Clusterin maintained epithelium viability during lung repair. Unlike normal and COPD lungs, IPF lungs were characterized by significantly increased extracellular Clusterin whereas the inverse was evident for intracellular Clusterin. In vitro and in vivo studies demonstrated that extracellular Clusterin promoted epithelial cell apoptosis while intercellular Clusterin modulated the expression of the DNA repair proteins, MSH2, MSH6, OGG1 and BRCA1. The fibrotic response in Clusterin deficient (CLU-/-) mice persisted after bleomycin and it was associated with increased DNA damage, reduced DNA repair responses, and elevated cellular senescence. Remarkably, this pattern mirrored that observed in IPF lung tissues. Together, our results show that cellular localization of Clusterin leads to divergent effects on epithelial cell regeneration and lung repair during fibrosis.

Antifibrotic role of vascular endothelial growth factor in pulmonary fibrosis.

The chronic progressive decline in lung function observed in idiopathic pulmonary fibrosis (IPF) appears to result from persistent nonresolving injury to the epithelium, impaired restitution of the epithelial barrier in the lung, and enhanced fibroblast activation. Thus, understanding these key mechanisms and pathways modulating both is essential to greater understanding of IPF pathogenesis. We examined the association of VEGF with the IPF disease state and preclinical models in vivo and in vitro. Tissue and circulating levels of VEGF were significantly reduced in patients with IPF, particularly in those with a rapidly progressive phenotype, compared with healthy controls. Lung-specific overexpression of VEGF significantly protected mice following intratracheal bleomycin challenge, with a decrease in fibrosis and bleomycin-induced cell death observed in the VEGF transgenic mice. In vitro, apoptotic endothelial cell-derived mediators enhanced epithelial cell injury and reduced epithelial wound closure. This process was rescued by VEGF pretreatment of the endothelial cells via a mechanism involving thrombospondin-1 (TSP1). Taken together, these data indicate beneficial roles for VEGF during lung fibrosis via modulating epithelial homeostasis through a previously unrecognized mechanism involving the endothelium.

Acute cigarette smoke exposure activates apoptotic and inflammatory programs but a second stimulus is required to induce epithelial to mesenchymal transition in COPD epithelium.

BACKGROUND: Smoking and aberrant epithelial responses are risk factors for lung cancer as well as chronic obstructive pulmonary disease and idiopathic pulmonary fibrosis. In these conditions, disease progression is associated with epithelial damage and fragility, airway remodelling and sub-epithelial fibrosis. The aim of this study was to assess the acute effects of cigarette smoke on epithelial cell phenotype and pro-fibrotic responses in vitro and in vivo. RESULTS: Apoptosis was significantly greater in unstimulated cells from COPD patients compared to control, but proliferation and CXCL8 release were not different. Cigarette smoke dose-dependently induced apoptosis, proliferation and CXCL8 release with normal epithelial cells being more responsive than COPD patient derived cells. Cigarette smoke did not induce epithelial-mesenchymal transition. In vivo, cigarette smoke exposure promoted epithelial apoptosis and proliferation. Moreover, mimicking a virus-induced exacerbation by exposing to mice to poly I:C, exaggerated the inflammatory responses, whereas expression of remodelling genes was similar in both. CONCLUSIONS: Collectively, these data indicate that cigarette smoke promotes epithelial cell activation and hyperplasia, but a secondary stimulus is required for the remodelling phenotype associated with COPD.

Characterisation of innate lymphoid cell populations at different sites in mice with defective T cell immunity.

Background: Innate lymphoid cells (ILCs) have now been identified within most tissues of the body and current evidence indicates that this family of cells play a fundamental role in maintaining tissue homeostasis. However, few studies have compared the ILC populations between several tissues. Methods: We sought to generate a comprehensive characterisation of the ILC populations in different tissues of C57BL/6 WT and genetically modified mice targeting costimulatory pathways, using transcription factor expression to define specific groups. Results: Consistent with studies individually describing the ILC composition in different tissues, our analysis revealed different ILC groups dominate the ILC population in different tissues. Additionally, we observed a population of  IL-7Rα +Id2 + cells lacking expression of lineage markers but also lacking expression of GATA-3, RORgt or T-bet. This population was most evident in ear skin where it outnumbered the defined ILC groups, however, further experiments demonstrated that detection of these cells was influenced by how the tissue was digested, raising concerns as to its real nature. Since both ILC2 and ILC3 express ICOS, we then investigated the requirement for ICOS:ICOSL interactions in the homeostasis of ILC populations at these sites. Surprisingly, no significant differences were detected in the number of ILC1, ILC2 or ILC3 between WT and ICOSL -/- mice in any tissue, indicating that this pathway is not required for ILC homeostasis at these sites. These data were compared with CD80 -/-CD86 -/- mice given evidence of CD28 expression by some ILC and ILC crosstalk with activated T cells. Notably, the absence of CD28 ligands resulted in a significant increase in ILC2 and ILC3 numbers in the intestine. Conclusions: Together, these data provide new insight into ILC composition in different tissues in both WT and genetically modified mice where key costimulatory pathways are genetically deleted, providing a useful resource for further research into ILC biology.

IL-33, IL-25, and TSLP induce a distinct phenotypic and activation profile in human type 2 innate lymphoid cells.

Innate lymphoid cells (ILCs) represent a distinct branch of the lymphoid lineage composed of 3 major subpopulations: ILC1, ILC2, and ILC3. ILCs are mainly described as tissue-resident cells but can be detected at low levels in human blood. However, unlike mouse ILCs, there is still no consistent methodology to purify and culture these cells that enables in-depth analysis of their intrinsic biology. Here, we describe defined culture conditions for ILC2s, which allowed us to dissect the roles of interleukin 2 (IL-2), IL-25, IL-33, and thymic stromal lymphopoietin (TSLP) individually, or in combination, in modulating ILC2 phenotype and function. We show that TSLP is important for ILC2 survival, while ILC2 activation is more dependent on IL-33, especially when in combination with IL-2 or TSLP. We found that activation of ILC2s by IL-33 and TSLP dramatically upregulated their surface expression of c-Kit and downregulated expression of the canonical markers IL-7Rα and CRTH2. IL-2 further amplified ILC2 production of IL-5, IL-13, and granulocyte-macrophage colony-stimulating factor but also induced a more natural killer (NK)-like phenotype in ILC2, with upregulation of granzyme B production by these cells. Furthermore, ILC2 plasticity was observed in serum-free SFEM II media in response to IL-33, IL-25, and TSLP stimulation and independently of IL-12 and IL-1ß. This is the first comprehensive report of an in vitro culture system for human ILC2s, without the use of feeder layers, which additionally evaluates the impact of IL-25, IL-33, and TSLP alone or in combination on ILC2 surface phenotype and activation status.

The epithelium in idiopathic pulmonary fibrosis: breaking the barrier.

Idiopathic pulmonary fibrosis is a progressive disease of unknown etiology characterized by a dysregulated wound healing response that leads to fatal accumulation of fibroblasts and extracellular matrix (ECM) in the lung, which compromises tissue architecture and lung function capacity. Injury to type II alveolar epithelial cells is thought to be the key event for the initiation of the disease, and so far both genetic factors, such as mutations in telomerase and MUC5B genes as well as environmental components, like cigarette smoking, exposure to asbestos and viral infections have been implicated as potential initiating triggers. The injured epithelium then enters a state of senescence-associated secretory phenotype whereby it produces both pro-inflammatory and pro-fibrotic factors that contribute to the wound healing process in the lung. Immune cells, like macrophages and neutrophils as well as activated myofibroblasts then perpetuate this cascade of epithelial cell apoptosis and proliferation by release of pro-fibrotic transforming growth factor beta and continuous deposition of ECM stiffens the basement membrane, altogether having a deleterious impact on epithelial cell function. In this review, we describe the role of the epithelium as both a physical and immunological barrier between environment and self in the homeostatic versus diseased lung and explore the potential mechanisms of epithelial cell injury and the impact of loss of epithelial cell permeability and function on cytokine production, inflammation, and myofibroblast activation in the fibrotic lung.

IL-33 is more potent than IL-25 in provoking IL-13-producing nuocytes (type 2 innate lymphoid cells) and airway contraction.

BACKGROUND: IL-25 and IL-33 belong to distinct cytokine families, but experimental mouse studies suggest their immunologic functions in type 2 immunity are almost entirely overlapping. However, only polymorphisms in the IL-33 pathway (IL1RL1 and IL33) have been significantly associated with asthma in large-cohort genome-wide association studies. OBJECTIVE: We sought to identify distinct pathways for IL-25 and IL-33 in the lung that might provide insight into their roles in asthma pathogenesis and potential for therapeutic intervention. METHODS: IL-25 receptor-deficient (Il17rb(-/-)), IL-33 receptor-deficient (ST2, Il1rl1(-/-)), and double-deficient (Il17rb(-/-)Il1rl1(-/-)) mice were analyzed in models of allergic asthma. Microarrays, an ex vivo lung slice airway contraction model, and Il13(+/eGFP) mice were then used to identify specific effects of IL-25 and IL-33 administration. RESULTS: Comparison of IL-25 and IL-33 pathway-deficient mice demonstrates that IL-33 signaling plays a more important in vivo role in airways hyperreactivity than IL-25. Furthermore, methacholine-induced airway contraction ex vivo increases after treatment with IL-33 but not IL-25. This is dependent on expression of the IL-33 receptor and type 2 cytokines. Confocal studies with Il13(+/eGFP) mice show that IL-33 more potently induces expansion of IL-13-producing type 2 innate lymphoid cells, correlating with airway contraction. This predominance of IL-33 activity is enforced in vivo because IL-33 is more rapidly expressed and released in comparison with IL-25. CONCLUSION: Our data demonstrate that IL-33 plays a critical role in the rapid induction of airway contraction by stimulating the prompt expansion of IL-13-producing type 2 innate lymphoid cells, whereas IL-25-induced responses are slower and less potent.

Blocking IL-25 signalling protects against gut inflammation in a type-2 model of colitis by suppressing nuocyte and NKT derived IL-13.

BACKGROUND: Interleukin-25 (IL-25) is a potent activator of type-2 immune responses. Mucosal inflammation in ulcerative colitis is driven by type-2 cytokines. We have previously shown that a neutralizing anti-IL-25 antibody abrogated airways hyperreactivity in an experimental model of lung allergy. Therefore, we asked whether blocking IL-25 via neutralizing antibodies against the ligand or its receptor IL-17BR could protect against inflammation in an oxazolone-induced mouse model of colitis. METHODS: Neutralizing antibodies to IL-25 or IL-17BR were administered to mice with oxazolone-induced colitis, a model of ulcerative colitis. The disease onset was evaluated by weight loss and degree of colon ulceration. Also, lamina propria and mesenteric lymph node (MLN) infiltrates were assessed for mucosal inflammation and cultured in vitro to determine cytokine production. RESULTS: We found that in oxazolone colitis IL-25 production derives from intestinal epithelial cells and that IL-17BR(+) IL-13-producing natural killer T (NKT) cells and nuocytes drive the intestinal inflammation. Blocking IL-25 signalling considerably improved the clinical aspects of the disease, including weight loss and colon ulceration, and resulted in fewer nuocytes and NKT cells infiltrating the mucosa. The improved pathology correlated with a decrease in IL-13 production by lamina propria cells, a decrease in the production of other type-2 cytokines by MLN cells, and a decrease in blood eosinophilia and IgE. CONCLUSION: IL-25 plays a pro-inflammatory role in the oxazolone colitis model, and neutralizing antibodies to IL-25 or IL-17BR can slow the ongoing inflammation in this disease. Because this model mimics aspects of human ulcerative colitis, these antibodies may represent potential therapeutics for reducing gut inflammation in patients.

Transcription factor RORα is critical for nuocyte development.

Nuocytes are essential in innate type 2 immunity and contribute to the exacerbation of asthma responses. Here we found that nuocytes arose in the bone marrow and differentiated from common lymphoid progenitors, which indicates they are distinct, previously unknown members of the lymphoid lineage. Nuocytes required interleukin 7 (IL-7), IL-33 and Notch signaling for development in vitro. Pro-T cell progenitors at double-negative stage 1 (DN1) and DN2 maintained nuocyte potential in vitro, although the thymus was not essential for nuocyte development. Notably, the transcription factor RORα was critical for the development of nuocytes and their role in the expulsion of parasitic worms.

Reduced c-Myb activity compromises HSCs and leads to a myeloproliferation with a novel stem cell basis.

Murine haematopoietic stem cells (HSCs) are contained in the Kit+Sca1+Lin(-) (KSL) population of bone marrow and are able to repopulate lethally irradiated mice. Myeloproliferative disorders (MPDs) are thought to be clonogenic diseases arising at the level of the HSC. Here, we show that mice expressing low levels of the transcription factor c-Myb, as the result of genetic knockdown, develop a transplantable myeloproliferative phenotype that closely resembles the human disease essential thrombocythaemia (ET). Unlike wild-type cells, the KSL population in c-myb knockdown bone marrow cannot repopulate irradiated mice and does not transfer the disease. Instead, cells positive for Kit and expressing low to medium levels of CD11b acquire self-renewing stem cell properties and are responsible for the perpetuation of the myeloproliferative phenotype.

Schwannoma intraósseo da coluna vertebral cervical: relato de caso / Intra-osseous cervical vertebral schwannoma: case report

Apresenta-se o caso clínico de um indivíduo do gênero masculino, de 75 anos de idade, com alterações clínicas compatíveis com um quadro de mielopatia cervical. A investigação por imagem revelou uma estenose do canal vertebral em C2-C3 e C3-C4, por alterações degenerativas nesses níveis, e a presença de uma lesão expansiva centrada aos corpos de C5 e C6. A tomografia axial computadorizada (TC) e a ressonância magnética (RM) mostraram ainda um componente paravertebral com características de sinal idênticas às da lesão vertebral. O doente foi operado e o exame histopatológico da massa tumoral demonstrou tratar-se de um schwannoma. Contudo, foram notadas algumas diferenças entre os dois componentes, intraósseo e paravertebral. O caso apresentado reveste-se de interesse especial pela localização e distribuição tumoral particularmente invulgares. Do nosso conhecimento, trata-se do primeiro caso descrito de schwannoma intraósseo com destruição simultânea de dois corpos vertebrais adjacentes. Salienta-se, ainda, a ocorrência de dois componentes tumorais anatomicamente distintos, um intraósseo e outro paravertebral, sem nítida continuidade entre si, como observado intraoperatoriamente e demonstrado pelas imagens de TC e RM. Julgamos importante considerar esse tipo de tumor no diagnóstico diferencial de lesões expansivas vertebrais, de forma a planejar adequadamente a abordagem terapêutica...

Streptococcus agalactiae GAPDH is a virulence-associated immunomodulatory protein.

Certain extracellular proteins produced by several pathogenic microorganisms interfere with the host immune system facilitating microbial colonization and were thus designated virulence-associated immunomodulatory proteins. In this study, a protein with B lymphocyte stimulatory activity was isolated from culture supernatants of Streptococcus agalactiae strain NEM316. This protein, with an apparent molecular mass of 45 kDa, was identified as GAPDH by N-terminal amino acid sequencing. The gapC gene was cloned and expressed in Escherichia coli for the production of a recombinant histidyl-tagged protein. The recombinant GAPDH (rGAPDH), purified in an enzymatically active form, induced in vitro an up-regulation of CD69 expression on B cells from normal and BCR transgenic mice. In addition, rGAPDH induced an increase in the numbers of total, but not of rGAPDH-specific, splenic Ig-secreting cells in C57BL/6 mice treated i.p. with this protein. These in vitro- and in vivo-elicited B cell responses suggest that the B cell stimulatory effect of rGAPDH is independent of BCR specificity. A S. agalactiae strain overexpressing GAPDH showed increased virulence as compared with the wild-type strain in C57BL/6 mice. This virulence was markedly reduced in IL-10-deficient and anti-rGAPDH antiserum-treated mice. These results suggest that IL-10 production, which was detected at higher concentrations in the serum of rGAPDH-treated mice, is important in determining the successfulness of the host colonization by S. agalactiae and they highlight the direct role of GAPDH in this process. Taken together, our data demonstrate that S. agalactiae GAPDH is a virulence-associated immunomodulatory protein.

A randomised bouble-blind placebo controlled trial of lidamidine HCL in irritable vowel syndrome

BACKGROUND: We have previously shown electro-mechanical recto-anal alterations in irritable bowel syndrome patients (Awad R. Neurogastroenterol Motil 1993; 5; 265-271). To assess whether the alpha 2-agonist lidamidine HCL is able to modify these physiological alterations and alleviate clinical symptoms, 50 patients with irritable bowel syndrome were studied in a random, double blind, placebo-controlled trial. METHODS: Lidamidine HCL (4 mg) or placebo was taken orally t.i.d. with food. Fasting and post-prandial electrical and mechanical activities of rectum and internal anal sphincter were recorded before and at the end of treatment. Recto-anal sensitivity was also tested. RESULTS: After treatment, post-prandial duration of spontaneous recto-anal inhibitory reflex diminished in the lidamidine group (18.9 +/- 1 vs. 15.1 +/- 1.3 sec; p < 0.05). Amplitude of induced rectoanal inhibitory reflex decreased after lidamidine (24.6 +/- 2.9 vs 17.3 +/- 3 mmHg; p = 0.02). Rectal electrical activity showed no changes during basal and post-prandial periods in any group. Rectal painful sensation decreased after treatment with lidamidine (54.8 +/- 5.4 vs 43.6 +/- 3.5 ml; p < 0.05) as well as with placebo (p < 0.05). Abdominal distension and requency, severity and duration of pain diminished in both groups (p < 0.05). CONCLUSION: Lidamidine decreased the augmented mechanical response to food, reduced rectal sensitivity, and relieved symptoms. These facts suggest that in spite of the strong placebo response obtained, lidamidine HCL can become a useful alternative for treatment of patients with irritable bowel syndrome.

A randomised bouble-blind placebo controlled trial of lidamidine HCL in irritable vowel syndrome

BACKGROUND: We have previously shown electro-mechanical recto-anal alterations in irritable bowel syndrome patients (Awad R. Neurogastroenterol Motil 1993; 5; 265-271). To assess whether the alpha 2-agonist lidamidine HCL is able to modify these physiological alterations and alleviate clinical symptoms, 50 patients with irritable bowel syndrome were studied in a random, double blind, placebo-controlled trial. METHODS: Lidamidine HCL (4 mg) or placebo was taken orally t.i.d. with food. Fasting and post-prandial electrical and mechanical activities of rectum and internal anal sphincter were recorded before and at the end of treatment. Recto-anal sensitivity was also tested. RESULTS: After treatment, post-prandial duration of spontaneous recto-anal inhibitory reflex diminished in the lidamidine group (18.9 +/- 1 vs. 15.1 +/- 1.3 sec; p < 0.05). Amplitude of induced rectoanal inhibitory reflex decreased after lidamidine (24.6 +/- 2.9 vs 17.3 +/- 3 mmHg; p = 0.02). Rectal electrical activity showed no changes during basal and post-prandial periods in any group. Rectal painful sensation decreased after treatment with lidamidine (54.8 +/- 5.4 vs 43.6 +/- 3.5 ml; p < 0.05) as well as with placebo (p < 0.05). Abdominal distension and requency, severity and duration of pain diminished in both groups (p < 0.05). CONCLUSION: Lidamidine decreased the augmented mechanical response to food, reduced rectal sensitivity, and relieved symptoms. These facts suggest that in spite of the strong placebo response obtained, lidamidine HCL can become a useful alternative for treatment of patients with irritable bowel syndrome. (Au)

Esophageal motility disorders in Mexican patioents with Duchenne's muscular dystrophy

Objetive: Myopathies are entities tahat mainly involve strieted muscle. In Duchenne's muscular dystrophy (DMD) there have been reported smooth muscle alterations in the pre-oral phase of swallowing, in gastric emptying, and pseudoobstruction. Nevertheless, esophageal motility alterations are not concluding. The objetive of this work was to determine if there are motor esophageal alterations is this patients, and if this alterations are related to the clinical manifestations of disease. Study design: nine consecutive patients with DMD (mean age 8, range 6-11 years; males) were evaluated, comparing clinical and manometric findings. Results: esophageal manometry alterations were found in all patients, mainly simultaneous non-peristaltic waves (60.86 percent) of diminished amplitude, in both striated and smooth muscle. Seventy seven percent presented with upper and lower gastrointestinal symptoms (dysphagia, regurgitation, epigastric pain, constipation, and distention). No correlation was found between esophageal motility alterations and gastrointestinal symptoms, nor with the clinical stage of disease in accordance to Brook (r=0.27). Conclusion: these results show that patients with DMD present esophageal motor disorders in both striated and smooth muscle, as well as upper and lower gastrointestinal symptoms. Specialized motility studies, could yield a better understanding of disease, and, possibly with adequate treatment, provide for a better quality of life in children with DMD.

Esophageal motility disorders in Mexican patioents with Duchennes muscular dystrophy

Objetive: Myopathies are entities tahat mainly involve strieted muscle. In Duchennes muscular dystrophy (DMD) there have been reported smooth muscle alterations in the pre-oral phase of swallowing, in gastric emptying, and pseudoobstruction. Nevertheless, esophageal motility alterations are not concluding. The objetive of this work was to determine if there are motor esophageal alterations is this patients, and if this alterations are related to the clinical manifestations of disease. Study design: nine consecutive patients with DMD (mean age 8, range 6-11 years; males) were evaluated, comparing clinical and manometric findings. Results: esophageal manometry alterations were found in all patients, mainly simultaneous non-peristaltic waves (60.86 percent) of diminished amplitude, in both striated and smooth muscle. Seventy seven percent presented with upper and lower gastrointestinal symptoms (dysphagia, regurgitation, epigastric pain, constipation, and distention). No correlation was found between esophageal motility alterations and gastrointestinal symptoms, nor with the clinical stage of disease in accordance to Brook (r=0.27). Conclusion: these results show that patients with DMD present esophageal motor disorders in both striated and smooth muscle, as well as upper and lower gastrointestinal symptoms. Specialized motility studies, could yield a better understanding of disease, and, possibly with adequate treatment, provide for a better quality of life in children with DMD. (AU)

Retroalimentación biológica y su aplicación clínica / Clinical applications of biofeedback

Antecedentes: La incontinencia fecal constituye un serio problema social que afecta a todos los grupos de edad. Su tratamiento es tan complejo como desconocido. Métodos: Efectuamos un estudio longitudinal, prospectivo, experimental, entre 47 pacientes consecutivos que presentaban incontinencia total por un periodo de 55.4 ñ 7.6 meses (intervalo: seis meses a 21 años), con 2.4 ñ 0.2 episodios de incontinencia (intervalo: 1-7 por día). A todos se les efectuó cuestionario para validar el diagnóstico de incontinencia, historia clínica completa, laboratorio, colon por enema, rectosigmoidoscopia, sensibilidad rectal, manometría rectoanal, y retroalimentación biológica sin instrumentación electrónica. Veintiún sujetos normales sirvieron como grupo control. Resultados: Los pacientes con incontinencia fecal presentaron disminución de la sensibilidad rectal (p<0.01) y alteraciones en el reflejo recto anal inhibitorio espontáneo. Todos obtuvieron curación completa en un periodo de 4 ñ 0.5 meses (intervalo: 15 días a 15 meses) y fueron seguidos por uno a ocho años. Conclusiones: La nueva modalidad de retroalimentación biológica aquí descrita no utiliza ningún instrumento electrónico. La curación y el tiempo de curación de los pacientes no solamente es comparable, sino superior a lo hasta ahora informados. Puede ser reproducido, con el entrenamiento adecuado, por mayor número de médicos en cualquier centro y condicionar, por tanto, un beneficio significativo en la calidad de vida de un mayor número de pacientes

Retroalimentacion biologica y cirugia en el tratamiento de la incontinencia fecal con lesion del esfinter anal externo: seguimento a largo plazo / Biofeedback and surgery in the treatment of fecal incontinence and lesion of the external anal sphincter: long-term follow-up

INTRODUCCION: En niños, el traumatismo de la región anal que afecta tanto al esfínter anal externo como al esfínter anal interno es un grave problema. La retroalimentación biológica no es efectiva si hay destrucción del esfínter anal externo, y la restitución de la morfologia con cirugía tampoco cura la incontinencia. CASO CLINICO: Niña de 6 años 8 meses de edad, que desde los 2 años sufrió tricocefalosis masiva recurrente; condicionándole prolapso rectal, abscesos y fístulas perianales, fistulectomías, y finalmente destrucción de la región perianal, con incontinencia total. Previa manometría rectoanal, y determinación de receptores rectales, se efectuó retroalimentación biológica antes y después de la transposición del músculo gracilis y colostomía. a los 12 meses se obtuvo continencia total, que aún persiste a 7 años de seguimiento. CONCLUSIONES: En la incontinencia fecal con destrucción del esfínter anal externo, y alteración fisiológica del esfínter anal interno, se debe efectuar: manometria y determinación de receptores rectales, reconstrucción del esfínter anal externo con transposición del músculo gracilis, y retroalimentación biológica