Handicap visible : de la reconnaissance du stigmate et du déni de déviance à la revendication de droits

This article brings new insight into the relationship between disability studies and the sociology of handicap as “deviance” and “stigma”. Disability studies grew up in a tight connection with the disability rights movement, but one of their roots was the new way of conceiving delinquency, addiction, madness, homosexuality, and handicap, which emerged in the 1960s. Eliot Freidson (1966) shifted the attention from the “disabled”, treated as patients to rehabilitate, to “handicap makers”. The relevant question was then: which are the professional jurisdictions of specialists appointed to “cure” disabled people? In which organizational arenas is disability institutionalized as a problem to be solved? Fred Davis (1961), for his part, explored another dimension, closer to Erving Goffman (1963): how are stigma co-produced, reified, or denied in encounter situations between people with and without disabilities? More specifically, how is the “visible handicap” handled in such face-to-face interactions? A third way has been worked by John Kitsuse in 1980 with his concept of “tertiary deviance.” In line with the 1960s sociology of deviance as “secondary deviation”, this concept of “tertiary deviance” recognizes the ability of persons with disabilities to act, to claim rights, to invent collective identities, and to experience and create new life ecologies.     

Suppressive effect of acetylcholine on automaticity of cannine atrioventricular node

The effects of acetylcholine on the spontaneous activity of the AV node of dog hearts were studied by recording transmembrane potentials of its fibers. Action potentials of most nodal fibers were characterized by prominent phase 4 depolarization and a smooth transition from phases 4 to 0. On the isolated AV nodes, acetylcholine at 1.0 μg/m1 suppressed the rate of phase 4 depolarization and increased the amplitude of the maximum diastolic potential, resulting in a slowing of spontaneous activity. At 2.0 μg/m1, spontaneous activity was completely suppressed. In comparison, spontaneous activity of the isolated His bundle was relatively insensitive to the suppressive effect of acetylcholine at the same concentrations. In the AV node-His bundle preparations in which the AV node was the pacemaker, acetylcholine decreased spontaneous activity by suppressing the phase 4 depolarization of the nodal fibers and shifted the pacemaker of the preparation to the His bundle. The findings provide a basis for predicting that under strong vagal influence, the automaticity of the AV node will be suppressed and the pacemaker of the junctional rhythm will be located at the His bundle.     

Endocardial cushion defect associated with cor triatriatum sinistrum or supravalve mitral ring

Clinical and angiographic or autopsy data, or both, on three children with a subdivided left atrium (cor triatriatum) and an associated endocardial cushion defect are reviewed. (One child had ostium primum defect, and two had complete atrioventricular [A-V] canal.) A fourth patient demonstrates the difficulties in differentiating subdivided left atrium from supravalve mitral stenosis in the presence of an endocardial cushion defect. The clinical findings are greatly influenced by the endocardial cushion defect. A pressure gradient between the pulmonary wedge and (left or right) ventricular end-diastolic pressures in patients with an endocardial cushion defect indicates pulmonary venous obstruction and should alert one to the possibility of these combined lesions. The exact diagnosis is made with injections of angiographic contrast medium into the proximal and distal left atrial chambers, to document the respective relations of the pulmonary veins, left atrial appendage and A-V valves to these atrial chambers. All three patients with an endocardial cushion defect and a subdivided left atrium had an associated patent ductus arteriosus. The common association of subdivided left atrium with intracardiac, pulmonary venous and aortic anomalies is again demonstrated.     

Electrophysiologic effects of atropine on human sinus node and atrium.

Electrophysiologic studies were conducted in 17 patients without apparent sinus node disease before and after intravenous administration of 1 to 2 mg of atropine. Mean values in milliseconds (+/- standard error of the mean) before and after administration of atropine were as follows: sinus cycle length 846 +/- 26.4 versus 647 +/- 20.0 (P less than 0.001); sinus nodal recovery time 1,029 +/- 37 versus 774 +/- 36 (P less than 0.001); mean calculated sinoatrial (S-A) conduction time 103 +/- 5.7 versus 58 +/- 3.9 (P less than 0.001); mean P-A interval 34 +/- 1.5 msec versus 31 +/- 1.5 (P less than 0.05); mean atrial effective and functional refractory periods during sinus rhythm 285 +/- 11.3 versus 238 +/- 7.9 and 331 +/0 11.6 versus 280 +/- 8.6, respectively (P less than 0.001 for both); mean atrial effective and functional refractory periods measured at equivalent driven cycle length 239 +/- 7.7 versus 213 +/- 7.4 and 277 +/- 11.4 versus 245 +/- 9.5, respectively (P less than 0.001 for both). In conclusion, atropine shortened sinus cycle length, sinus nodal recovery time and calculated S-A conduction time. The shortening of atrial refractory periods with atropine implies that vagotonia prolongs atrial refractoriness in man.