Video self-confrontation as a therapeutic tool in schizophrenia: A randomized parallel-arm single-blind trial.

BACKGROUND: Lack of insight is a barrier to treating psychosis. Preliminary studies have suggested that showing people videos of their psychotic behaviour may improve personal insight. This clinical trial aimed to assess the effect of video self-confrontation. METHODS: Inpatients between 18 and 65 years old with schizophrenia or schizoaffective disorder were filmed upon admission to two psychiatric hospitals while experiencing acute psychosis. After stabilization, individuals were randomized 1:1 to the "self-video" group where they watched their own video or to the "no video" control group. The primary outcome was the Scale to assess Unawareness of Mental Disorder (SUMD) at 48 h by a blinded assessor. Secondary objectives included psychotic and depressive symptoms, medication adherence and functioning using the Functional Remission of General Schizophrenia. Patients were followed up for four months. RESULTS: 60 participants were randomized and the level of insight did not differ between groups at 48 h (p = 0.98). There was no impact on SUMD subscores or the other insight questionnaires at any timepoint, nor on psychopathology or medication adherence. At one month, the level of functioning of those in the "self-video" group (n = 23) was higher (61.8 vs 53.5, p = 0.02), especially concerning "Treatment" and "Daily life". No adverse effects were reported. After video self-confrontation, people expressed more positive than negative emotions and were less lost to follow-up. CONCLUSION: Video self-confrontation did not change levels of insight, but may have a therapeutic impact nonetheless, by improving levels of self-care and adherence to care, indicating that this innovative therapeutic tool requires further study. TRIAL REGISTRATION NUMBER: NCT02664129.

Role of angiotensinogen in blood pressure homeostasis.

The role of angiotensinogen in blood pressure control was assessed in normotensive rats by observing the changes resulting from inhibition by specific rat angiotensinogen antiserum. The antiserum decreased blood pressure in rats on normal sodium as well as sodium-free diets (respectively delta BP = -30 +/- 6 mm Hg and -42 +/- 8 mm Hg). In binephrectomized sodium-replete rats, administration of antiserum did not reduce blood pressure, whereas in sodium-depleted animals it slightly decreased blood pressure by 11 +/- 3 mm Hg. These results suggest that angiotensinogen participates in the regulation of blood pressure in normotensive rats, even in the sodium-replete state.

Influence of converting enzyme inhibition on the hormonal and renal adaptation to hyper- and hyponatraemic dehydration.

The present study was designed to investigate in rats the influence of converting enzyme inhibition with captopril on blood pressure, plasma urea, plasma renin concentration (PRC), plasma aldosterone and plasma vasopressin, and to define the interrelationships between PRC and these variables during equal degrees of either hyponatraemic (furosemide, 40 mg/kg for 2 days) or hypernatraemic (48-h water deprivation) dehydration. Chronic treatment with captopril (40 mg/kg daily) decreased blood pressure by 19% in normally hydrated treated rats, by 27% in water-deprived treated rats and by 40% in furosemide-treated rats. Plasma renin concentration, plasma aldosterone and plasma vasopressin were increased during both hypo- and hypernatraemic dehydration. Captopril decreased plasma aldosterone in water-deprived and furosemide-treated rats, whereas plasma vasopressin was unchanged. The significant correlation observed between plasma aldosterone and PRC in non-treated rats persisted in treated rats, the same level of plasma aldosterone being observed at values of PRC 10 times higher. On the other hand, the correlation between plasma vasopressin and PRC did not persist in captopril-treated rats. An increase in plasma urea was observed in both water-deprived treated rats and furosemide-treated rats. These data indicate that during hypo- and hypernatraemic dehydration, the renin-angiotensin system plays a role in regulating blood pressure, urea elimination and plasma aldosterone, but vasopressin regulation is not modified by its inhibition.

Decreased renin release and constant kallikrein secretion after injection of L-NAME in isolated perfused rat kidney.

A possible role of the endothelial L-arginine/NO pathway in the control of renal hemodynamics, renin release and kallikrein secretion was studied in an isolated rat kidney model perfused in a closed-circuit. NG-nitro-L-arginine methyl ester (L-NAME, 1-50 microM), an inhibitor of nitric oxide biosynthesis, caused a dose-dependent increase in perfusion pressure (PP) and a dose-dependent decrease in renal perfusate flow. Renin release was inhibited independently of a rise in PP. L-NAME did not change the urinary kallikrein secretion. These results confirm the intervention of the L-arginine/NO pathway in the vasodilation of this isolated perfused kidney model and demonstrate the inhibitory effect of L-NAME on renin release. They suggest that nitric oxide synthesis plays a role in stimulating renin release and is not involved in the regulation of urinary kallikrein secretion.

[Kallikrein secretion by the isolated perfused rat kidney. Role of perfusion pressure and the renin-angiotensin system]. / Sécrétion de kallicréine par le rein de rat isolé perfusé. Rôle de la pression de perfusion et du système rénine-angiotensine.

The isolated perfused rat kidney (IPRK) releases kallikrein in urine and renin in perfusate. We have previously shown (Kidney Int 24: 58-65, 1983) and confirm here that kallikrein, as well as renin releases are influenced by changes in renal hemodynamics in this model: a rise in perfusion pressure (PP) from 80 to 98 mmHg increases renal perfusate flow (RPF) by 48 +/- 3 p. 100, inhibits renin release and stimulates kallikrein secretion to 234 +/- 84 p. 100 of control values (n = 8). Since the perfusate lacks angiotensinogen, we decided to study the effect on kallikrein of the reconstitution of the renin-angiotensin system in the IPRK by adding angiotensinogen + angiotensin converting enzyme (AG + ACE) to the perfusion medium. After AG + ACE, PP rose to 107 +/- 4 mmHg, RPF decreased by 82 +/- 3 p. 100 as a consequence of the vasoconstrictor effect of angiotensin II, and renin release was suppressed. Again kallikrein secretion was stimulated and increased to 333 +/- 153 p. 100 of control values (n = 4). It is concluded 1) that kallikrein release is influenced by changes in PP but not in RPF on the IPRK. 2) that reconstitution of the renin-angiotensin system by addition of AG + ACE to the perfusate leads to vasoconstriction, suppression of renin release and a marked increase in kallikrein secretion.

[Immunologic approach of the blockage of the renin angiotensin system in vivo]. / Approche immunologique du blocage du système rénine angiotensine in vivo.

To block the renin-angiotensin system by antibodies directed against renin or angiotensins is an old and recent goal. This goal can be attained by passive transfer of antibodies or by active immunization against the different molecules of the system. Only passive transfer of polyclonal antibodies directed against the native substrate (angiotensinogen) has been performed in rats. This acute blockade of angiotensinogen substrate availability decrease blood pressure about 30 mmHg in salt depleted rats. Passive transfer of anti-converting enzyme immunoglobulins has been already performed in rabbit and rat. It induced an immunoallergic reaction in the pulmonary capillary bed. Immunization against angiotensin II has been a powerful tool in the exploration of the role of the renin angiotensin system in hypertension. Passive and active immunization have been performed in different species: rabbit, rat. The majority of the results concerning the decrease in blood pressure was negative. However, some works reported positive results which could be related to the high affinity of antibodies for angiotensins. Passive and active immunizations against renin were also performed in different species: dog, pig, rat, rabbit, primates. The majority of the results concerning the decrease of blood pressure were positive, if species specificity of renin was taken into account. Recently passive transfer of polyclonal and monoclonal antibodies, directed against human renin have been performed in normotensive and hypertensive primates, demonstrating an acute fall in blood pressure comparable to that observed with converting enzyme inhibitors. Active immunization against human renin has also been performed in primates; and the chronic blockade of the renin-substrate reaction obtained in this way was associated with a significant decrease in blood pressure, aldosterone secretion and a disappearance of plasma renin activity. Unfortunately, such an active immunization was associated with an organ specific autoimmune disease within the kidney. In conclusion, passive and active immunization against the different proteins and peptides of the system offers specific models of blockade which can be compared with synthetic inhibitors of renin, converting enzyme and angiotensins. Therapeutic application of this immunological approach necessitates the verification of the total absence of autoimmune disease.

[Effects of clonidine on opiate withdrawal symptoms. Results - biochemical mechanisms (author's transl)]. / Application de la clonidine au traitement de l'état de manque des toxicomanies opiacées. Résultats thérapeutiques, mécanismes d'action.

Clonidine was administered to nineteen patients in an inpatient setting after abrupt discontinuation of chronic opiate addiction (morphine, héroin, dextromoramide). Clonidine produces a decrease sometimes very rapid in opiate withdrawal signs but does not suppress the whole affects associated with. These data support the hypothesis that clonidine has antiwithdrawal effect by replacing opiate-mediated inhibition with alpha 2 mediated inhibition of brain noradrenergic activity.

[Long-term review of homogeneous and consecutive series of 100 "Charnley"-type total hip prostheses]. / Révision á long terme d'une série homogéne et consécutive de 100 prothéses totales de hanche type "Charnley".

PURPOSE OF THE STUDY: Long-term studies of total hip replacements often give diverse results because the series studied are not homogeneous. We report the long-term result in a homogeneous, consecutive series of 100 Charnley total hip replacements for idiopathic hip osteoarthritis in patient without previous surgery, by the same operator. MATERIALS: Of 200 patients with 223 Charnley or Charnley-Kerboull total hip prostheses, implanted more than 13 years earlier, 94 patients with 104 implants were alive at the time of the study. Ninety of them (95.7 per cent) with 100 implants were clinically and radiographically examined. Mean follow-up was 14 yr 8 mo and minimum follow-up was over 13 yr 6 mo. METHODS: Hip function was clinically assessed according to Merle d'Aubigné's criteria. Immediate postoperative x-rays and x-rays at 1, 5 and 10 years and at maximum follow-up were examined. For the acetabulum, alignment, radiolucent line, loosening and wear of the socket were analysed. For the femur, the position of the implant, radiolucent line and loosening, changes in the calcar and cortical bone were analysed. RESULTS: Two femoral implants had to be replaced because of implant fracture. The acetabulum became loose in 3 cases and the femur in 2, but did not require revision at the time of examination. Mean acetabular wear was 0.93 mm (0-5 mm). Wear was greater if the subjects were active (p < 0.05) overweight (p < 0.05) and if the acetabulum was vertical (p < 0.05). Changes in calcar, generally lysis, were more frequent when wear was marked (p < 0.001). Thinning of cortical bone was more frequent in women (p < 0.05), sedentary subjects (p < 0.001) and those in poor general condition (p < 0.05) and was less frequently associated with acetabular wear (p < 0.01). DISCUSSION: This study is characterised by its homogeneity: same etiology, same operator, same implants. Functional outcome at a mean of 14 yr 8 mo after surgery was good, as in most series of Charnley's total hip prostheses. Acetabular wear gave most cause for concern. It was linked with the weight and activity of the patients and with socket alignment. This wear led to deterioration of the calcar, due to granulomas and not to stress shielding. In spite of the homogeneity of the series, no factor was found to account for cortical thickening, whereas cortical thinning occurred in light-weight, osteoporotic patients whose prosthesis did not entirely fill the medullary canal. CONCLUSION: Charnley's total hip prostheses are a good method for treatment of idiopathic hip osteoarthritis. Cement does not appear to be a major deterioration factor over time, unlike polyethylene sockets in which wear and its consequences are a matter for concern.

[Unstable painful shoulders (author's transl)]. / Epaules douloureuses et instables.

The authors have observed 23 cases of painful and unstable shoulders in athlets which could be related to unknown recurrent dislocations. The diagnosis was based on a radiological study demonstrating a deformity of the humeral upper extremity and of the glenoid. The patients were incapacited and had often been treated for "tendinitis". Most of the cases have been operated by a grafting of the anterior edge of the glenoid with success. It is thought that most of the glenoidal lesions are consequences and not causes of the dislocations.

[Reactions and psychic disorders in Besnier-Boeck-Schaumann disease. Clinical and psychological approach; application of a scale of aggressive behavior to the mental profile]. / Réactions et troubles psychiques au cours de la maladie de Besnier-Boeck-Schaumann. Approche clinique et psychologique; application d'une échelle de comportement agressif au profil mental.

35 cases of sarcoïdosis were studied at the onset of the disease. 25 cases of important or deep anxiety were recorded. None of them was correlated nor with organic lesions or medical seriousness, neither with psychopathic background, previous mental illness or treatment by corticoidic drugs. All patients were submitted to the Rorschach test, the self-assessment test of Catell, the Rosenzweig picture frustration test and the agressiveness rating scale test (L.-F. Gayral). It appears that, by comparison with three control groups: A) without sarcoïdosis but with another pulmonary disease, B) "normal", C) psychopathic personality. There is not a mental type profile for the patients with sarcoïdosis. Anxiety or/and with depression, or agressiveness are more important and frequent in patients not treated by corticoïdes than in patient treated. Another conclusion is the necessity to dispense careful psychotherapy to patients with sarcoïdosis, although the case does not require medical treatment. Quite contrary these last patients peculiarly need psychotherapy.

[Clinical trial of loxapine succinate in the treatment of 30 cases of psychotic states]. / Essai clinique du succinate de loxapine appliqué au traitement de 30 cas d'états psychotiques.

An open clinical study of loxapine succinate was developed on 30 hospitalized psychiatric patients in order to confirm its antipsychotic properties and its originality opposite the other major neuroleptics. Dosages ranged from 100 to 200 mg per day in 12 cases (40%), and more than 200 mg in serious psychosis or unamenable to therapeutic for which inferior dosages were inefficacious (11 cases). 56,7% of favourable results have been obtained, with a fair improvement of whole symptoms, paranoïd schizophrenic attack and acute delusions. Tolerance was remarkable: no neuro-vegetative manifestation was reported. The considerable sedative effect of loxapine had involved moderate and no invalidating drowsiness in 23% of cases. The extra-pyramidal occurring symptoms disappeared within 2 or 3 days. So loxapine succinate in proving to be a major first intention neuroleptic, suiting a considerable antipsychotic efficacy to a good tolerance, allowing new perspectives in the therapeutic and the approach of psychotic patients.

The role of the renin-angiotensin system in blood pressure regulation in normotensive animals and man.

The role of the renin-angiotensin system in the control of blood pressure in normal rodents, primates and man has been evaluated using inhibitors which block the system at various stages. Renin plays a major role in the maintenance of blood pressure under volume depletion. In subjects with a normal salt intake, the contribution of the renin-angiotensin system in maintaining blood pressure levels can be evaluated using angiotensin converting enzyme (ACE) inhibitors. The contribution of the renin-angiotensin system can now be evaluated more closely following the development of new substances which block the renin-angiotensinogen reaction. Available data strongly suggest that renin contributes to the maintenance of blood pressure levels in subjects with a normal salt intake, although to a lesser degree than in subjects on a low sodium intake. The renin-angiotensin system plays a role in the regulation of blood pressure levels in normal experimental animals and man--its importance depending on the state of sodium balance.