Differential Diagnosis Assessment in Ambulatory Care With an Automated Medical History-Taking Device: Pilot Randomized Controlled Trial.

BACKGROUND: Automated medical history-taking devices (AMHTDs) are emerging tools with the potential to increase the quality of medical consultations by providing physicians with an exhaustive, high-quality, standardized anamnesis and differential diagnosis. OBJECTIVE: This study aimed to assess the effectiveness of an AMHTD to obtain an accurate differential diagnosis in an outpatient service. METHODS: We conducted a pilot randomized controlled trial involving 59 patients presenting to an emergency outpatient unit and suffering from various conditions affecting the limbs, the back, and the chest wall. Resident physicians were randomized into 2 groups, one assisted by the AMHTD and one without access to the device. For each patient, physicians were asked to establish an exhaustive differential diagnosis based on the anamnesis and clinical examination. In the intervention group, residents read the AMHTD report before performing the anamnesis. In both the groups, a senior physician had to establish a differential diagnosis, considered as the gold standard, independent of the resident's opinion and AMHTD report. RESULTS: A total of 29 patients were included in the intervention group and 30 in the control group. Differential diagnosis accuracy was higher in the intervention group (mean 75%, SD 26%) than in the control group (mean 59%, SD 31%; P=.01). Subgroup analysis showed a between-group difference of 3% (83% [17/21]-80% [14/17]) for low complexity cases (1-2 differential diagnoses possible) in favor of the AMHTD (P=.76), 31% (87% [13/15]-56% [18/33]) for intermediate complexity (3 differential diagnoses; P=.02), and 24% (63% [34/54]-39% [14/35]) for high complexity (4-5 differential diagnoses; P=.08). Physicians in the intervention group (mean 4.3, SD 2) had more years of clinical practice compared with the control group (mean 5.5, SD 2; P=.03). Differential diagnosis accuracy was negatively correlated to case complexity (r=0.41; P=.001) and the residents' years of practice (r=0.04; P=.72). The AMHTD was able to determine 73% (SD 30%) of correct differential diagnoses. Patient satisfaction was good (4.3/5), and 26 of 29 patients (90%) considered that they were able to accurately describe their symptomatology. In 8 of 29 cases (28%), residents considered that the AMHTD helped to establish the differential diagnosis. CONCLUSIONS: The AMHTD allowed physicians to make more accurate differential diagnoses, particularly in complex cases. This could be explained not only by the ability of the AMHTD to make the right diagnoses, but also by the exhaustive anamnesis provided.

[From permanence to the group practice and then to the health center: New frameworks for new roles and skills of the primary care physician]. / De la permanence au cabinet de groupe, puis à la maison de santé.

Significant changes are needed in the future of primary care medicine: new health technologies allowing closer evaluation as well as a more reliable observation of patients' problems, new structural designs bringing together the different health care professionals and enabling integrative and multidisciplinary care as well as partnership with the community to better understand sociocultural aspects of the patients.

De nouveaux cadres de travail s'annoncent nécessaires pour les médecins de premier recours du futur : utilisation des technologies de santé mobile pour un suivi rapproché et en temps réel, réorganisation structurelle rapprochant les différents intervenants favorisant une approche multidisciplinaire coordonnée et partenariat communautaire prenant en compte la diversité socioculturelle des patients.

PINK1 and Parkin complementarily protect dopaminergic neurons in vertebrates.

Parkinson's disease (PD) is a common neurodegenerative disorder characterized by selective dopaminergic cell loss in the substantia nigra, but its pathogenesis remains unclear. The recessively inherited familial PD genes PARK2 and PARK6 have been attributed to mutations in the Parkin and PTEN-induced kinase 1 (PINK1) genes, respectively. Recent reports suggest that PINK1 works upstream of Parkin in the same pathway to regulate mitochondrial dynamics and/or conduct autophagic clearance of damaged mitochondria. This phenomenon is preserved from Drosophila to human cell lines but has not been demonstrated in a vertebrate animal model in vivo. Here, we developed a medaka fish (Oryzias latipes) model that is deficient in Pink1 and Parkin. We found that despite the lack of a conspicuous phenotype in single mutants for Pink1 or Parkin, medaka that are deficient in both genes developed phenotypes similar to that of human PD: late-onset locomotor dysfunction, a decrease in dopamine levels and a selective degeneration of dopaminergic neurons. Further analysis also revealed defects in mitochondrial enzymatic activity as well as cell death. Consistently, PINK1 and Parkin double-deficient MEF showed a further decrease in mitochondrial membrane potential and mitochondrial complex I activity as well as apoptosis compared with single-deficient MEF. Interestingly, these mitochondrial abnormalities in Parkin-deficient MEF were compensated by exogenous PINK1, but not by disease-related mutants. These results suggest that PINK1 and Parkin work in a complementary way to protect dopaminergic neurons by maintaining mitochondrial function in vertebrates.

Medaka fish Parkinson's disease model.

The teleost fish has been widely used in creating neurodegenerative models. Here we describe the teleost medaka fish Parkinson's disease (PD) models we developed using toxin treatment and genetic engineering. 1-Methyl-4-phenyl-1,2,3,4-tetrahydropyridine (MPTP), 6-hydroxydopamine (6-OHDA), proteasome inhibitors, lysosome inhibitors and tunicamycin treatment in our model fish replicated some salient features of PD: selective dopamine cell loss and reduced spontaneous movement with the last three toxins producing inclusion bodies ubiquitously in the brain. Despite the ubiquitous distribution of the inclusion bodies, the middle diencephalic dopaminergic neurons were particularly vulnerable to these toxins, supporting the idea that this dopamine cluster is similar to the human substantia nigra. PTEN-induced putative kinase 1 (PINK1) homozygous mutants also showed reduced spontaneous swimming movements. These data indicate that medaka fish can serve as a new model animal of PD. In this review we summarize our previous data and discuss future prospects.