7 research outputs found

    THE EMPIRICAL DIMENSIONS OF ANALYTIC PROCESS: AN EMPIRICAL INVESTIGATION

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    The aim of this study was to empirically identify the dimensions of the therapist’s, patient’s and interaction contributions to the analytic process. We performed an Exploratory Factor Analysis of patients’ contributions, therapists’ contributions and interaction dimensions, as assessed with the Analytic Process Scales (APS; Waldron et al., 2004) and Dynamic Interaction Scales (DIS; Waldron, Gazzillo et al., 2013) of 540 sessions from 27 analytic therapies. The EFA identified three dimensions of patients’ contributions (the patient reflects about her/his life and problems; the patient reflects about her/his relationship with the therapist; the patient dynamic competence); these factors explain 84.9% of the variance of patients’ contributions. We identified also three dimensions of the therapists’ contributions (therapist relational attitude, therapist dynamic competence, therapist confrontativeness), which explain 65.7% of the variance of therapists’ contributions; and one overall interaction factor explaining 59% of the variance of the APS and DIS interaction scales. Generalized Estimating Equations and partial correlation analyses enabled us to explore the interactions among these dimensions during the therapeutic process. In particular, we explored how the patient dynamic competence and the therapist dynamic competence and relational attitude contribute to the interaction, and how the interaction may strengthen the patient dynamic competence, i.e. the patients’ ability to participate productively to the analytic process and to oscillate between experiencing and reflecting on their experiences

    Fostering the capacity of the patients to oscillate between experiencing and reflecting: an empirical study on process and outcome of psychoanalyses

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    Aim: The aim of this study is to identify the technical and relation factors which contribute to the good outcome of psychoanalysis. Method: In order to accomplish this goal, we have assessed 600 sessions from 30 psychoanalytic treatments audio recorded an transcripted, 8 sessions from the first month, 4 from the middle of the therapy and 8 from the last month. The 8 sessions from the first month and the 8 sessions from the last month were assessed with the Shedler-Westen assessment Procedure-200 (SWAP-200; Shedler, Westen, 1999a, b), the Global Assessment of Functioning Scale (GAF, APA, 2000); the first 8 sessions were assessed also with the Helping Alliance Rating Scales (HAR; Luborsky, Crits-Cristoph, Alexander, Margolis, & Cohen, 1983) and all the sessions were assessed with the Analytic Process Scales (APS; Waldron et al., 2004) and the Dynamic Interaction Scales (DIS; Waldron et al., 2013). Results: The comparison between good and poor outcome treatments pointed out the relevance of both classical analytic interventions (clarification and interpretation of defenses, conflicts and emotional and behavioral patterns) and relational factors (straightforwardness, warmly and attuned responsiveness, empathy). Moreover, our data pointed out the correlation of the capacity of the patients to oscillate between experiencing and reflecting of the patients on their experience with the level of their Personality Health Index (PHI; Waldron et al., 2011).Finally, we explored what are the technical and relational elements of therapist communication that foster the patients capacity to oscillate between experiencing and reflecting. Discussion: The clinical and training implications of these data will be discussed

    Case report: Better late than never, but sooner is better: switch from CSII to sulfonylureas in two patients with neonatal diabetes due to KCNJ11 variants

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    Neonatal diabetes mellitus (NDM) is a rare genetic disease characterized by severe hyperglycemia requiring insulin therapy with onset mostly within the first 6 months and rarely between 6-12 months of age. The disease can be classified into transient (TNDM) or permanent neonatal diabetes mellitus (PNDM), or it can be a component of a syndrome. The most frequent genetic causes are abnormalities of the 6q24 chromosomal region and mutations of the ABCC8 or KCNJ11 genes coding for the pancreatic beta cell’s potassium channel (KATP). After the acute phase, patients with ABCC8 or KCNJ11 mutations treated with insulin therapy can switch to hypoglycemic sulfonylureas (SU). These drugs close the KATP channel binding the SUR1 subunit of the potassium channel and restoring insulin secretion after a meal. The timing of this switch can be different and could affect long-term complications. We describe the different management and clinical outcome over the time of two male patients with NDM due to KCNJ11 pathogenetic variants. In both cases, continuous subcutaneous insulin infusion pumps (CSII) were used to switch therapy from insulin to SU, but at different times after the onset. The two patients kept adequate metabolic control after the introduction of glibenclamide; during the treatment, insulin secretion was evaluated with c-peptide, fructosamine, and glycated hemoglobin (HbA1c), which were within the normal range. In neonates or infants with diabetes mellitus, genetic testing is an indispensable diagnostic tool and KCNJ11 variants should be considered. A trial of oral glibenclamide must be considered, switching from insulin, the first line of NDM treatment. This therapy can improve neurological and neuropsychological outcomes, in particular in the case of earlier treatment initiation. A new modified protocol with glibenclamide administered several times daily according to continuous glucose monitoring profile indications, was used. Patients treated with glibenclamide maintain good metabolic control and prevent hypoglycemia, neurological damage, and apoptosis of beta cells during long‐term administration

    A new mutation in the CAVIN1/PTRF gene in two siblings with congenital generalized lipodystrophy type 4: case reports and review of the literature

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    Lipodystrophy syndromes are characterized by a progressive metabolic impairment secondary to adipose tissue dysfunction and may have a genetic background. Congenital generalized lipodystrophy type 4 (CGL4) is an extremely rare subtype, caused by mutations in the polymerase I and transcript release factor (PTRF) gene. It encodes for a cytoplasmatic protein called caveolae-associated protein 1 (Cavin-1), which, together with caveolin 1, is responsible for the biogenesis of caveolae, being a master regulator of adipose tissue expandability. Cavin-1 is expressed in several tissues, including muscles, thus resulting, when dysfunctional, in a clinical phenotype characterized by the absence of adipose tissue and muscular dystrophy. We herein describe the clinical phenotypes of two siblings in their early childhood, with a phenotype characterized by a generalized reduction of subcutaneous fat, muscular hypertrophy, distinct facial features, myopathy, and atlantoaxial instability. One of the siblings developed paroxysmal supraventricular tachycardia leading to cardiac arrest at 3 months of age. Height and BMI were normal. Blood tests showed elevated CK, a mild increase in liver enzymes and triglycerides levels, and undetectable leptin and adiponectin concentrations. Fasting glucose and HbA1c were normal, while Homeostatic Model Assessment for Insulin Resistance (HOMA-IR) was mildly elevated. Both patients were hyperphagic and had cravings for foods rich in fats and sugars. Genetic testing revealed a novel pathogenic mutation of the CAVIN1/PTRF gene (NM_012232 exon1:c T21A:p.Y7X) at the homozygous state. The diagnosis of lipodystrophy can be challenging, often requiring a multidisciplinary approach, given the pleiotropic effect, involving several tissues. The coexistence of generalized lack of fat, myopathy with elevated CK levels, arrhythmias, gastrointestinal dysmotility, and skeletal abnormalities should prompt the suspicion for the diagnosis of CGL4, although phenotypic variability may occur

    Alpha-Synuclein Produces Early Behavioral Alterations via Striatal Cholinergic Synaptic Dysfunction by Interacting With GluN2D N-Methyl-D-Aspartate Receptor Subunit

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    Background Advanced Parkinson's disease (PD) is characterized by massive degeneration of nigral dopaminergic neurons, dramatic motor and cognitive alterations, and presence of nigral Lewy bodies, whose main constituent is \u3b1-synuclein (\u3b1-syn). However, the synaptic mechanisms underlying behavioral and motor effects induced by early selective overexpression of nigral \u3b1-syn are still a matter of debate. Methods We performed behavioral, molecular, and immunohistochemical analyses in two transgenic models of PD, mice transgenic for truncated human \u3b1-synuclein 1-120 and rats injected with the adeno-associated viral vector carrying wild-type human \u3b1-synuclein. We also investigated striatal synaptic plasticity by electrophysiological recordings from spiny projection neurons and cholinergic interneurons. Results We found that overexpression of truncated or wild-type human \u3b1-syn causes partial reduction of striatal dopamine levels and selectively blocks the induction of long-term potentiation in striatal cholinergic interneurons, producing early memory and motor alterations. These effects were dependent on \u3b1-syn modulation of the GluN2D-expressing N-methyl-D-aspartate receptors in cholinergic interneurons. Acute in vitro application of human \u3b1-syn oligomers mimicked the synaptic effects observed ex vivo in PD models. Conclusions We suggest that striatal cholinergic dysfunction, induced by a direct interaction between \u3b1-syn and GluN2D-expressing N-methyl-D-aspartate receptors, represents a precocious biological marker of the disease

    Efficacy of a multiple-component and multifactorial personalized fall prevention program in a mixed population of community-dwelling older adults with stroke, Parkinson's Disease, or frailty compared to usual care: The PRE.C.I.S.A. randomized controlled trial

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    Fall risk in the elderly is a major public health issue due to the injury-related consequences and the risk of associated long-term disability. However, delivering preventive interventions in usual clinical practice still represents a challenge
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