Narcissistic Personality Disorder: Are Psychodynamic Theories and the Alternative DSM-5 Model for Personality Disorders Finally Going to Meet?

Narcissistic Personality Disorder is the new borderline personality disorder of our current era. There have been recent developments on narcissism that are certainly worthwhile examining. Firstly, relational and intersubjective psychoanalysts have been rethinking the underlying concepts of narcissism, focusing on the development of self and relations to others. Secondly, in the DSM-5, the Alternative DSM-5 Model for Personality Disorders (AMPD) was presented for a dimensional evaluation of the severity of personality disorder pathology. The combined dimensional and trait conceptualization of NPD opened the door to new integrated diagnostic perspectives, including both internal and interpersonal functioning. Finally, Pincus and Lukowitsky encourage clinicians to use a hierarchical model of pathological narcissism, as it opens up opportunities for shared points of interest in empirical research from different scholarly perspectives. As for most non-psychodynamic clinicians and researchers the DSM-5 clearly bears dominant weight in their work, we will take the AMPD model for NPD as our point of reference. We will discuss the narcissist's unique pattern of self-impairments in identity and self-direction, and of interpersonal disfunctioning (evaluated by assessing empathy and intimacy). Subsequently, we will examine how contemporary psychodynamic theories and the hierarchical model of Pincus and Lukowitsky additionally inform or contradict the AMPD. For us, one of the big advantages of the AMPD is the use of structured clinical evaluations of disturbances of the self and interpersonal functioning and the dimensional evaluation of severity. As psychodynamically oriented therapists, we are enthusiastic about the opportunities for inclusion of psychodynamic concepts, but we also discuss a number of sticking points

Between session reliability of heel-to-toe progression measurements in the stance phase of gait

© 2018 Ade et al. This is an open access article distributed under the terms of the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original author and source are credited. The objective of the current study was to determine the test-retest reliability of heel-to-toe progression measures in the stance phase of gait using intraclass correlation coefficient (ICC) analysis. It has been proposed that heel-to-toe progression could be used as a functional measure of ankle muscle contracture/weakness in clinical populations. This was the first study to investigate the test-retest reliability of this measure. Eighteen healthy subjects walked over the GAITRite® mat three times at a comfortable speed on two sessions (≥ 48 hours apart). The reliability of the heel-to-toe progression measures; heel-contact time, mid-stance time and propulsive time were assessed. Also assessed were basic temporal-spatial parameters; velocity, cadence, stride length, step length, stride width, single and double leg support time. Reliability was determined using the ICC(3,1) model and, fixed and proportional biases, and measures of variability were assessed. Basic gait temporal-spatial parameters were not different between sessions (p > 0.05) and had excellent reliability (ICC(3,1) range: 0.871–0.953) indicating that subjects walked similarly between sessions. Measurement of heel-to-toe progression variables were not different between sessions (p > 0.05) and had excellent reliability (ICC(3,1) range: 0.845–0.926). However, these were less precise and more variable than the measurement of standard temporal-spatial gait variables. As the current study was performed on healthy populations, it represents the ‘best case’ scenario. The increased variability and reduced precision of heel-to-toe progression measurements should be considered if being used in clinical populations

Deletion of RAGE fails to prevent hepatosteatosis in obese mice due to impairment of other AGEs receptors and detoxifying systems

Abstract Advanced glycation endproducts (AGEs) are involved in several diseases, including NAFLD and NASH. RAGE is the main receptor mediating the pro-inflammatory signalling induced by AGEs. Therefore, targeting of RAGE has been proposed for prevention of chronic inflammatory diseases. However, the role of RAGE in the development of NAFLD and NASH remains poorly understood. We thus aimed to analyse the effect of obesity on AGEs accumulation, AGE-receptors and AGE-detoxification, and whether the absence of RAGE might improve hepatosteatosis and inflammation, by comparing the liver of lean control, obese (LeptrDb−/−) and obese RAGE-deficient (RAGE−/− LeptrDb−/−) mice. Obesity induced AGEs accumulation and RAGE expression with hepatosteatosis and inflammation in LeptrDb−/−, compared to lean controls. Despite the genetic deletion of RAGE in the LeptrDb−/− mice, high levels of intrahepatic AGEs were maintained accompanied by decreased expression of the protective AGE-receptor-1, impaired AGE-detoxifying system glyoxalase-1, and increased expression of the alternative AGE-receptor galectin-3. We also found sustained hepatosteatosis and inflammation as determined by persistent activation of the lipogenic SREBP1c and proinflammatory NLRP3 signalling pathways. Thus, RAGE targeting is not effective in the prevention of NAFLD in conditions of obesity, likely due to the direct liver specific crosstalk of RAGE with other AGE-receptors and AGE-detoxifying systems

Deletion of RAGE fails to prevent hepatosteatosis in obese mice due to impairment of other AGEs receptors and detoxifying systems

Advanced glycation endproducts (AGEs) are involved in several diseases, including NAFLD and NASH. RAGE is the main receptor mediating the pro-inflammatory signalling induced by AGEs. Therefore, targeting of RAGE has been proposed for prevention of chronic inflammatory diseases. However, the role of RAGE in the development of NAFLD and NASH remains poorly understood. We thus aimed to analyse the effect of obesity on AGEs accumulation, AGE-receptors and AGE-detoxification, and whether the absence of RAGE might improve hepatosteatosis and inflammation, by comparing the liver of lean control, obese (LeptrDb−/−) and obese RAGE-deficient (RAGE−/− LeptrDb−/−) mice. Obesity induced AGEs accumulation and RAGE expression with hepatosteatosis and inflammation in LeptrDb−/−, compared to lean controls. Despite the genetic deletion of RAGE in the LeptrDb−/− mice, high levels of intrahepatic AGEs were maintained accompanied by decreased expression of the protective AGE-receptor-1, impaired AGE-detoxifying system glyoxalase-1, and increased expression of the alternative AGE-receptor galectin-3. We also found sustained hepatosteatosis and inflammation as determined by persistent activation of the lipogenic SREBP1c and proinflammatory NLRP3 signalling pathways. Thus, RAGE targeting is not effective in the prevention of NAFLD in conditions of obesity, likely due to the direct liver specific crosstalk of RAGE with other AGE-receptors and AGE-detoxifying systems