This paper presents an integrative model of personality and personality disorder which incorporates psychoanalytic concepts with modern neuroscience. In addition, a dynamic, personalized, and context - and time-sensitive diagnosis of personality disorder is introduced. The authors cogently argue that all clinical variants of personality disorder share the same common deficit: fragmented basic units of experience at the nonconscious core of the mind (aka "partial object relations"). The fragmentation propagates through mental faculties (thought, motivation, emotion), as they self-organize into subsystems of personality, e.g., one's sense of self, identity, character, moral values, rendering them polarized into extreme and thus adaptively suboptimal. The syndrome of personality disorder arises as a nonconscious compensatory maneuver of the fragmented mind to organize itself through a defensive but unrealistic self-image (e.g., narcissistic, schizoid, antisocial, etc.), giving rise to a host of unique symptoms. Symptomatic pharmacotherapy of personality disorder is best organized around four empirically derived domains of symptoms, shared by all variants to a variable degree: i) mood and anxiety dysregulation; ii) impulsivity, aggression, and behavior dyscontrol; iii) emotional disinterest and detachment; and iv) cognitive distortions and brief reactive psychoses. Pharmacotherapy targeting the above domains is nonspecific, as medications affect multiple domains simultaneously. Modest empirical evidence and considerable clinical benefits continue to support the use of medications in the overall symptomatic treatment of personality disorder.
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http://dx.doi.org/10.24869/psyd.2019.2 | DOI Listing |
Alcohol Clin Exp Res (Hoboken)
January 2025
Department of Psychiatry, University of California San Diego Medical School, San Diego, California, USA.
Background: Preliminary evaluations of 212 drinking offspring from the San Diego Prospective Study (SDPD) indicated that over 50% developed alcohol use disorder (AUD) by their mid-20s. The present analysis evaluated if those findings remained robust when the group increased to 454 individuals, a sample size that facilitated a search for potential contributors to the high AUD prevalence.
Methods: Semistructured interviews were used to evaluate lifetime AUD diagnoses in 224 daughters and 230 sons from the SDPS (N = 454) by mean age 26.
Compr Psychiatry
December 2024
Laboratory of Behavioral Medicine, Neuroscience Institute, Lithuanian University of Health Sciences, Kaunas-Palanga, Lithuania.
Background: Cardiovascular diseases such as coronary artery disease (CAD) have a high prevalence of psychiatric comorbidities, that may impact clinically relevant outcomes (e.g., cognitive impairment and executive dysfunction).
View Article and Find Full Text PDFAlzheimers Dement
December 2024
Koc University, Department Biology and Genetics, Istanbul, Turkey.
Background: Valosin Containing Protein (VCP) mutations are responsible some genetic etiologies of amyotrophic lateral sclerosis (ALS) and frontotemporal dementia (FTD).
Method: A 67-year-old, male patient, applied to the clinic due to behavioral changes and difficulty swallowing. According the patient history it was reported that his first complaint started 6 years ago (at the age of 61).
Alzheimers Dement
December 2024
University of Exeter, Exeter, United Kingdom.
Background: When assessed in the Mild Behavioral Impairment (MBI) framework, late-life onset psychotic like symptoms (MBI-psychosis) are associated with incident cognitive decline and dementia. One approach to examining the genetic basis of this association, is to use Polygenic Risk Scores (PRS) to determine whether genetic propensity for late-life onset psychosis is shared with other traits. We aimed to elucidate the shared genetic liability between Educational Attainment, Intelligence, Reasoning, Memory, Neuroticism, Alzheimer's Disease, Major Depression, Schizophrenia and Bipolar Disorder and Mild Behavioral Impairment (MBI)-Psychosis in later life.
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