Personality disorder pathophysiology: Difference between revisions
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==Genetics== | ==Genetics== | ||
[ | genetic and [[prenatal]] factors also constitute a major role. Cluster-A PDs can have polymorphisms associated with the gene coding for [[dopamine 2-receptor]] (DRD2), [[catechol-0-methyltransferase]] (COMT), [[Dysbindin]] (DTNBP1), and [[D-aminoacid oxidase]] (DAAO). These genes are also associated with the development of schizophrenia, implying that both [[schizophrenia]] and schizotypal PD are related to [[dopaminergic dysfunction]]. Cluster B PDs have been found linked to polymorphisms in genes encoding serotonin transporter (5-HTTLPR), catabolic enzyme monoamine oxidase (MAOA), and [[tryptophan hydroxylase enzyme]] related genes [[TPH1]] and [[TPH2]]. This demonstrates the relation of the development of [[borderline]] personality and [[antisocial]] disorder with dysfunction in the [[serotonin system]]. Cluster-C PDs are linked with polymorphisms of the [[dopamine 3-receptor]] (DRD3) gene and [[COMT]], particularly [[obsessive-compulsive disorder]]<ref name="pmid20373672">{{cite journal| author=Reichborn-Kjennerud T| title=The genetic epidemiology of personality disorders. | journal=Dialogues Clin Neurosci | year= 2010 | volume= 12 | issue= 1 | pages= 103-14 | pmid=20373672 | doi= | pmc=3181941 | url=https://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=20373672 }} </ref>. Perinatal injuries like trauma, infections like [[encephalitis]], and [[hemorrhage]] may also be contributing factors. | ||
==Associated Conditions== | ==Associated Conditions== | ||
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Editor-In-Chief: C. Michael Gibson, M.S., M.D. [1]; Associate Editor(s)-in-Chief: Ayesha Anwar, M.B.B.S[2]
Overview
The exact pathogenesis of [disease name] is not fully understood.
OR
It is thought that [disease name] is the result of / is mediated by / is produced by / is caused by either [hypothesis 1], [hypothesis 2], or [hypothesis 3].
OR
[Pathogen name] is usually transmitted via the [transmission route] route to the human host.
OR
Following transmission/ingestion, the [pathogen] uses the [entry site] to invade the [cell name] cell.
OR
[Disease or malignancy name] arises from [cell name]s, which are [cell type] cells that are normally involved in [function of cells].
OR
The progression to [disease name] usually involves the [molecular pathway].
OR
The pathophysiology of [disease/malignancy] depends on the histological subtype.
Pathophysiology
Physiology
The personality development is a dynamic process that starts early in life and continue to evolve and change when subjected to environmental factors and consequential events. It results in establishing an organised pattern of behaviours and attitudes which are unique to every individual.
The theories to explain personality development has been presented throughout time. Freud's Psychoanalytic Theory was the pioneer. As discussed in historical perspectives, it is based on ideas of the id, the ego and the superego. The interaction and conflict among these is responsible for the creating the personality in an individual. He also proposed five stages of psychosexual development. Following it, new-Freudians (followers of Feud) elaborated the concept of Feud to formulate many new theories. However, the major problem was lack of ways to test the theories on wide variety of patients due to differences in dealings by different individuals and due to vague predictions made by it regarding defence mechanisms. Thus, it fails to pass empiricism. The five-factor theory/model is a remarkable widely-accepted model of personality development. It suggests personality constitutes of five traits; Conscientiousness, Agreeableness, Neuroticism, Openness to Experience, and Extraversion. Each personality trait is a spectrum and an individual can fall anywhere on this scale. The other trait theories just utilised binary values instead of a continuum. Each trait is influenced by genetic and environmental factors. The biological theories explain this as well.
Pathogenesis
Throughout time, a multitude of theories has been developed to explain the origin of these disorders. However still, the pathophysiology of PDs remains enigmatic. The five-factor model of personality was developed in the 1980s and 1990s, which demonstrated that it comprises five distinct traits. These include extraversion, Neuroticism, openness to experience/intellect, Agreeableness, and conscientiousness. A meta-analysis conducted by Saulsman and Page in 2004 reveals the association of personality disorders with the five-trait model. It concludes that extraversion is positively associated with disorders characterizing assertiveness or gregariousness like Histrionic and Narcissist. Neuroticism is positively associated with disorders causing emotional distress like Paranoid, Schizotypal, Borderline, Dependent, and Avoidant. Agreeableness is negatively associated with disorders characterized by interpersonal difficulties like Paranoid, Schizotypal, Antisocial, Borderline, and Narcissist. Those disorders which are distinguished by orderliness are positively associated with conscientiousness, like Obsessive-compulsive disorder. Schizoid is negatively associated with extraversion. Hence, PDs are primarily the result of positive correlation with Neuroticism and negative association with Agreeableness. Extraversion is associated in both ways [1].
It is a well-known fact that personality develops during childhood and interpersonal experiences and social interactions play a significant role in the development of PDs. Parental maltreatment, stress, and traumatic life events influence the personality adversely. In addition, genetic and prenatal factors also constitute a major role. Cluster-A PDs can have polymorphisms associated with the gene coding for dopamine 2-receptor (DRD2), catechol-0-methyltransferase (COMT), Dysbindin (DTNBP1), and D-aminoacid oxidase (DAAO). These genes are also associated with the development of schizophrenia, implying that both schizophrenia and schizotypal PD are related to dopaminergic dysfunction. Cluster B PDs have been found linked to polymorphisms in genes encoding serotonin transporter (5-HTTLPR), catabolic enzyme monoamine oxidase (MAOA), and tryptophan hydroxylase enzyme related genes TPH1 and TPH2. This demonstrates the relation of the development of borderline personality and antisocial disorder with dysfunction in the serotonin system. Cluster-C PDs are linked with polymorphisms of the dopamine 3-receptor (DRD3) gene and COMT, particularly obsessive-compulsive disorder[2]. Perinatal injuries like trauma, infections like encephalitis, and hemorrhage may also be contributing factors. Genetic factors interact with environmental stresses to result in PDs. Various parental behavior like excessive attachment, parental insensitivity or emotional neglect, physical and sexual abuse, and substance use disorders causes an essential impact on PDs development. Social bullying, racial discrimination, frequent dislocations during childhood, and lack of peer support are other risk factors.
Genetics
genetic and prenatal factors also constitute a major role. Cluster-A PDs can have polymorphisms associated with the gene coding for dopamine 2-receptor (DRD2), catechol-0-methyltransferase (COMT), Dysbindin (DTNBP1), and D-aminoacid oxidase (DAAO). These genes are also associated with the development of schizophrenia, implying that both schizophrenia and schizotypal PD are related to dopaminergic dysfunction. Cluster B PDs have been found linked to polymorphisms in genes encoding serotonin transporter (5-HTTLPR), catabolic enzyme monoamine oxidase (MAOA), and tryptophan hydroxylase enzyme related genes TPH1 and TPH2. This demonstrates the relation of the development of borderline personality and antisocial disorder with dysfunction in the serotonin system. Cluster-C PDs are linked with polymorphisms of the dopamine 3-receptor (DRD3) gene and COMT, particularly obsessive-compulsive disorder[2]. Perinatal injuries like trauma, infections like encephalitis, and hemorrhage may also be contributing factors.
Associated Conditions
Conditions associated with [disease name] include:
- [Condition 1]
- [Condition 2]
- [Condition 3]
Gross Pathology
On gross pathology, [feature1], [feature2], and [feature3] are characteristic findings of [disease name].
Microscopic Pathology
On microscopic histopathological analysis, [feature1], [feature2], and [feature3] are characteristic findings of [disease name].
References
- ↑ Saulsman LM, Page AC (2004). "The five-factor model and personality disorder empirical literature: A meta-analytic review". Clin Psychol Rev. 23 (8): 1055–85. doi:10.1016/j.cpr.2002.09.001. PMID 14729423.
- ↑ 2.0 2.1 Reichborn-Kjennerud T (2010). "The genetic epidemiology of personality disorders". Dialogues Clin Neurosci. 12 (1): 103–14. PMC 3181941. PMID 20373672.