Biological Markers in Borderline Personality Disorders: An Overview

1988 ◽  
Vol 33 (5) ◽  
pp. 350-354 ◽  
Author(s):  
Meir Steiner ◽  
Paul S. Links ◽  
Marilyn Korzekwa

The state of knowledge in the area of suggested biological markers that may delineate subpopulations of patients with borderline personality disorders (BPD) is reviewed. There is widespread disagreement as to the specificity of these markers. The clinical implications of Axis I — Axis II, state vs. trait, acute vs. chronic, and definite vs. probable diagnoses, all seem to contribute to the confusion in this area. Some patients with BPD and with schizotypal personality disorders (SPD) share neuroendocrine abnormalities with affective disorders (AD) and schizophrenic (SCH)patients respectively. This interface and/or potential overlap between personality disorders (PD) and the major mental disorders is discussed with special reference to the DST, TRH/TSH test, and REM latency which have already been established as valuable biological markers for certain subtypes of depression. In contrast, biologic abnormalities observed in chronic schizophrenia are also present in some SPD patients. Current data are supportive of the hypothesis that some PD patients are independent whereas others are genetically related to the major mental disorders.

2015 ◽  
Vol 206 (5) ◽  
pp. 355-356 ◽  
Author(s):  
Giles Newton-Howes ◽  
Roger Mulder ◽  
Peter Tyrer

SummaryBoth major classifications in psychiatry have now moved away from the multi-axial nosological model. This is clinically understandable as the specific categorical diagnoses, other than borderline personality disorder and personality disorder ‘NOS' (not otherwise specified) were so seldom used and empirical evidence would not support the polythetic categorical system. As a consequence, those with personality disorders, frequently referred to as Axis II disorders, now have to compete with all other mental disorders for clinical attention.


2018 ◽  
Vol 35 (4) ◽  
pp. 382-393
Author(s):  
Merete S. Johansen ◽  
Sigmund W. Karterud ◽  
Eivind Normann-Eide ◽  
Frida G. Rø ◽  
Elfrida H. Kvarstein ◽  
...  

1988 ◽  
Vol 21 (1) ◽  
pp. 44-50 ◽  
Author(s):  
Lee S. Mann ◽  
Thomas N. Wise ◽  
Errol A. Segall ◽  
Richard L. Goldberg ◽  
David M. Goldstein

2003 ◽  
Vol 18 (7) ◽  
pp. 350-355 ◽  
Author(s):  
Åsa Westrin ◽  
Karin Frii ◽  
Lil Träskman-Bendz

AbstractPrevious research on hypothalamic-pituitary adrenal (HPA) axis-activity in suicide attempter research has shown conflicting outcomes. The design of the present study was to test the influence of personality disorders and concominant axis I diagnoses on the dexamethasone suppression diagnostic test by use of multiple regression analyses. The sample consisted of 184 patients with a recent suicide attempt and 42 healthy controls. As expected, the lowest pre- and postdexamethasone cortisol levels were found in patients with personality disorders axis II, cluster B as compared to the other patients. The results remained significant when analysed for covariance with DSM-III-R axis I diagnoses, age or sex. Whether these low cortisol levels are due to previous experience of extreme stressful events or long-lasting burden, or whether they may be a consequence of biogenetic or psychological predisposal of interest, remains to be elucidated. Axis I comorbidity needs to be further examined.


2010 ◽  
Vol 12 (1) ◽  
pp. 103-114 ◽  

Genetic epidemiologic studies indicate that all ten personality disorders (PDs) classified on the DSM-IV axis II are modestly to moderately heritable. Shared environmental and nonadditive genetic factors are of minor or no importance. No sex differences have been identified, Multivariate studies suggest that the extensive comorbidity between the PDs can be explained by three common genetic and environmental risk factors. The genetic factors do not reflect the DSM-IV cluster structure, but rather: i) broad vulnerability to PD pathology or negative emotionality; ii) high impulsivity/low agreeableness; and iii) introversion. Common genetic and environmental liability factors contribute to comorbidity between pairs or clusters of axis I and axis II disorders. Molecular genetic studies of PDs, mostly candidate gene association studies, indicate that genes linked to neurotransmitter pathways, especially in the serotonergic and dopaminergic systems, are involved. Future studies, using newer methods like genome-wide association, might take advantage of the use of endophenotypes.


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