In daily clinical practice we use to make diagnoses in first consultations, but sometimes it is more complicated, requiring a cross-sectional study of the evolution of the case.In daily clinical practice we use to make diagnoses in first consultations, but sometimes it is more complicated, requiring a cross-sectional study of the evolution of the case.

44-year-old woman. Married and mother of one child. She has an hospitalization for alcohol dependence in the context of depressive syndrome. The patient attends the consultation regularly, presenting in the foreground alcohol consumption with evasive characteristics due to hypothymic mood. Many pharmacological approaches are tried with poor tolerance, as well as referral to an alcohol cessation unit. After that, it requires new income where partial disorientation is observed.

A CT scan is performed and is reported as normal.

In admissions, family-type interventions are performed to reduce accompanying family dysfunction. The evolution is torpid, with the appearance of dysfunctional hysteromorphic personality traits, with childish demands and refusal to go to prescribed consultations. Tendency to confabulation and demonstrative attitudes in the family context, which yield with hospitalization, presenting an absence of disruptive behaviors in the hospital context, but it does seem to present brain alterations due to alcoholism. It is sent home with appropriate indications.

Sometimes, a detailed investigation and follow-up of a case, in this case by way of admission, may result in a different diagnosis than the previous one, which entails a different management.

No significant relationships.

The personality disorders (PDs) in the ‘dramatic’ cluster B [antisocial (ASPD), histrionic (HPD), narcissistic (NPD) and borderline (BPD)] demonstrate co-morbidity. However, the degree to which genetic and/or environmental factors influence their co-occurrence is not known and, with the exception of ASPD, the relative impact of genetic and environmental risk factors on liability to the cluster B PDs has not been conclusively established.

PD traits were assessed in 1386 Norwegian twin pairs between the age of 19 and 35 years using the Structured Interview for DSM-IV Personality Disorders (SIDP-IV). Using the statistical package Mx, multivariate twin models were fitted to dimensional representations of the PDs.

The best-fitting model, which did not include sex or shared family environment effects, included common genetic and environmental factors influencing all four dramatic PD traits, and factors influencing only ASPD and BPD. Heritability was estimated at 38% for ASPD traits, 31% for HPD traits, 24% for NPD traits and 35% for BPD traits. BPD traits had the lowest and ASPD traits the highest disorder-specific genetic variance.

The frequently observed co-morbidity between cluster B PDs results from both common genetic and environmental influences. Etiologically, cluster B has a ‘substructure’ in which ASPD and BPD are more closely related to each other than to the other cluster B disorders.