Citation

New AS, Goodman M, Triebwasser J, Siever LJ. Psychiatr. Clin. North Am. 2008; 31(3): 441-61, vii.

Affiliation

The Mount Sinai School of Medicine, One Gustave L. Levy Place, Box 1217, New York, NY 10029, USA. antonia.new@mssm.edu

Copyright

(Copyright © 2008, Elsevier Publishing)

DOI

10.1016/j.psc.2008.03.011

PMID

18638645

Abstract

While it is premature to provide a simple model for the vulnerability to the development of either borderline (BPD) or schizotypal (SPD) personality disorder, it is clear that these heritable disorders lend themselves to fruitful neurobiological exploration. The most promising findings in BPD suggest that a diminished top-down control of affective responses, which is likely to relate to deceased responsiveness of specific midline regions of prefrontal cortex, may underlie the affective hyperresponsiveness in this disorder. In addition, genetic and neuroendocrine and molecular neuroimaging findings point to a role for serotonin in this affective disinhibition. Clearly SPD falls within the schizophrenia spectrum, but precisely the nature of what predicts full-blown schizophrenia as opposed to the milder symptoms of SPD is not yet clear.

Language: en