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The effect of trauma on expressive language impairment in borderline personality disorder
Author(s) -
Carter Phoebe E.,
Grenyer Brin F. S.
Publication year - 2012
Publication title -
personality and mental health
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.193
H-Index - 22
eISSN - 1932-863X
pISSN - 1932-8621
DOI - 10.1002/pmh.1177
Subject(s) - borderline personality disorder , psychology , amygdala , neuroimaging , emotive , clinical psychology , cognitive psychology , developmental psychology , neuroscience , philosophy , epistemology
Borderline personality disorder (BPD) is a disorder with known expressive language impairments that may be activated in treatment through interpersonal cues to the trauma memory system of these patients. However, there are few BPD studies investigating this phenomenon empirically. Our previous research is the first known investigation revealing expressive language deficits using clinically relevant trauma‐salient stimuli; the current study extends this to compare specific expressive language deficits on a neutral and emotive stimulus and relationships with trauma history. BPD and matched control ( N = 24) verbalizations were analysed by computerized measures of language impairment and pause profiles. BPD subjects evidenced greater overall language impairment and reduced syntactic complexity, but not semantic complexity compared with controls. No such differences were found between the two groups on the neutral condition. BPD subjects utilized significantly higher proportions of pauses for both the emotive and neutral condition. BPD subjects used significantly greater proportions of pauses when generating adjectives related to early relationship with mother, not father. Presence of physical abuse history and PTSD related to some expressive language deficits. These results support neuroimaging findings demonstrating reduced activation of the pre‐frontal cortex or anterior cingulate, alongside increased bilateral activation of the amygdala, during exposure to trauma‐salient stimuli. Copyright © 2012 John Wiley & Sons, Ltd.