Brain Functional Correlates of Recall of Life Events in Medication-Naïve Adolescents with Borderline Personality Disorder
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Published:2024
Issue:1
Volume:83
Page:49-60
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ISSN:0302-282X
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Container-title:Neuropsychobiology
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language:en
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Short-container-title:Neuropsychobiology
Author:
Salgado-Pineda Pilar,Ferrer Marc,Calvo Natàlia,Costa Xavier,Pozuelo-López María Ángeles,Ramos-Quiroga Josep Antoni,Tarragona Brenda,Fuentes-Claramonte Paola,Salvador Raymond,Pomarol-Clotet Edith
Abstract
<b><i>Introduction:</i></b> Recall of autobiographical events has been found to be impaired in borderline personality disorder (BPD), but few studies have examined if this impairment has brain functional correlates. This study evaluated brain functional alterations during autobiographical recall using medication-naive adolescent patients to avoid potential confounding effects of treatment. <b><i>Methods:</i></b> Thirty-two adolescent female patients with BPD who were never-medicated and without psychiatric comorbidity and 33 matched healthy females underwent fMRI while they viewed individualized cue words that evoked autobiographical memories. Control conditions included viewing non-memory-evoking cues and a low-level baseline (cross-fixation). <b><i>Results:</i></b> During autobiographical recall, in comparison to the low-level baseline, the BPD patients showed increased brain activity in regions including the posterior hippocampus, the lingual and calcarine cortex, and the precuneus compared to the healthy controls. The BPD patients also showed a failure to deactivate the right dorsolateral prefrontal cortex during autobiographical recall. No patient-control differences were found when memory-evoking words were compared to non-memory-evoking words. <b><i>Discussion/Conclusions:</i></b> This study finds evidence of hippocampal/lingual/calcarine/precuneus hyperactivation to stimuli that evoke autobiographical memories in patients with BPD. As the changes were seen in never-treated patients without other comorbidities, they could be considered intrinsic to the disorder. Our study also adds to existing evidence for failure of deactivation in BPD, this time outside the default mode network.