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Patterns of altered regional brain glucose metabolism in borderline personality disorder and bipolar II disorder
Author(s) -
Bøen E.,
Hjørnevik T.,
Hummelen B.,
Elvsåshagen T.,
Moberget T.,
Holtedahl J. E.,
Babovic A.,
Hol P. K.,
Karterud S.,
Malt U. F.
Publication year - 2019
Publication title -
acta psychiatrica scandinavica
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 2.849
H-Index - 146
eISSN - 1600-0447
pISSN - 0001-690X
DOI - 10.1111/acps.12997
Subject(s) - borderline personality disorder , bipolar disorder , psychology , medicine , pathophysiology , white matter , mood disorders , eating disorders , endocrinology , mania , insula , psychiatry , mood , neuroscience , magnetic resonance imaging , anxiety , radiology
Objective The relationship between borderline personality disorder ( BPD ) and bipolar II disorder ( BIP ‐ II ) is disputed but understudied. Here, we investigated brain glucose metabolism in these patient groups and healthy control subjects ( HC s). Methods Sixty‐five subjects, 22 BPD (19 females), 22 BIP ‐ II (17 females), and 21 HC (14 females), were examined using 2‐deoxy‐2[18F]‐fluoro‐d‐glucose positron‐emission tomography ( PET ) scanning. Only patients without reciprocal comorbidity were recruited; BPD participants without bipolar spectrum pathology; BIP ‐ II participants without cluster A/B personality pathology. Groups were compared pairwise. Associations with mood state and childhood trauma were analyzed. Results Both patient groups exhibited hypometabolism compared with HC s in insula, brainstem, and frontal white matter. Additionally, BPD patients showed hypometabolism in hypothalamus, midbrain, and striatum; BIP ‐ II patients in cerebellum. Uncorrected analyses showed cortical areas of higher metabolism in BIP ‐ II than BPD , and associations with clinical variables differed between the groups. Conclusion Reduced metabolism in the insula regions was shown in both disorders, suggesting shared pathophysiological mechanisms. The observed patterns of altered metabolism specific to each patient group, as well as the uncorrected results, may also suggest differential pathophysiology. However, these latter findings must be interpreted cautiously given the non‐significant corrected results in the direct comparison between the disorders.