Open AccessCortical activation abnormalities in bipolar and schizophrenia patients in a combined oddball–incongruence paradigm
Author(s) -
Lisa Rauer,
Sarah Trost,
Aleksandra Petrović,
Oliver Gruber
Publication year - 2020
Publication title -
european archives of psychiatry and clinical neuroscience
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.507
H-Index - 98
eISSN - 1433-8491
pISSN - 0940-1334
DOI - 10.1007/s00406-020-01168-1
Subject(s) - bipolar disorder , psychology , precentral gyrus , schizophrenia (object oriented programming) , neuroscience , superior frontal gyrus , prefrontal cortex , oddball paradigm , orbitofrontal cortex , middle frontal gyrus , frontal lobe , functional magnetic resonance imaging , cognition , audiology , psychiatry , medicine , magnetic resonance imaging , event related potential , radiology
Patients with bipolar disorder and schizophrenia often suffer from severe cognitive impairment even during times of remission. This study investigated the pathomechanisms underlying their deficits in cognitive control. A combined oddball-incongruence fMRI task was applied to examine similarities and differences of neural activation patterns between patients and healthy controls. Bipolar and schizophrenia patients demonstrated hyperactivations in the intraparietal cortex during the oddball condition. Furthermore, bipolar patients revealed diagnosis-specific hyperactivation in the left middle frontal gyrus, precentral gyrus, anteroventral prefrontal cortex and orbitofrontal cortex regions compared to schizophrenia patients and healthy individuals. In comparison to healthy controls the patients showed hypoactivations in the inferior frontal junction and ventral pathway during the cognitively more demanding incongruence. Taken together, bipolar patients seem to recruit frontal and parietal areas during the oddball condition to compensate for potential deficits in their attentional network. During more challenging tasks, i.e., the incongruence condition, their compensatory mechanisms seem to collapse leading to hypoactivations in the same frontal areas as well as the ventral pathway.