Abstract:
BACKGROUND:Depression is a heterogeneous mental illness. Neurostimulation treatments, by targeting specific nodes within the brain's emotion-regulation network, may be useful both as therapies and as probes for identifying clinically relevant depression subtypes. METHODS:Here, we applied 20 sessions of magnetic resonance imaging-guided repetitive transcranial magnetic stimulation (rTMS) to the dorsomedial prefrontal cortex in 47 unipolar or bipolar patients with a medication-resistant major depressive episode. RESULTS:Treatment response was strongly bimodal, with individual patients showing either minimal or marked improvement. Compared with responders, nonresponders showed markedly higher baseline anhedonia symptomatology (including pessimism, loss of pleasure, and loss of interest in previously enjoyed activities) on item-by-item examination of Beck Depression Inventory-II and Quick Inventory of Depressive Symptomatology ratings. Congruently, on baseline functional magnetic resonance imaging, nonresponders showed significantly lower connectivity through a classical reward pathway comprising ventral tegmental area, striatum, and a region in ventromedial prefrontal cortex. Responders and nonresponders also showed opposite patterns of hemispheric lateralization in the connectivity of dorsomedial and dorsolateral regions to this same ventromedial region. CONCLUSIONS:The results suggest distinct depression subtypes, one with preserved hedonic function and responsive to dorsomedial rTMS and another with disrupted hedonic function, abnormally lateralized connectivity through ventromedial prefrontal cortex, and unresponsive to dorsomedial rTMS. Future research directly comparing the effects of rTMS at different targets, guided by neuroimaging and clinical presentation, may clarify whether hedonia/reward circuit integrity is a reliable marker for optimizing rTMS target selection.
journal_name
Biol Psychiatryjournal_title
Biological psychiatryauthors
Downar J,Geraci J,Salomons TV,Dunlop K,Wheeler S,McAndrews MP,Bakker N,Blumberger DM,Daskalakis ZJ,Kennedy SH,Flint AJ,Giacobbe Pdoi
10.1016/j.biopsych.2013.10.026subject
Has Abstractpub_date
2014-08-01 00:00:00pages
176-85issue
3eissn
0006-3223issn
1873-2402pii
S0006-3223(13)01034-2journal_volume
76pub_type
杂志文章abstract:BACKGROUND:Mutations of MAGEL2 have been reported in patients presenting with autism, and loss of MAGEL2 is also associated with Prader-Willi syndrome, a neurodevelopmental genetic disorder. This study aimed to determine the behavioral phenotype of Magel2-deficient adult mice, to characterize the central oxytocin (OT) ...
journal_title:Biological psychiatry
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journal_title:Biological psychiatry
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journal_title:Biological psychiatry
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更新日期:2013-09-01 00:00:00
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pub_type: 杂志文章
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更新日期:2007-10-15 00:00:00
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更新日期:2009-08-01 00:00:00
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journal_title:Biological psychiatry
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更新日期:1998-07-15 00:00:00
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journal_title:Biological psychiatry
pub_type: 杂志文章
doi:10.1016/j.biopsych.2004.06.001
更新日期:2004-08-15 00:00:00
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journal_title:Biological psychiatry
pub_type: 杂志文章
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更新日期:2016-03-15 00:00:00
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pub_type: 杂志文章
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journal_title:Biological psychiatry
pub_type: 临床试验,杂志文章,随机对照试验
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更新日期:1997-07-15 00:00:00
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doi:10.1016/j.biopsych.2007.05.007
更新日期:2008-03-01 00:00:00