TY - JOUR
T1 - Modulation of Intrinsic Brain Activity by Electroconvulsive Therapy in Major Depression
AU - Leaver, Amber M.
AU - Espinoza, Randall
AU - Pirnia, Tara
AU - Joshi, Shantanu H.
AU - Woods, Roger P.
AU - Narr, Katherine L.
N1 - Funding Information:
This work was supported by the National Institutes of Health , including Grant No. R01 MH092301 (KLN and RE) and Grant No. K24 MH102743 (KLN).
Publisher Copyright:
© 2016 Society of Biological Psychiatry.
PY - 2016/1/1
Y1 - 2016/1/1
N2 - Background One of the most effective interventions for intractable major depressive episodes is electroconvulsive therapy (ECT). Because ECT is also relatively fast acting, longitudinal study of its neurobiological effects offers critical insight into the mechanisms underlying depression and antidepressant response. Here, we assessed modulation of intrinsic brain activity in corticolimbic networks associated with ECT and clinical response. Methods We measured resting-state functional connectivity (RSFC) in patients with treatment-resistant depression (n = 30) using functional magnetic resonance imaging acquired before and after completing a treatment series with right unilateral ECT. Using independent component analysis, we assessed changes in RSFC with 1) symptom improvement and 2) ECT, regardless of treatment outcome in patients, with reference to healthy control subjects (n = 32, also scanned twice). Results After ECT, consistent changes in RSFC within targeted depression-relevant functional networks were observed in the dorsal anterior cingulate cortex (ACC), mediodorsal thalamus (mdTh), hippocampus, and right anterior temporal, medial parietal, and posterior cingulate cortices in all patients. In a separate analysis, changes in depressive symptoms were associated with RSFC changes in the dorsal ACC, mdTh, putamen, medial prefrontal cortex, and lateral parietal cortex. RSFC of these regions did not change in healthy control subjects. Conclusions Neuroplasticity underlying clinical change was in part separable from changes associated with the effects of ECT observed in all patients. However, both ECT and clinical change were associated with RSFC modulation in dorsal ACC, mdTh, and hippocampus, which may indicate that these regions underlie the mechanisms of clinical outcome in ECT and may be effective targets for future neurostimulation therapies.
AB - Background One of the most effective interventions for intractable major depressive episodes is electroconvulsive therapy (ECT). Because ECT is also relatively fast acting, longitudinal study of its neurobiological effects offers critical insight into the mechanisms underlying depression and antidepressant response. Here, we assessed modulation of intrinsic brain activity in corticolimbic networks associated with ECT and clinical response. Methods We measured resting-state functional connectivity (RSFC) in patients with treatment-resistant depression (n = 30) using functional magnetic resonance imaging acquired before and after completing a treatment series with right unilateral ECT. Using independent component analysis, we assessed changes in RSFC with 1) symptom improvement and 2) ECT, regardless of treatment outcome in patients, with reference to healthy control subjects (n = 32, also scanned twice). Results After ECT, consistent changes in RSFC within targeted depression-relevant functional networks were observed in the dorsal anterior cingulate cortex (ACC), mediodorsal thalamus (mdTh), hippocampus, and right anterior temporal, medial parietal, and posterior cingulate cortices in all patients. In a separate analysis, changes in depressive symptoms were associated with RSFC changes in the dorsal ACC, mdTh, putamen, medial prefrontal cortex, and lateral parietal cortex. RSFC of these regions did not change in healthy control subjects. Conclusions Neuroplasticity underlying clinical change was in part separable from changes associated with the effects of ECT observed in all patients. However, both ECT and clinical change were associated with RSFC modulation in dorsal ACC, mdTh, and hippocampus, which may indicate that these regions underlie the mechanisms of clinical outcome in ECT and may be effective targets for future neurostimulation therapies.
KW - Anterior cingulate
KW - Connectivity
KW - Depression
KW - ECT
KW - Thalamus
KW - fMRI
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U2 - 10.1016/j.bpsc.2015.09.001
DO - 10.1016/j.bpsc.2015.09.001
M3 - Article
C2 - 26878070
AN - SCOPUS:84957818556
VL - 1
SP - 77
EP - 86
JO - Biological Psychiatry: Cognitive Neuroscience and Neuroimaging
JF - Biological Psychiatry: Cognitive Neuroscience and Neuroimaging
SN - 2451-9022
IS - 1
ER -