fMRI brain activation changes following treatment of a first bipolar manic episode

Objectives We tested the hypothesis that, with treatment, functional magnetic resonance imaging (fMRI) regional brain activation in first‐episode mania would normalize – i.e., that differences from healthy subjects would diminish over time, and would be associated with clinical remission status, pot...

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Published inBipolar disorders Vol. 18; no. 6; pp. 490 - 501
Main Authors Strakowski, Stephen M, Fleck, David E, Welge, Jeffrey, Eliassen, James C, Norris, Matthew, Durling, Michelle, Komoroski, Richard A, Chu, Wen-Jang, Weber, Wade, Dudley, Jonathan A, Blom, Thomas J, Stover, Amanda, Klein, Christina, Strawn, Jeffrey R, DelBello, Melissa P, Lee, Jing-Huei, Adler, Caleb M
Format Journal Article
LanguageEnglish
Published Denmark Blackwell Publishing Ltd 01.09.2016
Subjects
Online AccessGet full text
ISSN1398-5647
1399-5618
1399-5618
DOI10.1111/bdi.12426

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Abstract Objectives We tested the hypothesis that, with treatment, functional magnetic resonance imaging (fMRI) regional brain activation in first‐episode mania would normalize – i.e., that differences from healthy subjects would diminish over time, and would be associated with clinical remission status, potentially identifying neuroanatomic treatment response markers. Methods Forty‐two participants with bipolar I disorder were recruited during their first manic episode, pseudo‐randomized to open‐label lithium or quetiapine, and followed for 8 weeks. fMRI scans were obtained at baseline and then after 1 and 8 weeks of treatment, while participants performed a continuous performance task with emotional distracters. Healthy participants received fMRI scans at these same intervals. Specific region‐of‐interest (ROI) activations within prefrontal emotional networks were assessed as potential measures of treatment response. Results ROI data were reduced using exploratory factor analysis, which identified five factors that were organizationally consistent with functional anatomic models of human emotion modulation. Half of the participants with bipolar disorder achieved remission by Week 8 and were contrasted with the other half that did not. Analyses demonstrated that, in the bipolar disorder group in general, treatment led to decreases in activation across brain regions toward healthy subject values. However, differences in activation changes were observed between subjects with bipolar disorder who did or did not achieve remission in subcortical and amygdala factors. Conclusions These findings provide evidence for potential neuroanatomic treatment response markers in first‐episode bipolar disorder.
AbstractList Objectives We tested the hypothesis that, with treatment, functional magnetic resonance imaging (fMRI) regional brain activation in first‐episode mania would normalize – i.e., that differences from healthy subjects would diminish over time, and would be associated with clinical remission status, potentially identifying neuroanatomic treatment response markers. Methods Forty‐two participants with bipolar I disorder were recruited during their first manic episode, pseudo‐randomized to open‐label lithium or quetiapine, and followed for 8 weeks. fMRI scans were obtained at baseline and then after 1 and 8 weeks of treatment, while participants performed a continuous performance task with emotional distracters. Healthy participants received fMRI scans at these same intervals. Specific region‐of‐interest (ROI) activations within prefrontal emotional networks were assessed as potential measures of treatment response. Results ROI data were reduced using exploratory factor analysis, which identified five factors that were organizationally consistent with functional anatomic models of human emotion modulation. Half of the participants with bipolar disorder achieved remission by Week 8 and were contrasted with the other half that did not. Analyses demonstrated that, in the bipolar disorder group in general, treatment led to decreases in activation across brain regions toward healthy subject values. However, differences in activation changes were observed between subjects with bipolar disorder who did or did not achieve remission in subcortical and amygdala factors. Conclusions These findings provide evidence for potential neuroanatomic treatment response markers in first‐episode bipolar disorder.
We tested the hypothesis that, with treatment, functional magnetic resonance imaging (fMRI) regional brain activation in first-episode mania would normalize - i.e., that differences from healthy subjects would diminish over time, and would be associated with clinical remission status, potentially identifying neuroanatomic treatment response markers. Forty-two participants with bipolar I disorder were recruited during their first manic episode, pseudo-randomized to open-label lithium or quetiapine, and followed for 8 weeks. fMRI scans were obtained at baseline and then after 1 and 8 weeks of treatment, while participants performed a continuous performance task with emotional distracters. Healthy participants received fMRI scans at these same intervals. Specific region-of-interest (ROI) activations within prefrontal emotional networks were assessed as potential measures of treatment response. ROI data were reduced using exploratory factor analysis, which identified five factors that were organizationally consistent with functional anatomic models of human emotion modulation. Half of the participants with bipolar disorder achieved remission by Week 8 and were contrasted with the other half that did not. Analyses demonstrated that, in the bipolar disorder group in general, treatment led to decreases in activation across brain regions toward healthy subject values. However, differences in activation changes were observed between subjects with bipolar disorder who did or did not achieve remission in subcortical and amygdala factors. These findings provide evidence for potential neuroanatomic treatment response markers in first-episode bipolar disorder.
We tested the hypothesis that, with treatment, functional magnetic resonance imaging (fMRI) regional brain activation in first-episode mania would normalize - i.e., that differences from healthy subjects would diminish over time, and would be associated with clinical remission status, potentially identifying neuroanatomic treatment response markers.OBJECTIVESWe tested the hypothesis that, with treatment, functional magnetic resonance imaging (fMRI) regional brain activation in first-episode mania would normalize - i.e., that differences from healthy subjects would diminish over time, and would be associated with clinical remission status, potentially identifying neuroanatomic treatment response markers.Forty-two participants with bipolar I disorder were recruited during their first manic episode, pseudo-randomized to open-label lithium or quetiapine, and followed for 8 weeks. fMRI scans were obtained at baseline and then after 1 and 8 weeks of treatment, while participants performed a continuous performance task with emotional distracters. Healthy participants received fMRI scans at these same intervals. Specific region-of-interest (ROI) activations within prefrontal emotional networks were assessed as potential measures of treatment response.METHODSForty-two participants with bipolar I disorder were recruited during their first manic episode, pseudo-randomized to open-label lithium or quetiapine, and followed for 8 weeks. fMRI scans were obtained at baseline and then after 1 and 8 weeks of treatment, while participants performed a continuous performance task with emotional distracters. Healthy participants received fMRI scans at these same intervals. Specific region-of-interest (ROI) activations within prefrontal emotional networks were assessed as potential measures of treatment response.ROI data were reduced using exploratory factor analysis, which identified five factors that were organizationally consistent with functional anatomic models of human emotion modulation. Half of the participants with bipolar disorder achieved remission by Week 8 and were contrasted with the other half that did not. Analyses demonstrated that, in the bipolar disorder group in general, treatment led to decreases in activation across brain regions toward healthy subject values. However, differences in activation changes were observed between subjects with bipolar disorder who did or did not achieve remission in subcortical and amygdala factors.RESULTSROI data were reduced using exploratory factor analysis, which identified five factors that were organizationally consistent with functional anatomic models of human emotion modulation. Half of the participants with bipolar disorder achieved remission by Week 8 and were contrasted with the other half that did not. Analyses demonstrated that, in the bipolar disorder group in general, treatment led to decreases in activation across brain regions toward healthy subject values. However, differences in activation changes were observed between subjects with bipolar disorder who did or did not achieve remission in subcortical and amygdala factors.These findings provide evidence for potential neuroanatomic treatment response markers in first-episode bipolar disorder.CONCLUSIONSThese findings provide evidence for potential neuroanatomic treatment response markers in first-episode bipolar disorder.
Objectives We tested the hypothesis that, with treatment, functional magnetic resonance imaging (fMRI) regional brain activation in first-episode mania would normalize - i.e., that differences from healthy subjects would diminish over time, and would be associated with clinical remission status, potentially identifying neuroanatomic treatment response markers. Methods Forty-two participants with bipolar I disorder were recruited during their first manic episode, pseudo-randomized to open-label lithium or quetiapine, and followed for 8 weeks. fMRI scans were obtained at baseline and then after 1 and 8 weeks of treatment, while participants performed a continuous performance task with emotional distracters. Healthy participants received fMRI scans at these same intervals. Specific region-of-interest (ROI) activations within prefrontal emotional networks were assessed as potential measures of treatment response. Results ROI data were reduced using exploratory factor analysis, which identified five factors that were organizationally consistent with functional anatomic models of human emotion modulation. Half of the participants with bipolar disorder achieved remission by Week 8 and were contrasted with the other half that did not. Analyses demonstrated that, in the bipolar disorder group in general, treatment led to decreases in activation across brain regions toward healthy subject values. However, differences in activation changes were observed between subjects with bipolar disorder who did or did not achieve remission in subcortical and amygdala factors. Conclusions These findings provide evidence for potential neuroanatomic treatment response markers in first-episode bipolar disorder.
Author Stover, Amanda
Blom, Thomas J
Strawn, Jeffrey R
Dudley, Jonathan A
DelBello, Melissa P
Weber, Wade
Welge, Jeffrey
Norris, Matthew
Lee, Jing-Huei
Komoroski, Richard A
Fleck, David E
Eliassen, James C
Strakowski, Stephen M
Chu, Wen-Jang
Durling, Michelle
Klein, Christina
Adler, Caleb M
AuthorAffiliation b Department of Psychiatry, Dell Medical School, University of Texas at Austin, Austin, TX, USA
a Department of Psychiatry and Behavioral Neuroscience and Center for Imaging Research, University of Cincinnati College of Medicine, Cincinnati, OH
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  surname: Adler
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  organization: Department of Psychiatry and Behavioral Neuroscience and Center for Imaging Research, University of Cincinnati College of Medicine, OH, Cincinnati, USA
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Keywords fMRI
first-episode
treatment
amygdala
bipolar disorder
prefrontal
mania
Language English
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2016 John Wiley & Sons A/S. Published by John Wiley & Sons Ltd.
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Drs. Strakowski and Fleck equally contributed to this manuscript.
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PublicationDecade 2010
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PublicationPlace_xml – name: Denmark
PublicationTitle Bipolar disorders
PublicationTitleAlternate Bipolar Disord
PublicationYear 2016
Publisher Blackwell Publishing Ltd
Publisher_xml – name: Blackwell Publishing Ltd
References Lee JH, Garwood M, Menon R et al. High contrast and fast three-dimensional magnetic resonance imaging at high fields. Magn Reson Med. 1995;34:308-312.
DelBello MP, Hanseman D, Adler CM, Fleck DE, Strakowski SM. Twelve-month outcome of adolescents with bipolar disorder following first hospitalization for a manic or mixed episode. Am J Psychiatry. 2007;164:582-590.
Elliott R, Ogilvie A, Rubinsztein JS, Calderon G, Dolan RJ, Sahakian BM. Abnormal ventral frontal response during performance of an affective go/no go task in patients with mania. Biol Psychiatry. 2004;55:1163-1170.
Strakowski SM, Adler CM, Cerullo M et al. Magnetic resonance imaging brain activation in first-episode bipolar mania during a response inhibition task. Early Interv Psychiatry. 2008;2:225-233.
Hulvershorn LA, Karne H, Gunn AD et al. Neural activation during facial emotion processing in unmedicated bipolar depression, euthymia, and mania. Biol Psychiatry. 2012;71:603-610.
Diler RS, Segreti AM, Ladouceur CD et al. Neural correlates of treatment in adolescents with bipolar depression during response inhibition. J Child Adolesc Psychopharmacol. 2013;23:214-221.
Chang KD, Wagner C, Garrett A, Howe M, Reiss A. A preliminary functional magnetic resonance imaging study of prefrontal-amygdalar activation changes in adolescents with bipolar depression treated with lamotrigine. Bipolar Disord. 2008;10:426-431.
Passarotti AM, Sweeney JA, Pauluri MN. Fronto-limbic dysfunction in mania pre-treatment and persistent amygdala over-activity post-treatment in pediatric bipolar disorder. Psychopharmacology. 2011;216:485-499.
Strakowski SM, Eliassen JC, Lamy M et al. Functional magnetic resonance imaging brain activation in bipolar mania: evidence for disruption of the ventrolateral prefrontal-amygdala emotional pathway. Biol Psychiatry. 2011;69:381-388.
Chen YC, Thaler D, Nixon P, Stern CE, Passingham RE. The functions of the medial premotor cortex. II. The timing and selection of learned movements. Exp Brain Res. 1995;102:461-473.
Cox RW, Hyde JS. Software tools for analysis and visualization of fMRI data. NMR Biomed. 1997;10:171-178.
Kaufman J, Birmaher B, Brent D et al. Schedule for Affective Disorders and Schizophrenia for School-Age Children-Present and Lifetime Version (K-SADS-PL): initial reliability and validity data. J Am Acad Child Adolesc Psychiatry. 1997;36:980-988.
First MB, Spitzer RL, Gibbon M, Williams JBW. Structured Clinical Interview for DSM-IV Axis I Disorders - Patient Edition (SCID-I/P). New York: Biometrics Research Department, New York State Psychiatric Institute; 1995.
Welge JA, Strakowski SM, Eliassen JC et al. Factor analysis of regional brain activation in bipolar and healthy individuals reveals a consistent modular structure. Biol Psychiatry. 2014;75:240S.
Phan KL, Wager T, Taylor SF, Liberzon I. Functional neuroanatomy of emotion: a meta-analysis of emotional activation studies in PET and fMRI. NeuroImage. 2002;16:331-348.
Schneider MR, Adler CM, Whitsel R et al. The effects of ziprasidone on prefrontal and amygdala activation in manic youth with bipolar disorder. Isr J Psychiatry Relat Sci. 2012;49:112-120.
Page SJ, Harnish SM, Lamy M, Eliassen JC, Szaflarski JP. Affected arm use and cortical change in stroke patients exhibiting minimal hand movement. Neurorehabil Neural Repair. 2010;24:195-203.
Cerullo MA, Fleck DE, Eliassen JC et al. A longitudinal functional connectivity analysis of the amygdala in bipolar I disorder across mood states. Bipolar Disord. 2012;14:175-184.
Hafeman DM, Chang KD, Garrett AS, Sanders EM, Phillips ML. Effects of medication on neuroimaging findings in bipolar disorder: an updated review. Bipolar Disord. 2012;14:375-410.
Schmithorst VJ, Dardzinski BJ, Holland SK. Simultaneous correction of ghost and geometric distortion artifacts in EPI using a multiecho reference scan. IEEE Trans Med Imaging. 2001;20:535-539.
Maxwell E. Family Interview for Genetics Studies. Washington, DC: National Institutes of Mental Health; 1999.
Yamasaki H, LaBar KS, McCarthy G. Dissociable prefrontal brain systems for attention and emotion. Proc Natl Acad Sci USA. 2002;99:11447-11451.
Young RC, Biggs JT, Ziegler VE, Meyer DA. A rating scale for mania: reliability, validity and sensitivity. Br J Psychiatry. 1978;133:429-435.
Cox RW. AFNI: software for analysis and visualization of functional magnetic resonance neuroimages. Comput Biomed Res. 1996;29:162-173.
Strakowski SM, Adler CM, Almeida J et al. The functional neuroanatomy of bipolar disorder: a consensus model. Bipolar Disord. 2012;14:313-325.
Altshuler LL, Bookheimer SY, Townsend J et al. Blunted activation in orbitofrontal cortex during mania: a functional magnetic resonance imaging study. Biol Psychiatry. 2005;58:763-769.
Strakowski SM, Adler CM, Holland SK, Mills N, DelBello MP. A preliminary fMRI study of sustained attention in euthymic, unmedicated bipolar disorder. Neuropsychopharmacology. 2004;29:1734-1740.
Tohen M, Zarate CA Jr, Hennen J et al. The McLean-Harvard first-episode mania study: prediction of recovery and first recurrence. Am J Psychiatry. 2003;160:2099-2107.
Bienvenu OJ, Davydow DS, Kendler KS. Psychiatric "diseases" versus behavioral disorders and degree of genetic influence. Psychol Med. 2011;41:33-40.
Goodwin FK, Jamison KR. Chapter 4: Course and Outcome. Manic-Depressive Illness: Bipolar Disorder and Recurrent Depression, Second edition. New York: Oxford University Press; 2007.
Lane RD, Reiman EM, Axelrod B, Yun LS, Holmes A, Schwartz GE. Neural correlates of level of emotional awareness: evidence of an interaction between emotion and attention in the anterior cingulate cortex. J Cogn Neurosci. 1998;10:525-535.
Chang KD, Adleman NE, Dienes K, Simeonova DL, Menon V, Reiss A. Anomalous prefrontal-subcortical activation in familial pediatric bipolar disorder: a functional magnetic resonance imaging investigation. Arch Gen Psychiatry. 2004;61:781-792.
Davis AK, DelBello MD, Eliassen J et al. Neurofunctional effects of quetiapine in patients with bipolar mania. Bipolar Disord. 2015;17:444-449.
Hamilton M. A rating scale for depression. J Neurol Neurosurg Psychiatry. 1960;25:56-61.
Cox RW, Jesmanowicz A. Real-time 3D image registration for functional MRI. Magn Reson Med. 1999;42:1014-1018.
Schneider MR, Klein CC, Weber W et al. The effects of carbamazepine on prefrontal activation in manic youth with bipolar disorder. Psychiatry Res. 2014;223:268-270.
McClellan AT, Kushner H, Metzger D et al. The fifth edition of the Addiction Severity Index. J Subst Abuse Treat. 1992;9:199-213.
2002; 16
2015; 17
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2010; 24
1960; 25
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2011; 41
2003; 160
1995; 102
2012; 49
2011; 69
1998; 10
2014; 223
2014; 75
2005; 58
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– reference: Maxwell E. Family Interview for Genetics Studies. Washington, DC: National Institutes of Mental Health; 1999.
– reference: Schneider MR, Adler CM, Whitsel R et al. The effects of ziprasidone on prefrontal and amygdala activation in manic youth with bipolar disorder. Isr J Psychiatry Relat Sci. 2012;49:112-120.
– reference: Yamasaki H, LaBar KS, McCarthy G. Dissociable prefrontal brain systems for attention and emotion. Proc Natl Acad Sci USA. 2002;99:11447-11451.
– reference: Strakowski SM, Adler CM, Almeida J et al. The functional neuroanatomy of bipolar disorder: a consensus model. Bipolar Disord. 2012;14:313-325.
– reference: Schmithorst VJ, Dardzinski BJ, Holland SK. Simultaneous correction of ghost and geometric distortion artifacts in EPI using a multiecho reference scan. IEEE Trans Med Imaging. 2001;20:535-539.
– reference: Strakowski SM, Adler CM, Cerullo M et al. Magnetic resonance imaging brain activation in first-episode bipolar mania during a response inhibition task. Early Interv Psychiatry. 2008;2:225-233.
– reference: Strakowski SM, Eliassen JC, Lamy M et al. Functional magnetic resonance imaging brain activation in bipolar mania: evidence for disruption of the ventrolateral prefrontal-amygdala emotional pathway. Biol Psychiatry. 2011;69:381-388.
– reference: Cox RW. AFNI: software for analysis and visualization of functional magnetic resonance neuroimages. Comput Biomed Res. 1996;29:162-173.
– reference: McClellan AT, Kushner H, Metzger D et al. The fifth edition of the Addiction Severity Index. J Subst Abuse Treat. 1992;9:199-213.
– reference: Phan KL, Wager T, Taylor SF, Liberzon I. Functional neuroanatomy of emotion: a meta-analysis of emotional activation studies in PET and fMRI. NeuroImage. 2002;16:331-348.
– reference: Bienvenu OJ, Davydow DS, Kendler KS. Psychiatric "diseases" versus behavioral disorders and degree of genetic influence. Psychol Med. 2011;41:33-40.
– reference: Chen YC, Thaler D, Nixon P, Stern CE, Passingham RE. The functions of the medial premotor cortex. II. The timing and selection of learned movements. Exp Brain Res. 1995;102:461-473.
– reference: Cox RW, Jesmanowicz A. Real-time 3D image registration for functional MRI. Magn Reson Med. 1999;42:1014-1018.
– reference: Altshuler LL, Bookheimer SY, Townsend J et al. Blunted activation in orbitofrontal cortex during mania: a functional magnetic resonance imaging study. Biol Psychiatry. 2005;58:763-769.
– reference: Hamilton M. A rating scale for depression. J Neurol Neurosurg Psychiatry. 1960;25:56-61.
– reference: Strakowski SM, Adler CM, Holland SK, Mills N, DelBello MP. A preliminary fMRI study of sustained attention in euthymic, unmedicated bipolar disorder. Neuropsychopharmacology. 2004;29:1734-1740.
– reference: Lane RD, Reiman EM, Axelrod B, Yun LS, Holmes A, Schwartz GE. Neural correlates of level of emotional awareness: evidence of an interaction between emotion and attention in the anterior cingulate cortex. J Cogn Neurosci. 1998;10:525-535.
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– reference: Welge JA, Strakowski SM, Eliassen JC et al. Factor analysis of regional brain activation in bipolar and healthy individuals reveals a consistent modular structure. Biol Psychiatry. 2014;75:240S.
– reference: Lee JH, Garwood M, Menon R et al. High contrast and fast three-dimensional magnetic resonance imaging at high fields. Magn Reson Med. 1995;34:308-312.
– reference: Page SJ, Harnish SM, Lamy M, Eliassen JC, Szaflarski JP. Affected arm use and cortical change in stroke patients exhibiting minimal hand movement. Neurorehabil Neural Repair. 2010;24:195-203.
– reference: Tohen M, Zarate CA Jr, Hennen J et al. The McLean-Harvard first-episode mania study: prediction of recovery and first recurrence. Am J Psychiatry. 2003;160:2099-2107.
– reference: Hulvershorn LA, Karne H, Gunn AD et al. Neural activation during facial emotion processing in unmedicated bipolar depression, euthymia, and mania. Biol Psychiatry. 2012;71:603-610.
– reference: Schneider MR, Klein CC, Weber W et al. The effects of carbamazepine on prefrontal activation in manic youth with bipolar disorder. Psychiatry Res. 2014;223:268-270.
– reference: Diler RS, Segreti AM, Ladouceur CD et al. Neural correlates of treatment in adolescents with bipolar depression during response inhibition. J Child Adolesc Psychopharmacol. 2013;23:214-221.
– reference: DelBello MP, Hanseman D, Adler CM, Fleck DE, Strakowski SM. Twelve-month outcome of adolescents with bipolar disorder following first hospitalization for a manic or mixed episode. Am J Psychiatry. 2007;164:582-590.
– reference: Elliott R, Ogilvie A, Rubinsztein JS, Calderon G, Dolan RJ, Sahakian BM. Abnormal ventral frontal response during performance of an affective go/no go task in patients with mania. Biol Psychiatry. 2004;55:1163-1170.
– reference: Chang KD, Wagner C, Garrett A, Howe M, Reiss A. A preliminary functional magnetic resonance imaging study of prefrontal-amygdalar activation changes in adolescents with bipolar depression treated with lamotrigine. Bipolar Disord. 2008;10:426-431.
– reference: Davis AK, DelBello MD, Eliassen J et al. Neurofunctional effects of quetiapine in patients with bipolar mania. Bipolar Disord. 2015;17:444-449.
– reference: Hafeman DM, Chang KD, Garrett AS, Sanders EM, Phillips ML. Effects of medication on neuroimaging findings in bipolar disorder: an updated review. Bipolar Disord. 2012;14:375-410.
– reference: Young RC, Biggs JT, Ziegler VE, Meyer DA. A rating scale for mania: reliability, validity and sensitivity. Br J Psychiatry. 1978;133:429-435.
– reference: Passarotti AM, Sweeney JA, Pauluri MN. Fronto-limbic dysfunction in mania pre-treatment and persistent amygdala over-activity post-treatment in pediatric bipolar disorder. Psychopharmacology. 2011;216:485-499.
– reference: Goodwin FK, Jamison KR. Chapter 4: Course and Outcome. Manic-Depressive Illness: Bipolar Disorder and Recurrent Depression, Second edition. New York: Oxford University Press; 2007.
– reference: Cerullo MA, Fleck DE, Eliassen JC et al. A longitudinal functional connectivity analysis of the amygdala in bipolar I disorder across mood states. Bipolar Disord. 2012;14:175-184.
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Snippet Objectives We tested the hypothesis that, with treatment, functional magnetic resonance imaging (fMRI) regional brain activation in first‐episode mania would...
We tested the hypothesis that, with treatment, functional magnetic resonance imaging (fMRI) regional brain activation in first-episode mania would normalize -...
Objectives We tested the hypothesis that, with treatment, functional magnetic resonance imaging (fMRI) regional brain activation in first-episode mania would...
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StartPage 490
SubjectTerms Adult
amygdala
Amygdala - diagnostic imaging
Amygdala - physiopathology
Antimanic Agents - therapeutic use
bipolar disorder
Bipolar Disorder - diagnosis
Bipolar Disorder - psychology
Bipolar Disorder - therapy
Emotions - physiology
Episode of Care
Female
first-episode
fMRI
Humans
Lithium - therapeutic use
Magnetic Resonance Imaging - methods
Male
mania
prefrontal
Psychiatric Status Rating Scales
Quetiapine Fumarate - therapeutic use
Task Performance and Analysis
treatment
Treatment Outcome
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Title fMRI brain activation changes following treatment of a first bipolar manic episode
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