Preliminary evidence for increased frontosubcortical activation on a motor impulsivity task in mixed episode bipolar disorder.

Division of Bipolar Disorders Research, Department of Psychiatry, University of Cincinnati College of Medicine, Cincinnati, OH 45267–0583, USA.
Journal of Affective Disorders (Impact Factor: 3.76). 05/2011; 133(1-2):333-9. DOI: 10.1016/j.jad.2011.03.053
Source: PubMed

ABSTRACT Of all mood states, patients in mixed episodes of bipolar disorder are at the greatest risk for impulsive behaviors including attempted suicide. The aim of this study was to examine whether the neural correlates of motor impulsivity are distinct in patients with mixed mania.
Ten patients with bipolar disorder in a mixed episode (BP-M), 10 bipolar comparison participants in a depressed episode (BP-D), and 10 healthy comparison (HC) participants underwent functional MRI while performing a Go/No-Go task of motor impulsivity.
Both patient groups had elevated, self-rated motor impulsiveness scores. The BP-M group also had a trend-level increase in commission errors relative to the HC group on the Go/No-Go task. While the full sample strongly activated a ventrolateral prefrontal-subcortical brain network, the BP-M group activated the amygdala and frontal cortex more strongly than the HC group, and the thalamus, cerebellum, and frontal cortex more strongly than the BP-D group.
This study is primarily limited by a relatively small sample size.
Higher commission error rates on the Go/No-Go task suggest increased vulnerability to impulsive responding during mixed episodes of bipolar disorder. Moreover, the distinct pattern of increased brain activation during mixed mania may indicate a connection between behavioral impulsivity and a failure of neurophysiological "inhibition", especially in the amygdala.

  • [Show abstract] [Hide abstract]
    ABSTRACT: Despite the growing number of neuroimaging studies in bipolar disorder over the past years, the brain regions involved in mood dysregulation in this disease are still poorly understood. If some neurofunctional abnormalities seem to be independent of mood state, others were preferentially associated with mania or depression, involving the amygdala and other limbic regions as well as ventral frontal regions, with a likely hemispheric lateralization of these abnormalities according to the thymic state that was examined. Very few imaging studies became interested in bipolar patients in a mixed state, making it harder to connect brain malfunction to a given mood state. However, data obtained so far support the hypothesis of a lateralization of brain abnormalities in relation to bipolar symptomatology, suggesting that neurofonctional abnormalities preferentially located in the right ventral frontal and limbic areas may underlie the depressive component, associated with abnormalities of the left similar regions for the manic component. Identifi cation of brain dysfunctions that may explain the emergence of mixed symptoms will likely provide useful information to better understand the respective roles of each hemisphere in the pathophysiology of bipolar disorder.
    L Encéphale 12/2013; 39 Suppl 3:162-6. · 0.60 Impact Factor
  • [Show abstract] [Hide abstract]
    ABSTRACT: OBJECTIVE In this critical review, the authors appraise neuroimaging findings in bipolar disorder in emotion-processing, emotion-regulation, and reward-processing neural circuitry in order to synthesize the current knowledge of the neural underpinnings of bipolar disorder and provide a neuroimaging research road map for future studies. METHOD The authors examined findings from all major studies in bipolar disorder that used functional MRI, volumetric analysis, diffusion imaging, and resting-state techniques, integrating findings to provide a better understanding of larger-scale neural circuitry abnormalities in bipolar disorder. RESULTS Bipolar disorder can be conceptualized, in neural circuitry terms, as parallel dysfunction in prefrontal cortical (especially ventrolateral prefrontal cortical)-hippocampal-amygdala emotion-processing and emotion-regulation circuits bilaterally, together with an "overactive" left-sided ventral striatal-ventrolateral and orbitofrontal cortical reward-processing circuitry, resulting in characteristic behavioral abnormalities associated with bipolar disorder: emotional lability, emotional dysregulation, and heightened reward sensitivity. A potential structural basis for these functional abnormalities is gray matter volume decreases in the prefrontal and temporal cortices, the amygdala, and the hippocampus and fractional anisotropy decreases in white matter tracts connecting prefrontal and subcortical regions. CONCLUSIONS Neuroimaging studies of bipolar disorder clearly demonstrate abnormalities in neural circuits supporting emotion processing, emotion regulation, and reward processing, although there are several limitations to these studies. Future neuroimaging research in bipolar disorder should include studies adopting dimensional approaches; larger studies examining neurodevelopmental trajectories in youths with bipolar disorder or at risk for bipolar disorder; multimodal neuroimaging studies using integrated systems approaches; and studies using pattern recognition approaches to provide clinically useful individual-level data. Such studies will help identify clinically relevant biomarkers to guide diagnosis and treatment decision making for individuals with bipolar disorder.
    American Journal of Psychiatry 03/2014; 171(8). DOI:10.1176/appi.ajp.2014.13081008 · 14.72 Impact Factor
  • Source
    [Show abstract] [Hide abstract]
    ABSTRACT: AimsCompare regional brain activation among adolescents with bipolar disorder and co-occurring cannabis use disorder.DesignCross-sectional study.SettingCincinnati, OH, USA.ParticipantsAdolescents with bipolar disorder (BP, n=14), adolescents with cannabis use disorder (MJ, n=13), adolescents with co-occurring cannabis use and bipolar disorders (BPMJ, n=25), and healthy adolescents (HC, n=15).MeasurementsCannabis craving, substance use, BOLD signal assessed by the Marijuana Craving Questionnaire (MCQ), Teen-Addiction Severity Index (T-ASI), and a cannabis cue reactivity task during a fMRI session, respectively.FindingsThe BP group exhibited significantly greater brain activation than the BPMJ group in the right amygdala (F=4.14, p=0.046), left nucleus accumbens (F=3.8, p=0.02), left thalamus (F=3.8, p<0.05) and the right thalamus (F=6.2, p=0.02). The BP group exhibited significantly greater activation than the HC group in the left nucleus accumbens (F=11.5, p=0.0001), right thalamus (F=4.9, p=0.03), and the left striatum (F=3.6, p=0.04). Left amygdala activation of the BPMJ group trended towards being significantly negatively correlated with the number of joints smoked (R=-0.4, p=0.06).Conclusions Bipolar adolescents with comorbid cannabis use do not exhibit the same over-activation of the regions involved in emotional processing as seen in adolescents with bipolar disorder alone. The absence of these findings in patients with comorbid bipolar and cannabis use disorders suggests that these individuals may have a unique endophenotype of bipolar disorder or that cannabis use may alter brain activation uniquely in bipolar disorder patients who use cannabis.
    Addiction 06/2014; 109(11). DOI:10.1111/add.12668 · 4.60 Impact Factor

Full-text (2 Sources)

Available from
Jun 10, 2014