MRI during affect discrimination in bipolar affective disorder. Bipolar Disord 2(3 Pt 2):237-248

Cognitive Neuroimaging Laboratory, Brain Imaging Center, McLean Hospital, Harvard Medical School, Belmont, MA 02478, USA.
Bipolar Disorders (Impact Factor: 4.97). 10/2000; 2(3 Pt 2):237-48.
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It has been hypothesized that disturbances in affect may represent distinct etiologic factors for bipolar affective disorder. The neural mechanisms mediating affective processes and their relationship to brain development and the pathophysiology of bipolar affective disorder remain to be clarified. Recent advances in neuroimaging techniques have made possible the non-invasive examination of specific brain regions during cortical challenge paradigms. This study reports findings based on fMRI data acquired during fearful and happy affect recognition paradigms in patients with bipolar affective disorder and in healthy adult subjects.
Prior to the scan, subjects were instructed to view the stimuli and to identify the type of facial expression presented. Echo planar scanning was performed on a 1.5 Tesla scanner which had been retrofitted with a whole body echo planar coil, using a head coil.
The data indicate that in adult subjects with bipolar affective disorder, there is a reduction in dorsolateral prefrontal cortex activation and an increase in amygdalar activation in response to fearful facial affect. In a healthy comparison group, signal intensity changes were not found in these regions. In addition, although the patients with bipolar affective disorder completed the task demands, they demonstrated an impaired ability to correctly identify fearful facial affect but not the happy facial affect displayed.
These findings are consistent with the hypothesis that in some patients with bipolar affective disorder, there may be a reduction of frontal cortical function which may be associated with affective as well as attentional processing deficits.

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Available from: William D. S. Killgore
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    • "Given mood symptoms are the key component of bipolar disorder, most neuroimaging studies of social cognition in bipolar disorder to date have appropriately focused on brain activity during emotion processing tasks (for a review see Cusi, Nazarov, Holshausen, MacQueen, & McKinnon, 2012). Most often, these studies have revealed overactive limbic networks and corresponding underactivity in areas of the prefrontal cortex, indicating reduced cognitive control over emotional responding (Hassel et al., 2008; Malhi et al., 2007; Yurgelun-Todd et al., 2000). Few studies have examined the neural basis of theory of mind in bipolar disorder. "
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    • "In 2008, Mitchell et al. tackled this issue, and found that higher rates of psychomotor retardation occur relatively more in bipolar than in unipolar depression, and this also applies for greater difficulty thinking, more early morning awakening, more morning worsening of mood and more frequent psychotic symptoms [11]. Functional imaging studies suggest an increased activation of some limbic regions in respond to sad stimuli, in both unipolar and bipolar depression [12]. At the level of physiology, bipolar and unipolar depressive episodes are characterized by similar levels of dopamine and serotonin [10] with some differences at the level of intracellular transduction pathways. "

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    • "Similarly, both PFC and striatal hyperactivation (Pavuluri et al. 2007) and hypoactivation (Blumberg et al. 2005; Pavuluri et al. 2007; Killgore et al. 2008) have been reported in passive viewing paradigms. Explicit face emotion processing paradigms, in which the task directs attention toward the face emotion, have also elicited amygdala hyperactivity in BD (Yurgelun-Todd et al. 2000; Rich et al. 2006; Foland et al. 2008; Almeida et al. 2010; Chen et al. 2010; Versace et al. 2010; Hulvershorn et al. 2012), although some find hypoactivation (Lennox et al. 2004; Chen et al. 2006; Vizueta et al. 2012). These mixed findings in BD are consistent with meta-analyses in healthy adults (Sergerie et al. 2008), suggesting that explicit face emotion processing may probe the amygdala less effectively than do passive viewing paradigms, and may even be associated with decreased amygdala activation (Costafreda et al. 2008). "
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