Neuroimaging Studies of Mood Disorders

Biological Vulnerabilities to the Development of Psychopathology

“…It is interesting to note that increased amygdala activity has also been associated with bipolar disorder and anxiety disorders (Davidson et al, 2002). Bilateral reductions in anterior cingulate activity have also been noted and have been found to correlate with the extent of gray matter reduction, which is consistent with the finding that antidepressant treatment does not generally lead to a normalization of activity in this region (Davidson et al, 2002;Drevets, 2000).…”

“…Decreased bilateral or left prefrontal cortex activation is one of the most often reported functional anomalies in the imaging literature on depression (Davidson et al, 2002). Resting state imaging studies have shown hypometabolism of the frontal lobes, more specifically of the dorsolateral and dorsomedial prefrontal cortex (Davidson et al, 2002;Drevets, 2000;Liotti & Mayberg, 2001). Specificity of reduced activity to the left hemisphere has been replicated numerous times by electroencephalogram (EEG) studies, although negative evidence has also been found (Davidson et al, 2002).…”

“…More specifically, it has been suggested that some brain anomalies may characterize specific subtypes of patients (Davidson et al, 2002). For example, patients with a family history of major depression have been shown to be more likely to have increased activity of the amygdala, orbital cortex, and medial thalamus and decreased activity in specific subregions of the prefrontal cortex, as well as volumetric anomalies of the basal ganglia (Drevets, 2000). As well, patients with a family history of major depression do not exhibit the reduced amygdala activity usually associated with remission of symptoms, suggesting that amygdala hyperactivity may constitute a marker of a depressive trait rather than a depressive state in this subpopulation (Davidson et al, 2002).…”

“…As well, patients with a family history of major depression do not exhibit the reduced amygdala activity usually associated with remission of symptoms, suggesting that amygdala hyperactivity may constitute a marker of a depressive trait rather than a depressive state in this subpopulation (Davidson et al, 2002). Patients with a late onset of the disorder have also been shown to exhibit a specific pattern of anomalies (Drevets, 2000). They exhibit sulcal and ventricular enlargement, as well as reduced volumes of the frontal lobes and the basal ganglia.…”

Behavioral Neurobiology of Bipolar Disorder and its Treatment

“…Previous neurobiological studies of mood disorders focused primarily on abnormalities of the monoaminergic neurotransmitter systems, on characterizing alterations of individual neurotransmitters in disease states, and on assessing response to mood stabilizer, antipsychotic, and antidepressant medications. The monoaminergic systems are v extensively distributed throughout the network of limbic, striatal, and prefrontal cortical neuronal circuits thought to support the behavioral and visceral manifestations of mood disorders (Drevets 2000). Studies of cerebrospinal fluid (CSF) chemistry, neuroendocrine responses to pharmacological challenge, and neuroreceptor and transporter binding demonstrated a number of abnormalities in monoaminergic neurotransmitter and neuropeptide systems in mood disorders (Goodwin and Jamison 2007).…”