Anterior cingulate cortical volumes and treatment remission of geriatric depression

Abstract

SUMMARYBackground Structural abnormalities of the anterior cingulate cortex (ACC) may interfere with the interaction of cortical and limbic networks involved in emotional regulation and contribute to chronic depressive syndromes in the elderly. This study examined the relationship of regional anterior cingulate cortical volumes with treatment remission of elderly depressed patients. We hypothesized that patients who failed to remit during a 12-week controlled treatment trial of escitalopram would exhibit smaller anterior cingulate gray matter volumes than patients who remitted. Methods The participants were 41 non-demented individuals with non-psychotic major depression. After a 2-week singleblind placebo period, subjects who still had a Hamilton Depression Rating Scale (HDRS) of 18 or greater received escitalopram 10 mg daily for 12 weeks. Remission was defined as a HDRS score of 7 or below for at least 2 consecutive weeks. The patient sample consisted of 22 depressed patients who achieved remission during the study and 19 depressed patients who remained symptomatic. High-resolution magnetization-prepared rapidly acquired gradient echo (MPRAGE) sequences were acquired on a 1.5 T scanner and regional ACC volumes were manually outlined (dorsal, rostral, anterior subgenual, and posterior subgenual). Results Repeated measure analyses revealed that patients who failed to remit following escitalopram treatment had smaller dorsal and rostral anterior cingulate gray matter volumes than patients who remitted, whereas subgenual cortical volumes did not differ between the groups. Conclusions Structural abnormalities of the dorsal and rostral anterior cingulate may perpetuate late-life depression.

Imaging predictors of remission to anti-depressant medications in major depressive disorder

“…Although two studies associated a smaller right superior frontal gyrus with remitters (Costafreda et al, 2009;Li et al, 2010), Jung et al (2014) showed significantly smaller volumes in patients who did not respond to 8 weeks of ADM, compared to healthy controls (Jung et al, 2014). More consistent findings have been seen with the anterior and posterior cingulate cortices, with larger sizes of both structures predicting remission (Costafreda et al, 2009;Gunning et al, 2009;Jarnum et al, 2011). Although no more than 2 reviewed papers have corroborated these findings, a small number of ADM treatment response studies have provided further support for cingulate size (Chen et al, 2007;Samann et al, 2013).…”

“…In these patients, larger dorsal and rostral ACC volumes were associated with remission (Gunning et al, 2009). A subsequent study showed significantly reduced PCC thickness in 9 patients who did not remit after 6 months of mixed ADM, compared with 8 remitters.…”

Specificity of abnormal brain volume in major depressive disorder: A comparison with borderline personality disorder

“…Reduced ACC volume was found to be associated with attention biases towards negative, depressionrelated cues (Leung et al, 2009), with a diminished ability to down-regulate negative -but not positive -emotions (Mak et al, 2009), with worse executive performance (Vasic et al, 2008), and with higher risk for suicidal behavior (Wagner et al, 2011). Lastly, ACC volume decrease was found to correlate with negative antidepressant treatment response in cross-sectional imaging studies of MDD (Chen et al, 2007;Gunning et al, 2009). …”

Cognitive Effects of Late Life Depression: Review of Neuropsychological Findings

“…The functioning of the rostal ACC has been found to be altered due to depression, as shown by deviating ERP responses in depressed older adults following an emotional go-no/go paradigm [93]. Also, smaller gray matter volumes of the ACC correlated with poor effects of antidepressant treatment [96], indicating that preexisting conditions affecting the anterior cingulate may be one reason why many elderly depressed patients do not respond to common antidepressant treatments [18]. Reduced N2 components within ACC correlate with poorer performance on the inhibition control task, suggesting that depression causes less efficient processing within the ACC, or perhaps that brain plasticity has shifted inhibition control processing to less specialized areas [13] [18].…”