Article

From high anxiety trait to depression: a neurocognitive hypothesis.

Laboratory of Behavioral Genetics, Brain Mind Institute, Ecole Polytechnique Federale de Lausanne (EPFL), Lausanne CH-1015, Switzerland.
Trends in Neurosciences (Impact Factor: 12.9). 05/2009; 32(6):312-20. DOI: 10.1016/j.tins.2009.02.004
Source: PubMed

ABSTRACT Although exposure to substantial stress has a major impact on the development of depression, there is considerable variability in the susceptibility of individuals to the adverse effects of stress. The personality trait of high anxiety has been identified as a vulnerability factor to develop depression. We propose here a new unifying model based on a series of neurocognitive mechanisms (and fed with crucial information provided by research on the fields of emotion, stress and cognition) whereby individuals presenting a high anxiety trait are particularly vulnerable to develop depression when facing stress and adversity. Our model highlights the importance of developing prevention programs addressed to restrain, in high anxious individuals, the triggering of a dysfunctional neurocognitive cascade while coping with stress.

0 Bookmarks
 · 
243 Views
  • Source
    [Show abstract] [Hide abstract]
    ABSTRACT: Whether trait anxiety is associated with a general impairment of cognitive control is a matter of debate. This study investigated whether and how experimentally manipulated working memory (WM) load modulates the relation between trait anxiety and cognitive control. This question was investigated using a dual-task design in combination with event-related potentials. Participants were required to remember either one (low WM load) or six letters (high WM load) while performing a flanker task. Our results showed that a high WM load disrupted participants' ability to overcome distractor interference and this effect was exacerbated for the high trait-anxious (HTA) group. This exacerbation was reflected by larger interference effects (i.e., incongruent minus congruent) on reaction times (RTs) and N2 amplitudes for the HTA group than for the low trait-anxious group under high WM load. The two groups, however, did not differ in their ability to inhibit task-irrelevant distractors under low WM load, as indicated by both RTs and N2 amplitudes. These findings underscore the significance of WM-related cognitive demand in contributing to the presence (or absence) of a general cognitive control deficit in trait anxiety. Furthermore, our findings show that when limited WM resources are depleted by high WM load, HTA individuals exhibit less efficient recruitments of cognitive control required for the inhibition of distractors, therefore resulting in a greater degree of response conflict.
    PLoS ONE 11/2014; 9(11):e111791. DOI:10.1371/journal.pone.0111791 · 3.53 Impact Factor
  • [Show abstract] [Hide abstract]
    ABSTRACT: Comorbidity with anxiety disorder is a relatively common occurrence in major depressive disorder. However, the unique and shared neuroanatomical characteristics of depression and anxiety disorders have not been fully identified. The aim of this study was to identify gray matter abnormalities and their clinical correlates in depressive patients with and without anxiety disorders.We applied voxel-based morphometry and region-of-interest analyses of gray matter volume (GMV) in normal controls (NC group, n = 28), depressive patients without anxiety disorder (DP group, n = 18), and depressive patients with anxiety disorder (DPA group, n = 20). The correlations between regional GMV and clinical data were analyzed.The DP group showed decreased GMV in the left insula (INS) and left triangular part of the inferior frontal gyrus when compared to the NC group. The DPA group showed greater GMV in the midbrain, medial prefrontal cortex, and primary motor/somatosensory cortex when compared to the NC group. Moreover, the DPA group showed greater GMV than the DP group in the frontal, INS, and temporal lobes. Most gray matter anomalies were significantly correlated with depression severity or anxiety symptoms. These correlations were categorized into 4 trend models, of which 3 trend models (ie, Models I, II, and IV) revealed the direction of the correlation between regional GMV and depression severity to be the opposite of that between regional GMV and anxiety symptoms. Importantly, the left INS showed a trend Model I, which might be critically important for distinguishing depressive patients with and without anxiety disorder.Our findings of gray matter abnormalities, their correlations with clinical data, and the trend models showing opposite direction may reflect disorder-specific symptom characteristics and help explain the neurobiological differences between depression and anxiety disorder.
    Medicine 12/2014; 93(29):e345. DOI:10.1097/MD.0000000000000345 · 4.87 Impact Factor
  • Source
    [Show abstract] [Hide abstract]
    ABSTRACT: Background: The experience of early life stress is a consistently identified risk factor for the development of mood and anxiety disorders. Preclinical research employing animal models of early life stress has made inroads in understanding this association and suggests that the negative sequelae of early life stress may be mediated by developmental disruption of corticolimbic structures supporting stress responsiveness. Work in humans has corroborated this idea, as childhood adversity has been associated with alterations in gray matter volumes of the hippocampus, amygdala, and medial prefrontal cortex. Yet, missing from this body of research is a full understanding of how these neurobiological vulnerabilities may mechanistically contribute to the reported link between adverse childhood experiences and later affective psychopathology. Results: Analyses revealed that self-reported childhood maltreatment was associated with reduced gray matter volumes within the medial prefrontal cortex and left hippocampus. Furthermore, reduced left hippocampal and medial prefrontal gray matter volume mediated the relationship between childhood maltreatment and trait anxiety. Additionally, individual differences in corticolimbic gray matter volume within these same structures predicted the anxious symptoms as a function of life stress 1 year after initial assessment. Conclusions: Collectively, these findings provide novel evidence that reductions in corticolimbic gray matter, particularly within the hippocampus and medial prefrontal cortex, are associated with reported childhood maltreatment and individual differences in adult trait anxiety. Furthermore, our results suggest that these structural alterations contribute to increased affective sensitivity to stress later in life in those that have experienced early adversity. More broadly, the findings contribute to an emerging literature highlighting the critical importance of early stress on the development of corticolimbic structures supporting adaptive functioning later in life.
    11/2014; 4:12. DOI:10.1186/2045-5380-4-12

Preview

Download
2 Downloads
Available from