Abstract

Suicidal ideation (SUI) can occur in the absence of concomitant psychiatric diagnoses, and even normal levels can be problematic among individuals experiencing excess stress or lack of social support. The objective of this study was to investigate the neuroanatomical basis of SUI in non-clinical human populations who are within the normal limits of SUI, after accounting for elevated stress and perceived lack of social support. Neuroanatomical data were collected from 55 healthy individuals (mean age 30.9 ± 8.1 years, 27 females) whose depression severity levels were below the Diagnostic and Statistical Manual of Mental Disorders criteria. Measures of SUI, aggression, stress, non-support, and treatment rejection were collected from the treatment-consideration scales (TCS) of the Personality Assessment Inventory (PAI). Correlations between standardized SUI scores and three brain morphometry measures, including vertex wise cortical thickness (CT), cortical surface area (CSA), and cortical volume (CV), were estimated for each participant, controlling for age, sex, intracranial volume, and the remaining TCS measures. We observed a significant negative association between scores on SUI and both CSA and CV (cluster-forming threshold of p < 0.005, clusterwise threshold of p < 0.05, FDR corrected for multiple comparisons) within the left rostral middle frontal gyrus. Our findings suggest that greater CSA and CV within the dorsolateral prefrontal cortex are associated with reduced SUI in a non-clinical population with mild levels of stress and perceived lack of social support. Because the dorsolateral prefrontal cortex has been broadly linked to cognitive reappraisal, self-critical thoughts, and emotional regulation, greater CSA and CV within these regions may lead to better mental health by protecting healthy individuals from engaging in SUI during periods of stress and perceived insufficient social support. As our data consisted of only healthy individuals with non-clinical levels of SUI, further investigation will be necessary to explore the neural basis of SUI in populations who may be at greater risk of future suicidal behavior

Highlights

  • Introduction150,000 people in Europe die because of suicide every year [1], and the percentage of annual suicide attempts in the United States has reportedly increased significantly from 0.62% to 0.79% (from the sample recruited between 2004 and 2005 and between 2012 and 2013) among individuals aged 21 years and older [2], making suicide one of the primary causes of death [3]

  • 150,000 people in Europe die because of suicide every year [1], and the percentage of annual suicide attempts in the United States has reportedly increased significantly from 0.62% to 0.79% among individuals aged 21 years and older [2], making suicide one of the primary causes of death [3]

  • At a cluster-wise threshold (CWT) of p < 0.05 and clusterforming threshold (CFT) of p < 0.005: We found a cluster with its peak in the left rostral middle frontal gyrus (L.RMFG), which is part of the dorsolateral prefrontal cortex, FIGURE 1 | Subjectwise distribution of T-scores from the Personality Assessment Inventory–treatment-consideration scales (PAI-TCS)

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Summary

Introduction

150,000 people in Europe die because of suicide every year [1], and the percentage of annual suicide attempts in the United States has reportedly increased significantly from 0.62% to 0.79% (from the sample recruited between 2004 and 2005 and between 2012 and 2013) among individuals aged 21 years and older [2], making suicide one of the primary causes of death [3]. Neuroanatomical differences, i.e., reduced volume within the frontal lobe [11, 12], have been associated with suicide or suicidal behavior, including suicide attempts. The orbitofrontal cortex (OFC) and amygdala are key regions linked to emotion and impulse regulation, with work suggesting that structural abnormalities within these regions can potentially influence these functions and increase the risk for suicidal behavior [15]. From a clinical point of view, Baeken and colleagues recently explored the SUI attenuation following 4 days of a high-frequency brain stimulation procedure, called accelerated intermittent theta burst stimulation (aiTBS)

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