Individual differences in the Behavioral Inhibition System are associated with orbitofrontal cortex and precuneus gray matter volume

Please cite this article in press as: Vuilleumier P. Brain circuits implicated in psychogenic paralysis in conversion disorders and hypnosis. REVIEW/MISE AU POINT Brain circuits implicated in psychogenic paralysis in conversion disorders and hypnosis Circuits cérébraux des paralysies psychogènes liées aux troubles de conversion et à l'hypnose P. Vuilleumier Laboratory for Behavioral Neurology and Imaging of Cognition (LABNIC), Department of Neuroscience (NEUFO), University Medical Center (CMU), 1, rue Micheli du Crest, 1205 Geneva, SwitzerlandReceived 27 December 2013; accepted 12 January 2014 KEYWORDSConversion; Hysteria; Hypnosis; Paralysis; Brain; Neuroimaging; Affect; Self; Precuneus; VMPFC Summary Conversion disorders are defined as neurological symptoms arising without organic damage to the nervous system, presumably in relation to various emotional stress factors, but the exact neural substrates of these symptoms and the mechanisms responsible for their production remain poorly understood. In the past 15 years, novel insights have been gained with the advent of functional neuroimaging studies in patients suffering from conversion disorders in both motor and non-motor (e.g. somatosensory, visual) domains. Several studies have also compared brain activation patterns in conversion to those observed during hypnosis, where similar functional losses can be evoked by suggestion. The current review summarizes these recent results and the main neurobiological hypotheses proposed to account for conversion symptoms, in particular motor deficits. An emerging model points to an important role of ventromedial prefrontal cortex (VMPFC), precuneus, and perhaps other limbic structures (including amygdala), all frequently found to be hyperactivated in conversion disorders in parallel to impaired recruitment of primary motor and/or sensory pathways at the cortical or subcortical (basal ganglia) level. These findings are only partly shared with hypnosis, where increases in precuneus predominate, together with activation of attentional control systems, but without any activation of VMPFC. Both VMPFC and precuneus are key regions for access to internal representations about the self, integrating information from memory and imagery with affective relevance (in VMPFC) and sensory or agency representations (in precuneus). It is therefore postulated that conversion deficits might result from an alteration of conscious sensorimotor functions and self-awareness under the influence of affective and sensory representations generated in these regions, which might promote certain patterns of behaviors in response to self-relevant emotional states. © 2014 Elsevier Masson SAS. All rights reserved. IntroductionConversion disorders have been known to physicians since ancient times and consist of neurological dysfunction that occurs in the absence of organic lesions within the nervous system, but is distinct from other major psychiatric symptoms such as psychosis or depression. Thus, patients may present with a paralysis of one or ...

ObjectivesThe State-Trait Anxiety Inventory (STAI) and the Hamilton scale for anxiety (HARS) are two of the most important scales employed in clinical and psychological realms for the evaluation of anxiety. Although the reliability and sensibility of these scales are widely demonstrated there is an open debate on what exactly their scores reflect. Neuroimaging provides the potential to validate the quality and reliability of clinical scales through the identification of specific biomarkers. For this reason, we evaluated the neural correlates of these two scales in a large cohort of healthy individuals using structural neuroimaging methods.Case reportNeuroimaging analysis included thickness/volume estimation of cortical and subcortical limbic structures, which were regressed on anxiety inventory scores with age and gender used for assessing discriminant validity. A total of 121 healthy subjects were evaluated. Despite the two anxiety scales, at a behavioral level, displaying significant correlations among them (HARS with STAI-state (r = 0.24; P = 0.006) and HARS with STAI-trait (r = 0.42; P < 0.001)), multivariate neuroimaging analyses demonstrated that anatomical variability in the anterior cingulate cortex was the best predictor of the HARS scores (all β's ≥ 0.31 and P's ≤ 0.01), whereas STAI-related measures did not show any significant relationship with regions of limbic circuits, but their scores were predicted by gender (all β's ≥ 0.23 and P's ≤ 0.02).ConclusionAlthough the purpose of HARS and STAI is to quantify the degree and characteristics of anxiety-like behaviors, our neuroimaging data indicated that these scales are neurobiologically different, confirming that their scores might reflect different aspects of anxiety: the HARS is more related to subclinical expression of anxiety disorders, whereas the STAI captures sub-dimensions of personality linked to anxiety.

While many studies have reported that individual differences in personality traits are genetically influenced, the neurobiological bases mediating these influences have not yet been well characterized. To advance understanding concerning the pathway from genetic variation to personality, here we examined whether measures of heritable variation in neuroanatomical size in candidate regions (amygdala and medial orbitofrontal cortex) were associated with heritable effects on personality. A sample of 486 middle-aged (mean = 55 years) male twins (complete MZ pairs = 120; complete DZ pairs = 84) underwent structural brain scans and also completed measures of two core domains of personality: positive and negative emotionality. After adjusting for estimated intracranial volume, significant phenotypic (rp) and genetic (rg) correlations were observed between left amygdala volume and positive emotionality (rp = .16, p < .01; rg = .23, p < .05, respectively). In addition, after adjusting for mean cortical thickness, genetic and nonshared-environmental correlations (re) between left medial orbitofrontal cortex thickness and negative emotionality were also observed (rg = .34, p < .01; re = −.19, p < .05, respectively). These findings support a model positing that heritable bases of personality are, at least in part, mediated through individual differences in the size of brain structures, although further work is still required to confirm this causal interpretation.