Social cognition and neurocognition as predictors of conversion to psychosis in individuals at ultra-high risk

Kim, Hee Sun; Shin, Na Young; Jang, Joon Hwan; Kim, Euitae; Shim, Geumsook; Park, Hye Yoon; Hong, Kyung Sue; Kwon, Jun Soo

doi:10.1016/j.schres.2011.04.023

Cited by 152 publications

(111 citation statements)

References 37 publications

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“…This assumption is based also on studies of subjects at CHR that report similar but more attenuated findings compared to those reported for schizophrenia, including cognitive impairments, [26][27][28] structural, [29][30][31][32] and functional alterations. 33,34 Moreover, characterizing those at the prepsychotic phase of illness, who evince potential prodromal symptoms, is critical for establishing biomarkers that can be used to follow the effects of treatment or to identify subjects who are at higher risk for developing the illness.…”

Section: Introductionmentioning

confidence: 94%

Altered Thalamo-Cortical White Matter Connectivity: Probabilistic Tractography Study in Clinical-High Risk for Psychosis and First-Episode Psychosis

Cho

Shenton

Kubicki

et al. 2015

SCHBUL

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105

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Disrupted thalamo-cortical connectivity is regarded as a core psychopathology in patients diagnosed with schizophrenia. However, whether the thalamo-cortical white matter connectivity is disrupted before the onset of psychosis is still unknown. To determine this gap in knowledge, the strength of thalamo-cortical white matter anatomical connectivity in subjects at clinical-high risk for psychosis (CHR) was compared to that of first-episode psychosis (FEP) and healthy controls. A total of 37 CHR, 21 FEP, and 37 matched healthy controls underwent diffusion-weighted magnetic resonance imaging to examine the number of probabilistic tractography "counts" representing thalamo-cortical white matter connectivity. We also investigated the relationship with psychopathology. For FEP, the connectivity between the thalamus and parietal cortex was significantly increased (F = 5.65, P < .05) compared to that of healthy controls. However, the connectivity between thalamus and orbitofrontal cortex was significantly reduced compared to both healthy controls (F = 11.86, P < .005) and CHR (F = 6.63, P < .05). Interestingly, CHR exhibited a similar pattern as FEP, albeit with slightly reduced magnitude. Compared to healthy controls, there was a significant decrease (F = 4.16, P < .05) in CHR thalamo-orbitofrontal connectivity. Also, the strength of the thalamo-orbitofrontal connectivity was correlated with the Global Assessment of Functioning score in CHR (r = .35, P < .05). This observed pattern of white matter connectivity disruptions in FEP and in CHR suggests that this pattern of disconnectivity not only highlights the involvement of thalamus but also might be useful as an early biomarker for psychosis.

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Section: Introductionmentioning

confidence: 94%

Altered Thalamo-Cortical White Matter Connectivity: Probabilistic Tractography Study in Clinical-High Risk for Psychosis and First-Episode Psychosis

Cho

Shenton

Kubicki

et al. 2015

SCHBUL

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105

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“…Some of the altered node centrality measures correlated with duration and severity of disease. Structural and functional network changes (of genetic origin) are implicated in Attention Deficit Hyperactivity Disorder (ADHD) [92], similarly, complex genetic and developmental factors are implicated in schizophrenia where in, normal development of long range fronto-temporal connection is disrupted [93,94].…”

Section: Network Disorder and Neuropsychiatric Diseasesmentioning

confidence: 99%

Disruption of Neurosynaptic Physiology and Neuron Network Dysfunction in Brain Disorders: An Environmental and Occupational Health Perspective

Pandey¹

2017

AND

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Networks of signaling cascades regulate synaptic transmission and morphology. Signaling molecules and their dynamics are subject to impact of environmental insults as well as genes predisposing to disease risks. Pollutants may impact brain through cellular, molecular and inflammatory pathways, causing direct damage or predisposing to damage by other insults, leading to diseases. Disruptions in structure and function of neurotransmission elements and protein networks contribute to pathogenesis of neuropsychiatric diseases. Different affected brain regions and/or synaptic connections between excitatory and inhibitory neurons charecterise specific clinical states. Functional identification of synaptic signaling networks and specific neuronal pathways would facilitate understanding of specific pathomechanisms relevant to preventive and corrective interventions. Physiology of neural networks and pathogenesis, therapeutics and prevention of diseases arising of their disruption, specially with environmental afflictions, deserve holistic and not fragmentary understanding. Present article attempts to present such diverse information with possible coherence to emphasize necessary address in contemporary medical teaching and continuing education for young researchers. The mounting challenge of prevention and management of pollution inflicted disruption of neurophysiology associated with brain dysfunction and diseases in contemporary world may be better addressed by integrated interdisciplinary understanding of the problems.

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“…Maladaptive ER strategies (e.g., suppression, rumination, self-blame, catastrophizing), commonly assessed using the Cognitive Emotion Regulation Reduced ACC and LPFC activation during ECA in anxiety [84]; reduced DLPFC and increased amygdala activation in depression [85] Findings in psychosis-spectrum samples Behavioral Suppression associated with more severe paranoia [87], auditory hallucinations [88], and poorer social functioning [94] Impaired ECA associated with paranoia [99], disorganized symptoms [100], and reduced positive affect [108] Neuroimaging Reduced frontal-limbic connectivity during reappraisal in schizophrenia [103] and PP [104] Reduced LPFC, medial PFC, and ACC activation during ECA in schizophrenia [105] and PP [104] ACC anterior cingulate cortex, BPD borderline personality disorder, CERQ Cognitive Emotion Regulation Questionnaire, DLPFC dorsolateral prefrontal cortex, ECA emotion conflict adaptation, ER emotion regulation, LPFC lateral prefrontal cortex, PFC prefrontal cortex, PP psychosis proneness Questionnaire (CERQ) [75], are increasingly recognized as vulnerability factors that contribute to the development and maintenance of psychopathology [28], particularly disorders characterized by affective instability, such as anxiety [76], depression [77,78], and substance use [79]. Similarly, impaired performance on ECA paradigms requiring inhibition of irrelevant negative emotional stimuli has been observed in depression [80], anxiety [81], borderline personality disorder [82], and those at risk for developing a mood disorder [83].…”

Section: Relevance Of Cognitive Control Of Emotion To Transdiagnosticmentioning

confidence: 99%

Beyond “Cold” Cognition: Exploring Cognitive Control of Emotion as a Risk Factor for Psychosis

Tully

Niendam

2014

Curr Behav Neurosci Rep

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The past 20 years of research examining psychosis risk factors has predominantly focused on "cold" cognitive (i.e., non-affective) processes. Despite identification of potential cognitive and associated brain-based vulnerability markers, our ability to identify those individuals at highest risk for future psychosis has not substantially improved. Consequently, researchers have begun to examine emotionprocessing deficits as potential psychosis vulnerability markers. Here we propose that a particular emotionprocessing domain, cognitive control of emotion, is a potential transdiagnostic mechanism underlying the heterogeneity of clinical presentation and psychosocial impairments observed in high-risk populations. Recent investigations indicate impaired cognitive control of emotion is observable across the psychosis spectrum and relates to important clinical and psychosocial outcomes relevant to the high-risk state. Moreover, preliminary evidence indicates treatment interventions aimed at improving cognitive control of emotion could reduce psychotic symptoms and improve functioning. We highlight gaps in current knowledge and propose five key avenues for future investigations.

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Social cognition and neurocognition as predictors of conversion to psychosis in individuals at ultra-high risk

Cited by 152 publications

References 37 publications

Altered Thalamo-Cortical White Matter Connectivity: Probabilistic Tractography Study in Clinical-High Risk for Psychosis and First-Episode Psychosis

Altered Thalamo-Cortical White Matter Connectivity: Probabilistic Tractography Study in Clinical-High Risk for Psychosis and First-Episode Psychosis

Disruption of Neurosynaptic Physiology and Neuron Network Dysfunction in Brain Disorders: An Environmental and Occupational Health Perspective

Beyond “Cold” Cognition: Exploring Cognitive Control of Emotion as a Risk Factor for Psychosis

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