Shared and divergent neurocognitive impairments in adult patients with schizophrenia and bipolar disorder: Whither the evidence?

Kuswanto, Carissa Nadia; Chin, Rowena; Sum, Min Yi; Sengupta, Somnath; Fagiolini, Andrea; McIntyre, Roger S.; Vieta, Eduard; Sim, Kang

doi:10.1016/j.neubiorev.2015.12.002

Cited by 43 publications

(43 citation statements)

References 148 publications

Supporting

Mentioning

Contrasting

Unclassified

Order By: Relevance

“…Recently, converging clinical, cognitive, biological, and genetic evidence across psychotic spectrum disorders, and at both early and chronic stages, has supported a dimensional model of psychosis (Craddock et al , 2009; Hill et al , 2013; Kuswanto et al , 2016; O'Donovan et al , 2009; Reininghaus et al , 2013; Tamminga et al , 2013). Consistent with this model, the findings of minimal CA1 volume trajectory differences between the non-remitters who remained persistently symptomatic at a subthreshold level and those who progressed to full-blown psychosis suggest that the CA1 volume changes may be most closely linked, in a dimensional manner, to the emergence of psychotic symptoms, rather than to the diagnosis of schizophrenia per se .…”

Section: Discussionmentioning

confidence: 99%

Progressive Decline in Hippocampal CA1 Volume in Individuals at Ultra-High-Risk for Psychosis Who Do Not Remit: Findings from the Longitudinal Youth at Risk Study

Holt

Cheung

et al. 2017

Neuropsychopharmacol

View full text Add to dashboard Cite

Most individuals identified as ultra-high-risk (UHR) for psychosis do not develop frank psychosis. They continue to exhibit subthreshold symptoms, or go on to fully remit. Prior work has shown that the volume of CA1, a subfield of the hippocampus, is selectively reduced in the early stages of schizophrenia. Here we aimed to determine whether patterns of volume change of CA1 are different in UHR individuals who do or do not achieve symptomatic remission. Structural MRI scans were acquired at baseline and at 1–2 follow-up time points (at 12-month intervals) from 147 UHR and healthy control subjects. An automated method (based on an ex vivo atlas of ultra-high-resolution hippocampal tissue) was used to delineate the hippocampal subfields. Over time, a greater decline in bilateral CA1 subfield volumes was found in the subgroup of UHR subjects whose subthreshold symptoms persisted (n=40) and also those who developed clinical psychosis (n=12), compared with UHR subjects who remitted (n=41) and healthy controls (n=54). No baseline differences in volumes of the overall hippocampus or its subfields were found among the groups. Moreover, the rate of volume decline of CA1, but not of other hippocampal subfields, in the non-remitters was associated with increasing symptom severity over time. Thus, these findings indicate that there is deterioration of CA1 volume in persistently symptomatic UHR individuals in proportion to symptomatic progression.

show abstract

Section: Discussionmentioning

confidence: 99%

Progressive Decline in Hippocampal CA1 Volume in Individuals at Ultra-High-Risk for Psychosis Who Do Not Remit: Findings from the Longitudinal Youth at Risk Study

Holt

Cheung

et al. 2017

Neuropsychopharmacol

View full text Add to dashboard Cite

show abstract

“…In schizophrenia, schizoaffective disorder, bipolar I disorder, and schizotypal personality disorder, cognitive deficits were documented in all domains: sensorimotor, attention, learning and memory, executive functions, language, and social cognition 180‐184 . These deficits were most pronounced in schizophrenia, but the other disorders showed a similar, although less extreme, profile of cognitive impairment 185‐188 . With regard to dimensions, negative and disorganized symptoms were linked to all aforementioned deficits, whereas reality distortion was essentially unrelated to cognitive impairment 189‐191 .…”

Section: Validity Evidencementioning

confidence: 99%

Validity and utility of Hierarchical Taxonomy of Psychopathology (HiTOP): I. Psychosis superspectrum

et al. 2020

View full text Add to dashboard Cite

The Hierarchical Taxonomy of Psychopathology (HiTOP) is a scientific effort to address shortcomings of traditional mental disorder diagnoses, which suffer from arbitrary boundaries between psychopathology and normality, frequent disorder co‐occurrence, heterogeneity within disorders, and diagnostic instability. This paper synthesizes evidence on the validity and utility of the thought disorder and detachment spectra of HiTOP. These spectra are composed of symptoms and maladaptive traits currently subsumed within schizophrenia, other psychotic disorders, and schizotypal, paranoid and schizoid personality disorders. Thought disorder ranges from normal reality testing, to maladaptive trait psychoticism, to hallucinations and delusions. Detachment ranges from introversion, to maladaptive detachment, to blunted affect and avolition. Extensive evidence supports the validity of thought disorder and detachment spectra, as each spectrum reflects common genetics, environmental risk factors, childhood antecedents, cognitive abnormalities, neural alterations, biomarkers, and treatment response. Some of these characteristics are specific to one spectrum and others are shared, suggesting the existence of an overarching psychosis superspectrum. Further research is needed to extend this model, such as clarifying whether mania and dissociation belong to thought disorder, and explicating processes that drive development of the spectra and their subdimensions. Compared to traditional diagnoses, the thought disorder and detachment spectra demonstrated substantially improved utility: greater reliability, larger explanatory and predictive power, and higher acceptability to clinicians. Validated measures are available to implement the system in practice. The more informative, reliable and valid characterization of psychosis‐related psychopathology offered by HiTOP can make diagnosis more useful for research and clinical care.

show abstract

“…Notably, varying degrees of impairment in both executive function and reward processing are a common feature of the psychiatric disorders associated with childhood stress (e.g., Brown, 2008; Etkin et al, 2013; Green, 2006; Lewandowski et al, 2016; Whitton et al, 2015). As an example, working memory and other executive function deficits are seen in ADHD, substance abuse and other addictive disorders, bipolar disorder, major depressive disorder, and schizophrenia (Brown, 2008; Craig et al, 2016; Crews & Boettiger, 2009; Cullen et al, 2016; Etkin et al, 2013; Grant & Chamberlain, 2014; Kuswanto et al, 2016; Leeman et al, 2014). Furthermore, disrupted reward processing as a function of diminished executive processes is demonstrated in individuals with major depressive disorder (Whitton et al, 2015), who show deficits in working memory, sustained attention, and task switching (Etkin et al, 2013).…”

Section: Childhood Stress and Later Psychiatric Illness – A Functimentioning

confidence: 99%

Impact of juvenile chronic stress on adult cortico-accumbal function: Implications for cognition and addiction

Watt

Weber

Davies

et al. 2017

Progress in Neuro-Psychopharmacology and Biological Psychiatry

View full text Add to dashboard Cite

Repeated exposure to stress during childhood is associated with increased risk for neuropsychiatric illness, substance use disorders and other behavioral problems in adulthood. However, it is not clear how chronic childhood stress can lead to emergence of such a wide range of symptoms and disorders in later life. One possible explanation lies in stress-induced disruption to the development of specific brain regions associated with executive function and reward processing, deficits in which are common to the disorders promoted by childhood stress. Evidence of aberrations in prefrontal cortex and nucleus accumbens function following repeated exposure of juvenile (pre- and adolescent) organisms to a variety of different stressors would account not only for the similarity in symptoms across the wide range of childhood stress-associated mental illnesses, but also their persistence into adulthood in the absence of further stress. Therefore, the goal of this review is to evaluate the current knowledge regarding disruption to executive function and reward processing in adult animals or humans exposed to chronic stress over the juvenile period, and the underlying neurobiology, with particular emphasis on the prefrontal cortex and nucleus accumbens. First, the role of these brain regions in mediating executive function and reward processing is highlighted. Second, the neurobehavioral development of these systems is discussed to illustrate how juvenile stress may exert long-lasting effects on prefrontal cortex-accumbal activity and related behavioral functions. Finally, a critical review of current animal and human findings is presented, which strongly supports the supposition that exposure to chronic stress (particularly social aggression and isolation in animal studies) in the juvenile period produces impairments in executive function in adulthood, especially in working memory and inhibitory control. Chronic juvenile stress also results in aberrations to reward processing and seeking, with increased sensitivity to drugs of abuse particularly noted in animal models, which is in line with greater incidence of substance use disorders seen in clinical studies. These consequences are potentially mediated by monoamine and glutamatergic dysfunction in the prefrontal cortex and nucleus accumbens, providing translatable therapeutic targets. However, the predominant use of male subjects and social-based stressors in preclinical studies points to a clear need for determining how both sex differences and stressor heterogeneity may differentially contribute to stress-induced changes to substrates mediating executive function and reward processing, before the impact of chronic juvenile stress in promoting adult psychopathology can be fully understood.

show abstract

Shared and divergent neurocognitive impairments in adult patients with schizophrenia and bipolar disorder: Whither the evidence?

Cited by 43 publications

References 148 publications

Progressive Decline in Hippocampal CA1 Volume in Individuals at Ultra-High-Risk for Psychosis Who Do Not Remit: Findings from the Longitudinal Youth at Risk Study

Progressive Decline in Hippocampal CA1 Volume in Individuals at Ultra-High-Risk for Psychosis Who Do Not Remit: Findings from the Longitudinal Youth at Risk Study

Validity and utility of Hierarchical Taxonomy of Psychopathology (HiTOP): I. Psychosis superspectrum

Impact of juvenile chronic stress on adult cortico-accumbal function: Implications for cognition and addiction

Contact Info

Product

Resources

About