Neuropsychological Impairments in Schizophrenia and Psychotic Bipolar Disorder: Findings from the Bipolar-Schizophrenia Network on Intermediate Phenotypes (B-SNIP) Study

Abstract

Objective Familial neuropsychological deficits are well established in schizophrenia but remain less well characterized in other psychotic disorders. This study from the Bipolar-Schizophrenia Network on Intermediate Phenotypes (B-SNIP) consortium 1) compares cognitive impairment in schizophrenia and bipolar disorder with psychosis, 2) tests a continuum model of cognitive dysfunction in psychotic disorders, 3) reports familiality of cognitive impairments across psychotic disorders, and 4) evaluates cognitive impairment among nonpsychotic relatives with and without cluster A personality traits. Method Participants included probands with schizophrenia (N=293), psychotic bipolar disorder (N=227), schizoaffective disorder (manic, N=110; depressed, N=55), their first-degree relatives (N=316, N=259, N=133, and N=64, respectively), and healthy comparison subjects (N=295). All participants completed the Brief Assessment of Cognition in Schizophrenia (BACS) neuropsychological battery. Results Cognitive impairments among psychotic probands, compared to healthy comparison subjects, were progressively greater from bipolar disorder (z=−0.77) to schizoaffective disorder (manic z=−1.08; depressed z=−1.25) to schizophrenia (z=−1.42). Profiles across subtests of the BACS were similar across disorders. Familiality of deficits was significant and comparable in schizophrenia and bipolar disorder. Of particular interest were similar levels of neuropsychological deficits in relatives with elevated cluster A personality traits across proband diagnoses. Nonpsychotic relatives of schizophrenia probands without these personality traits exhibited significant cognitive impairments, while relatives of bipolar probands did not. Conclusions Robust cognitive deficits are present and familial in schizophrenia and psychotic bipolar disorder. Severity of cognitive impairments across psychotic disorders was consistent with a continuum model, in which more prominent affective features and less enduring psychosis were associated with less cognitive impairment. Cognitive dysfunction in first-degree relatives is more closely related to psychosis-spectrum personality disorder traits in psychotic bipolar disorder than in schizophrenia.

Involvement of NRN1 gene in schizophrenia-spectrum and bipolar disorders and its impact on age at onset and cognitive functioning

“…This selective impact of NRN1 on intelligence may suggest its involvement in processes underlying cognitive functioning, which are described to be more quantitatively impaired in SSD (Hill et al 2013). Again, although results did not reach significance after permutation, it is of interest that the haplotypes identified in the present study contain the same haplotype that Chandler et al (2010) described to be associated with better fluid intelligence in schizophrenia patients and not in healthy subjects (SNP10-SNP11: C-A).…”

“…Available evidence also supports that a generalised deficit is present across SSD and BPD, even though quantitative differences may exist (Hill et al 2013). In view of these similarities, the integration of categorical and dimensional approaches has been suggested of particular interest to the complete understanding of psychotic disorders (Peralta and Cuesta 2007).…”

Cognitive impairments in psychotic disorders: common mechanisms and measurement

“…The literature on the comparison of schizoaffective disorder to schizophrenia is mixed, with some studies finding very similar magnitudes of cognitive impairments in these two disorders (108)(109)(110) and others reporting worse impairment in schizophrenia (107,111).…”

Neuroanatomical voxel-based profile of schizophrenia and bipolar disorder

“…However, the Kreaepelian dichotomous conceptualisation of the two disorders has been recently challenged by evidence of an intimate relationship. Indeed, SCZ and BD exhibit considerable overlaps in terms of genetic risk factors (Lichtenstein et al 2009), clinical features (Fischer & Carpenter, 2009), neuropsychological impairment (Hill et al 2013), as well as morphological brain changes compared with healthy controls (HC), including impaired white matter (WM) connectivity (Brambilla et al 2005(Brambilla et al , 2009, ventricular enlargement and global brain volume reduction (Arnone et al 2009). These similarities contribute to raise questions on the degree of distinctiveness of the two disorders.…”