Brain Morphological Characteristics of Cognitive Subgroups of Schizophrenia-Spectrum Disorders and Bipolar Disorder: A Systematic Review with Narrative Synthesis.

Despite a growing body of research, there is yet to be a cohesive synthesis of studies examining differences in brain morphology according to patterns of cognitive function among both schizophrenia-spectrum disorder (SSD) and bipolar disorder (BD) individuals. We aimed to provide a systematic overview of the morphological differences-inclusive of grey and white matter volume, cortical thickness, and cortical surface area-between cognitive subgroups of these disorders and healthy controls, and between cognitive subgroups themselves. An initial search of PubMed and Scopus databases resulted in 1486 articles of which 20 met inclusion criteria and were reviewed in detail. The findings of this review do not provide strong evidence that cognitive subgroups of SSD or BD map to unique patterns of brain morphology. There is preliminary evidence to suggest that reductions in cortical thickness may be more strongly associated with cognitive impairment, whilst volumetric deficits may be largely tied to the presence of disease.

Neurocognitive trajectories and their clinical implications in first-episode schizophrenia after one year of antipsychotic treatment.

Neurocognitive impairment is a core feature of schizophrenia, and patients with first-episode schizophrenia (FES) are optimal candidates for cognitive remediation, but we do not know enough about the incidence, severity and longitudinal changes in neurocognitive impairment in those with FES. This study aimed to assess the neurocognitive trajectories of patients with FES and to compare the clinical and functional outcomes among those with different trajectories. A total of 562 untreated patients with FES completed a neurocognitive test battery and psychopathological and functional assessment. A total of 373 patients attended the follow-up. Group-based trajectory modelling (GBTM) was applied to identify neurocognitive trajectories. Analysis of variance and chi-square tests were conducted to compare demographic characteristics, multiple neurocognitive domains, and clinical and functional outcomes among the different subgroups. We identified three neurocognitive subgroups: preserved (n = 133), mildly to moderately impaired (n = 187) and severely impaired (n = 53). Neurocognitive function in the two impaired subgroups improved within a year but failed to reach the normal level. The processing speed followed trajectories similar to those of overall cognition. The three subgroups did not significantly differ in antipsychotic usage or clinical remission rate. The severely impaired subgroup had poorer functional outcomes than the preserved subgroup, but the mildly to moderately impaired subgroup did not. Patients with FES followed distinct neurocognitive trajectories during the first year of treatment. Patients with severe neurocognitive impairment have poorer functional outcomes, which require and are more likely to benefit from cognitive remediation. Processing speeding is a potential indicator for screening overall cognition.

Cognitive reserve attenuates age-related cognitive decline in the context of putatively accelerated brain ageing in schizophrenia-spectrum disorders.

BACKGROUND: In schizophrenia, relative stability in the magnitude of cognitive deficits across age and illness duration is inconsistent with the evidence of accelerated deterioration in brain regions known to support these functions. These discrepant brain-cognition outcomes may be explained by variability in cognitive reserve (CR), which in neurological disorders has been shown to buffer against brain pathology and minimize its impact on cognitive or clinical indicators of illness. METHODS: Age-related change in fluid reasoning, working memory and frontal brain volume, area and thickness were mapped using regression analysis in 214 individuals with schizophrenia or schizoaffective disorder and 168 healthy controls. In patients, these changes were modelled as a function of CR. RESULTS: Patients showed exaggerated age-related decline in brain structure, but not fluid reasoning compared to controls. In the patient group, no moderation of age-related brain structural change by CR was evident. However, age-related cognitive change was moderated by CR, such that only patients with low CR showed evidence of exaggerated fluid reasoning decline that paralleled the exaggerated age-related deterioration of underpinning brain structures seen in all patients. CONCLUSIONS: In schizophrenia-spectrum illness, CR may negate ageing effects on fluid reasoning by buffering against pathologically exaggerated structural brain deterioration through some form of compensation. CR may represent an important modifier that could explain inconsistencies in brain structure - cognition outcomes in the extant literature.