To explore the links between neuropsychological performance, diagnostic category and duration of illness in subjects with psychotic and affective disorders.

Memory and executive abilities were tested in consecutively admitted patients with schizophrenia (N = 20), other non-schizophrenic psychotic disorders (N = 29), bipolar disorder (N = 33) and major depression (N = 19).

Subjects with schizophrenia had poorer global memory performances than subjects with major depression, and poorer delayed verbal memory abilities than those from the other three diagnostic groups. Executive abilities explored by the Stroop test and the Wisconsin Card Sorting Test did not differ between diagnostic groups. Neuropsychological performances were not influenced by previous duration of illness.

Memory deficits are the most discriminatory cognitive features between subjects with schizophrenia and those with other psychotic or mood disorders. The fact that cognitive deficits are static whatever the diagnostic group indirectly suggests that they may have a neurodevelopmental origin in subjects with schizophrenia, but perhaps also in subjects with other psychotic and mood disorders.

In the past decade, network analysis (NA) has been applied to psychopathology to quantify complex symptom relationships. This statistical technique has demonstrated much promise, as it provides researchers the ability to identify relationships across many symptoms in one model and can identify central symptoms that may predict important clinical outcomes. However, network models are highly influenced by node selection, which could limit the generalizability of findings. The current study (N = 6850) tests a comprehensive, cognitive–behavioral model of eating-disorder symptoms using items from two, widely used measures (Eating Disorder Examination Questionnaire and Eating Pathology Symptoms Inventory).

We used NA to identify central symptoms and compared networks across the duration of illness (DOI), as chronicity is one of the only known predictors of poor outcome in eating disorders (EDs).

Our results suggest that eating when not hungry and feeling fat were the most central symptoms across groups. There were no significant differences in network structure across DOI, meaning the connections between symptoms remained relatively consistent. However, differences emerged in central symptoms, such that cognitive symptoms related to overvaluation of weight/shape were central in individuals with shorter DOI, and behavioral central symptoms emerged more in medium and long DOI.

Our results have important implications for the treatment of individuals with enduring EDs, as they may have a different core, maintaining symptoms. Additionally, our findings highlight the importance of using comprehensive, theoretically- or empirically-derived models for NA.

Brain structure alterations have been reported in anorexia nervosa, but findings have been inconsistent. This may be due to inadequate sample size, sample heterogeneity or differences in methodology.

High resolution magnetic resonance images were acquired of 33 adult participants with anorexia nervosa and 33 healthy participants, the largest study sample to date, in order to assess whole-brain volume, ventricular cerebrospinal fluid, white matter and grey matter volume. Voxel-based morphometry was conducted to assess regional grey matter volume. Levels of depression, anxiety, obsessionality and eating disorder-related symptoms were measured and used to explore correlations with brain structure.

Participants with anorexia nervosa had smaller brain volumes as well as a global decrease in grey matter volume with ventricular enlargement. Voxel-based morphometry revealed a decrease in grey matter volume spanning across the cerebellum, temporal, frontal and occipital lobes. A correlation was found between grey matter volume loss and duration of illness in the cerebellum and mesencephalon. No correlations were found with clinical measures.

Findings are in accordance with several previous studies on brain structure and match functional studies that have assessed the symptomatology of anorexia nervosa, such as body image distortion and cognitive bias to food. The correlation with duration of illness supports the implication of cerebellar atrophy in the maintenance of low weight and disrupted eating behaviour and illustrates its role in the chronic phase of anorexia nervosa. The lack of other correlations suggests that these findings are not related to the presence of co-morbid disorders.

Several studies have shown cortical volume loss in frontotemporal regions in schizophrenia patients, and it is known that these reductions may be associated with disease symptoms and cognitive deficits. The aim of this study was to investigate possible cortical thickness correlations in frontotemporal regions in relation to age at onset and duration of illness.

One hundred forty-eight schizophrenia patients (97 males; age and SD 36.30 ± 10.06) and 87 (57 males; age and SD 36.48 ± 10.10) age-matched healthy subjects underwent a brain MRI scan. Cortical segmentation and surface statistical analysis were performed using the FreeSurfer software package. Results were corrected for multiple comparisons using the Monte Carlo method considering a cluster-corrected Type I Error of 5%.

Compared to controls, schizophrenia patients presented significant cortical thinning in the frontotemporal, parietal, and occipital cortices. No correlation between prefrontal cortex thickness and duration of illness in patients with schizophrenia or between frontotemporal cortical thickness and age at onset was found. However, a significant interaction between age and diagnosis was observed on frontal cortical thickness with patients presenting a thinner cortex than expected for age.

Although there was no correlation between age of onset and duration of illness with brain volume, our findings suggest that there is an accelerated cortical loss in schizophrenia, thus reinforcing the progressive processes of the disease.

Predicting cognitive deficits in early psychosis may well be crucial to identify those individuals most in need of receiving intensive intervention. As yet, however, the identification of potential pretreatment predictors for cognitive performance has been hampered by inconsistent findings across studies. We aimed to examine the associations of functional and clinical pretreatment variables with cognitive functioning after a first psychotic episode.

One hundred and thirty-one patients experiencing first-episode psychosis were assessed for psychopathology, pre-morbid functioning, duration of illness, age of onset, and family history of psychosis and neurocognitive functioning. Multiple regression analyses were conducted for six basic cognitive dimensions known to be affected in this population: verbal learning, verbal memory, verbal comprehensive abilities, executive functioning, motor dexterity and sustained attention.

Pre-morbid functioning was the main predictor for five out of the six basic cognitive domains. Pre-morbid social adjustment difficulties were associated with worse performance in executive functioning, motor dexterity and sustained attention. Academic functioning was associated with verbal comprehension, and verbal learning and memory. Gender, age of onset, duration of untreated psychosis, and family history of psychosis had no or limited value as predictors of neurocognitive outcome.

Poor pre-morbid functioning was related to a worse performance in the six basic cognitive dimensions evaluated; however, this accounted for only a small amount of the explained variance. Cognitive impairment is a prominent feature in patients with early psychosis regardless of favorable prognostic features such as short duration of illness, female gender, later age of onset, and non-family history of psychosis.