Psychological trauma, mood and social isolation do not explain elevated dissociation in functional neurological disorder (FND)

Functional Neurological Disorder (FND) results in altered motor, sensory and cognitive function in the absence of evident organic disease. It often co-occurs alongside dissociative disorders and dissociation has been found to be high in patients across FND subtypes (particularly in those with Non-Epileptic Attack Disorder; NEADs). However, the presence of dissociation in FND is varied and there are contradictory definitions and suggestions for elevated levels. Here, three studies show that dissociation is a prominent, defining feature of people with FND compared to those who are healthy or have other, similar long-term health conditions, and that this heightened dissociation is not explained by a history of trauma (study 1, N = 121), mood (study 2, N = 589) and is not associated with social isolation/social exclusion (study 3, N = 542). As dissociation appeared to occur in FND in the absence of the usual contributing factors, and as higher levels of dissociation were associated with increased disability and illness impacts, understanding its role is of fundamental importance to developing our understanding of FND. These findings have further applications, beyond the theoretical, in clinical settings and in research; the implications for further research are discussed

Neural changes following cognitive behaviour therapy for psychosis: A longitudinal study

A growing body of evidence demonstrates that persistent positive symptoms, particularly delusions, can be improved by cognitive behaviour therapy for psychosis. Heightened perception and processing of threat are believed to constitute the genesis of delusions. The present study aimed to examine functional brain changes following cognitive behaviour therapy for psychosis. The study involved 56 outpatients with one or more persistent positive distressing symptoms of schizophrenia. Twenty-eight patients receiving cognitive behaviour therapy for psychosis for 6–8 months in addition to their usual treatment were matched with 28 patients receiving treatment as usual. Patients’ symptoms were assessed by a rater blind to treatment group, and they underwent functional magnetic resonance imaging during an affect processing task at baseline and end of treatment follow-up. The two groups were comparable at baseline in terms of clinical and demographic parameters and neural and behavioural responses to facial and control stimuli. The cognitive behaviour therapy for psychosis with treatment-as-usual group (22 subjects) showed significant clinical improvement compared with the treatment-as-usual group (16 subjects), which showed no change at follow-up. The cognitive behaviour therapy for psychosis with treatment-as-usual group, but not the treatment-as-usual group, showed decreased activation of the inferior frontal, insula, thalamus, putamen and occipital areas to fearful and angry expressions at treatment follow-up compared with baseline. Reduction of functional magnetic resonance imaging response during angry expressions correlated directly with symptom improvement. This study provides the first evidence that cognitive behaviour therapy for psychosis attenuates brain responses to threatening stimuli and suggests that cognitive behaviour therapy for psychosis may mediate symptom reduction by promoting processing of threats in a less distressing way

Smooth pursuit and antisaccade eye movements in siblings discordant for schizophrenia

Smooth pursuit eye movement (SPEM) and antisaccade deficits have been proposed as endophenotypes in the search for schizophrenia genes. We assessed these measures in 24 schizophrenia patients, 24 of their healthy siblings, and 24 healthy controls closely matched to the siblings. Between-group differences were assessed using a random effects regression model taking into account the relatedness between patients and siblings. Patients showed reduced SPEM gain, increased frequency of saccades during pursuit, increased antisaccade error rate, and reduced antisaccade gain compared to controls. Siblings performed intermediate, i.e. between patients and controls, on most measures, but were particularly characterised by reduced antisaccade gain. SPEM gain at one target velocity was significantly correlated between patients and siblings, highlighting the necessity of taking into account within-family correlations in the statistical analysis of between-group differences. It is concluded that subtle SPEM and antisaccade deficits are observed in clinically unaffected siblings of schizophrenia patients; these deficits may be useful markers of genetic liability to schizophrenia