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We examined demographic, clinical, and psychological characteristics of a large cohort (n = 368) of adults with dissociative seizures (DS) recruited to the CODES randomised controlled trial (RCT) and explored differences associated with age at onset of DS, gender, and DS semiology.
Prior to randomisation within the CODES RCT, we collected demographic and clinical data on 368 participants. We assessed psychiatric comorbidity using the Mini-International Neuropsychiatric Interview (M.I.N.I.) and a screening measure of personality disorder and measured anxiety, depression, psychological distress, somatic symptom burden, emotional expression, functional impact of DS, avoidance behaviour, and quality of life. We undertook comparisons based on reported age at DS onset (<40 v. ⩾40), gender (male v. female), and DS semiology (predominantly hyperkinetic v. hypokinetic).
Our cohort was predominantly female (72%) and characterised by high levels of socio-economic deprivation. Two-thirds had predominantly hyperkinetic DS. Of the total, 69% had ⩾1 comorbid M.I.N.I. diagnosis (median number = 2), with agoraphobia being the most common concurrent diagnosis. Clinical levels of distress were reported by 86% and characteristics associated with maladaptive personality traits by 60%. Moderate-to-severe functional impairment, high levels of somatic symptoms, and impaired quality of life were also reported. Women had a younger age at DS onset than men.
Our study highlights the burden of psychopathology and socio-economic deprivation in a large, heterogeneous cohort of patients with DS. The lack of clear differences based on gender, DS semiology and age at onset suggests these factors do not add substantially to the heterogeneity of the cohort.
The results of one randomised control trial testing a psychological rehabilitation programme aimed at information processing strategies showed improvements in cognition post-treatment.
To determine whether there are concomitant brain activation changes as a result of engaging in cognitive remediation therapy (CRT).
Three groups (patients receiving control therapyor CRT and a healthy control group) were investigated in a repeated measures design using the two-back test. Functional magnetic resonance imaging (fMRI) data and a broad assessment of executive functioning were completed at baseline and post-treatment. Brain activation changes were identified after accounting for possible task-correlated motion artefact.
fMRI analyses indicate that the control group showed decreased activation butthetwo patient groups showed an increase in activation over time. The patient group that received successful CRT had significantly increased brain activation in regions associated with working memory particularly the frontocortical areas.
This isthefirsttimethat brain activation changes in a seriously disabled group of patients with schizophrenia can be associated clearly with psychological rather than pharmacological therapy.
The association between temporal lobe epilepsy and schizophrenia suggests that the critical abnormality may be pathology within the temporal lobes. People with schizophrenia-like psychosis of epilepsy (SLPE) provide a useful group in which to examine the importance of temporal and frontal lobe dysfunction in schizophrenia.
A verbal fluency activation paradigm and a 99mTc HMPAO SPET were used to study frontotemporal function in people with SLPE (n = 12), schizophrenia (n = 11) and epilepsy (n = 16).
People with SLPE differed from both other groups by showing lower blood flow in the left superior temporal gyrus during performance of a verbal fluency task compared with a word repetition task (F=5.4, P=0.01). During the verbal fluency task people with primary schizophrenia showed a greater increase in blood flow in anterior cingulate (F=4.5, P=0.02) than the other two groups. There were no between-group differences in frontal brain regions.
Our findings support an association between left temporal lobe abnormality and SLPE. The different patterns of activation observed in people with primary schizophrenia and SLPE suggests that different pathophysiological mechanisms may operate in these two groups. In SLPE the pathophysiology may be relatively confined to the dominant temporal lobe.
The growth hormone (GH) response to apomorphine, thought to reflect central dopaminergic receptor sensitivity, has been reported as enhanced in acute schizophrenia. We investigated this response in relation to the psychotic episodes associated with Parkinson's disease (PD).
The GH response to apomorphine was measured in three groups of patients with Parkinson's disease: those currently psychotic (n = 9), those with a past history of psychosis (n = 7) and those who had never been psychotic (n = 8).
Apomorphine-induced GH response was not related to psychosis but was unexpectedly associated with measures of depression.
Visual hallucinations were a prominent feature in the psychotic patients and the atypical nature of these psychoses might explain why we found no evidence of dopaminergic sensitivity. Serotonergic dysfunction would be in keeping with this. Dopaminergic mechanisms may contribute to the minor depressive symptomatology seen in PD.
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