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Social and environmental factors such as poverty or violence modulate the risk and course of schizophrenia. However, how they affect the brain in patients with psychosis remains unclear.
We studied how environmental factors are related to brain structure in patients with schizophrenia and controls in Latin America, where these factors are large and unequally distributed.
This is a multicentre study of magnetic resonance imaging in patients with schizophrenia and controls from six Latin American cities. Total and voxel-level grey matter volumes, and their relationship with neighbourhood characteristics such as average income and homicide rates, were analysed with a general linear model.
A total of 334 patients with schizophrenia and 262 controls were included. Income was differentially related to total grey matter volume in both groups (P = 0.006). Controls showed a positive correlation between total grey matter volume and income (R = 0.14, P = 0.02). Surprisingly, this relationship was not present in patients with schizophrenia (R = −0.076, P = 0.17). Voxel-level analysis confirmed that this interaction was widespread across the cortex. After adjusting for global brain changes, income was positively related to prefrontal cortex volumes only in controls. Conversely, the hippocampus in patients with schizophrenia, but not in controls, was relatively larger in affluent environments. There was no significant correlation between environmental violence and brain structure.
Our results highlight the interplay between environment, particularly poverty, and individual characteristics in psychosis. This is particularly important for harsh environments such as low- and middle-income countries, where potentially less brain vulnerability (less grey matter loss) is sufficient to become unwell in adverse (poor) environments.
One hypothesis proposed to underlie formal thought disorder (FTD), the incoherent speech is seen in some patients with schizophrenia, is that it reflects impairment in frontal/executive function. While this proposal has received support in neuropsychological studies, it has been relatively little tested using functional imaging. This study aimed to examine brain activations associated with FTD, and its two main factor-analytically derived subsyndromes, during the performance of a working memory task.
Seventy patients with schizophrenia showing a full range of FTD scores and 70 matched healthy controls underwent fMRI during the performance of the 2-back version of the n-back task. Whole-brain corrected, voxel-based correlations with FTD scores were examined in the patient group.
During 2-back performance the patients showed clusters of significant inverse correlation with FTD scores in the inferior frontal cortex and dorsolateral prefrontal cortex bilaterally, the left temporal cortex and subcortically in the basal ganglia and thalamus. Further analysis revealed that these correlations reflected an association only with ‘alogia’ (poverty of speech, poverty of content of speech and perseveration) and not with the ‘fluent disorganization’ component of FTD.
This study provides functional imaging support for the view that FTD in schizophrenia may involve impaired executive/frontal function. However, the relationship appears to be exclusively with alogia and not with the variables contributing to fluent disorganization.
Functional brain activity has been only studied marginally in schizoaffective disorder (SAD), a disorder whose nosological status is controversial. The present study investigated the prefrontal cortex (PFC) activity of schizomanic patients during performance of a working memory task.
13 schizoaffective patients, with current schizomanic episode (Young> 18); and 26 sex- and age-matched healthy controls underwent functional magnetic resonance imaging (fMRI) while performing baseline, 1-back and 2-back versions of the n-back task. Linear models were used to obtain maps of activations and deactivations in the groups.
During performance of the n-back task, controls showed activation in a cluster of frontal areas and de-activation in the medial orbitofrontal and anterior cingulate cortex. The SAD patients showed significantly less activation in prefrontal areas than the controls. They also showed a marked failure to de-activate in medial frontal cortex. The SAD patients’ impaired task performance was associated with both reduced activation of the dorsolateral PFC and reduced de-activation of the medial frontal areas.
Schizomanic patients show failure of activation in a network of cortical regions, and also a failure to de-activate the ventromedial PFC and anterior cingulate cortex. This latter area corresponds to the one of the components of the 'default mode network´. This pattern of abnormality is similar to that found by our group to characterise schizophrenia (failure to activate and failure to de-activate), but different from that which characterises manic patients (failure to de-activate only).
The aim of this pilot study is to assess, in a sample of patients with chemical (alcohol) and behavioural (gambling) dependence, the specifical association between core symptoms and Separation Anxiety Disorder, both in Childhood and in Adulthood.
Materials and methods
After a stabilization period of three months, outpatients with alcohol dependence (n = 30), patological gambling (n = 30) and a control group of anxiety disorders (n = 30) will be assessed with the following psychometric battery:
• SCI-SAS (Structured Clinical Interview for Separation Anxiety) Child and Adult
• SASI (Separation Anxiety Symptom Inventory)
• ASA-27 (Adult Separation Anxiety Questionnaire)
• TCI-R (Temperament anc Character Inventory Revised)
• GAF (Global Assess of Functioning)
• SCL-90-R (Symptom Checklist Revised)
• SOGS (South Oaks Gambling Scale)
• ADS (Alcohol Dependence Scale)
• HAM-A (Hamilton Anxiety Rating Scale)
A preliminary analisys of collected datas (n = 33) shows a strong inter-reliability of the Separation Anxiety Scales (SCI-SAS, SASI and ASA-27) with a p = 0.001 and an association between levels of functioning (GAF) and ASA-27 and SASI scores (p = 0.010 and p = 0,001).
It shows a statistical correlation between ASA-27 and TCI-R: inverse proportion with Self Directness (SD) (p = 0.004) and direct relation with Self Trascendency (ST) (p = 0.003).
Even if the sample is still limited we found an interesting trend between Separation Anxiety symptoms, TCI-R dimensions and core symptoms of dependance. We should focus better, when the study will be over, on narrow and specific sub-analisys that should lead us to a better understanding of the disorders.
Adult Separation Anxiety Disorder (ASAD) is related to greater personal dysfunction and to a reduced sensitivity to conventional treatment, such as cognitive-behavioural therapy or anti-panic drugs, even considering severity of anxiety symptoms, number of co-morbid disorders, socioeconomical status, disease duration, and severity of agoraphobia.
To evaluate separation anxiety, psychiatric co-morbidity, levels of anxiety, character and temperament personality traits, and global functioning, in subjects with anxiety disorders attending a tertiary-level outpatient clinic.
To predict the outcome and customize treatment for anxiety disorders.
After symptom stabilization of one month (T0) 40 patients with anxiety disorders were assessed by means of SCI- SAS, SASI, ASA -27, MINI, HAM- A, TCI-R, GAF. Prospective evaluation is planned at T60 and T180.
According to preliminary cross-sectional data, higher scores of separation anxiety show statistically significant correlations with some domains of the TCI-R; in addition, patients with ASAD show greater psychiatric co-morbidity. No correlations were found between the presence of separation anxiety and levels of anxiety at HAM-A or GAF scores at baseline.
The prospective study of long-term response to treatment is ongoing and the sample will be expanded. The comprehension of anxiety symptoms appraisal in the framework of psychobiological personality characteristics is expected to influence the choice of both pharmacological and psychological therapeutic tools, particularly in patients showing higher levels of dysfunction.
Pathological Gambling (PG) includes extremely different types of game and many gamblers suffer from anxiety disorders. According to the self-medication hypothesis, Gambling Behaviour may be a strategy to tolerate suffering and compensate uneasiness; otherwise social problems related to gambling may lead to anxiety disorders, possibly unmasking an adult form of Separation Anxiety Disorder (SAD).
To investigate possible relationships between PG and SAD, considering the different games, the age of onset, the symptom severity, and the distinction between Adult and Child SAD.
32 gamblers attending an outpatient psychiatric clinic completed the following tests: SOGS and ASI to investigate the kind of gambling, the age of onset and the social conditions of gamblers; SCI-SAS, SASI, ASA-27 to evaluate the Separation Anxiety in childhood and adulthood; HAM-A; GAF.
There are statistically significant correlations between later age of onset of PG and development of SAD in adults. Higher scores in GAF are related to lower scores in Separation Anxiety scales and HAM-A. There is a strong inter-correlation among the Separation Anxiety scales. Higher scores in HAM-A correlate with higher scores in SASI and ASA-27. Male gamblers have an earlier onset and increasing with the age of onset increases the addiction to “dissociative” games instead of “active” ones.
Our preliminary data do not support self-medication hypothesis; possibly, a later-onset gambling is related to a more neurotic and less impulsive psychopathological pattern.
Attention-deficit/hyperactivity disorder (ADHD) is a developmental disorder that persists into adulthood. Though symptoms of inattention and hyperactivity-impulsivity are the two core symptom sets of the disorder, recent reviews argue that emotional dysregulation is an additional feature of ADHD criteria. In the DSM-5 emotional dysregulation does not appear. In a study by the Mental Health Center (MHC) of Arganda, 42 outpatients, all older than 18, we'll look for:
○ Examine the comorbidity of ADHD, in relation to Axis I and personality disorder (PD) from the DSM-IV. In addition, to see if emotional dysregulation is present in these patients.
○ The proposal is that there exist comorbidity with PD, in addition to emotional dysregulation symptoms.
○ Transversal descriptive study of out-patients.
○ A diagnosis of ADHD with: ASRS-V1.1, the ADHD, the CAADID and the WURS scale, reduced version.
○ Emotion dysregulation was assessed by the Impulsivity/Emotional Lability scale from the CAARS and by the DERS and PD with the SCID-II questionary.
A high comorbidity is observed with PD and depressive symptoms. The combined type of ADHD is the most frequently found, with higher severity and frequency of PD. The association with depressive symptoms is more often found in the inattentive subtype and the combined type with substance abuse. Preliminary data is included on emotional dysregulation and ADHD.
ADHD is a disease observed in out-patient adults with a high frequency of comorbidity with PD and depression.
It is necessary to look for the dimension of emotional dysregulation.
Disease surveillance can be made more effective by either improving disease detection, providing cost savings, or doing both. Currently, cattle herds in low-risk areas (LRAs) for bovine tuberculosis (bTB) in England are tested once every 4 years. In Scotland, the default herd testing frequency is also 4 years, but a risk-based system exempts some herds from testing altogether. To extend this approach to other areas, a bespoke understanding of at-risk herds and how risk-based surveillance can affect bTB detection is required. Here, we use a generalized linear mixed model to inform a Bayesian probabilistic model of freedom from infection and explore risk-based surveillance strategies in LRAs and Scotland. Our analyses show that in both areas the primary herd-level risk factors for bTB infection are the size of the herd and purchasing cattle from high-risk areas of Great Britain and/or Ireland. A risk-based approach can improve the current surveillance system by both increasing detection (9% and 7% fewer latent infections), and reducing testing burden (6% and 26% fewer animal tests) in LRAs and Scotland, respectively. Testing at-risk herds more frequently can also improve the level of detection by identifying more infected cases and reducing the hidden burden of the disease, and reduce surveillance effort by exempting low-risk herds from testing.
Understanding the processes that shape parasite diversification, their distribution and abundance provides valuable information on the dynamics and evolution of disease. In this study, we assessed the diversity, distribution, host-specificity and infection patterns of apicomplexan parasites in amphibians and reptiles from Oman, Arabia. Using a quantitative PCR approach we detected three apicomplexan parasites (haemogregarines, lankesterellids and sarcocystids). A total of 13 haemogregarine haplotypes were identified, which fell into four main clades in a phylogenetic framework. Phylogenetic analysis of six new lankesterellid haplotypes revealed that these parasites were distinct from, but phylogenetically related to, known Lankesterella species and might represent new taxa. The percentage of infected hosts (prevalence) and the number of haemogregarines in the blood (parasitaemia) varied significantly between gecko species. We also found significant differences in parasitaemia between haemogregarine parasite lineages (defined by phylogenetic clustering of haplotypes), suggesting differences in host–parasite compatibility between these lineages. For Pristurus rupestris, we found significant differences in haemogregarine prevalence between geographical areas. Our results suggest that host ecology and host relatedness may influence haemogregarine distributions and, more generally, highlight the importance of screening wild hosts from remote regions to provide new insights into parasite diversity.
Relatively few studies have investigated whether relatives of patients with bipolar disorder show brain functional changes, and these have focused on activation changes. Failure of de-activation during cognitive task performance is also seen in the disorder and may have trait-like characteristics since it has been found in euthymia.
A total of 20 euthymic patients with bipolar disorder, 20 of their unaffected siblings and 40 healthy controls underwent functional magnetic resonance imaging during performance of the n-back working memory task. An analysis of variance (ANOVA) was fitted to individual whole-brain maps from each set of patient–relative–matched pair of controls. Clusters of significant difference among the groups were used as regions of interest to compare mean activations/de-activations between them.
A single cluster of significant difference among the three groups was found in the whole-brain ANOVA. This was located in the medial prefrontal cortex, a region of task-related de-activation in the healthy controls. Both the patients and their siblings showed significantly reduced de-activation compared with the healthy controls in this region, but the failure was less marked in the relatives.
Failure to de-activate the medial prefrontal cortex in both euthymic bipolar patients and their unaffected siblings adds to evidence for default mode network dysfunction in the disorder, and suggests that it may act as a trait marker.
In a background of interest in staging models in psychiatry, we tested the validity of a simple staging model of cognitive impairment to predict incident dementia.
A large community sample of adults aged ≥55 years (N = 4803) was assessed in the baseline of a longitudinal, four-wave epidemiological enquiry. A two-phase assessment was implemented in each wave, and the instruments used included the Mini-Mental Status Examination (MMSE); the History and Aetiology Schedule and the Geriatric Mental State-AGECAT. For the standardised degree of cognitive impairment Perneczky et al's MMSE criteria were applied. A panel of psychiatrists diagnosed cases of dementia according to DSM-IV criteria, and cases and sub-cases of dementia were excluded for the follow-up waves. Competing risk regression models, adjusted by potential confounders, were used to test the hypothesised association between MMSE levels and dementia risk.
Out of the 4057 participants followed up, 607 (14.9%) were classified as ‘normal’ (no cognitive impairment), 2672 (65.8%) as ‘questionable’ cognitive impairment, 732 (18.0%) had ‘mild’ cognitive impairment, 38 (0.9%) had ‘moderate’ cognitive impairment and eight (0.2%) had ‘severe’ impairment.
Cognitive impairment was associated with risk of dementia, the risk increasing in parallel with the level of impairment (hazard ratio: 2.72, 4.78 and 8.38 in the ‘questionable’, ‘mild’ and ‘moderate’ level of cognitive impairment, respectively).
The documented gradient of increased risk of dementia associated with the severity level of cognitive impairment supports the validity of the simple staging model based on the MMSE assessment.
Functional imaging studies in relatives of schizophrenic patients have had inconsistent findings, particularly with respect to altered dorsolateral prefrontal cortex activation. Some recent studies have also suggested that failure of deactivation may be seen.
A total of 28 patients with schizophrenia, 28 of their siblings and 56 healthy controls underwent functional magnetic resonance imaging during performance of the n-back working memory task. An analysis of variance was fitted to individual whole-brain maps from each set of patient–relative–matched pair of controls. Clusters of significant difference among the groups were then used as regions of interest to compare mean activations and deactivations among the groups.
In all, five clusters of significant differences were found. The schizophrenic patients, but not the relatives, showed reduced activation compared with the controls in the lateral frontal cortex bilaterally, the left basal ganglia and the cerebellum. In contrast, both the patients and the relatives showed significant failure of deactivation compared with the healthy controls in the medial frontal cortex, with the relatives also showing less failure than the patients. Failure of deactivation was not associated with schizotypy scores or presence of psychotic-like experiences in the relatives.
Both schizophrenic patients and their relatives show altered task-related deactivation in the medial frontal cortex. This in turn suggests that default mode network dysfunction may function as a trait marker for schizophrenia.
To test the hypothesis that cognitive impairment in older adults is associated with all-cause mortality risk and the risk increases when the degree of cognitive impairment augments; and then, if this association is confirmed, to report the population-attributable fraction (PAF) of mortality due to cognitive impairment.
A representative random community sample of individuals aged over 55 was interviewed, and 4557 subjects remaining alive at the end of the first year of follow-up were included in the analysis. Instruments used in the assessment included the Mini-Mental Status Examination (MMSE), the History and Aetiology Schedule (HAS) and the Geriatric Mental State (GMS)-AGECAT. For the standardised degree of cognitive impairment Perneczky et al's MMSE criteria were applied. Mortality information was obtained from the official population registry. Multivariate Cox proportional hazard models were used to test the association between MMSE degrees of cognitive impairment and mortality risk. We also estimated the PAF of mortality due to specific MMSE stages.
Cognitive impairment was associated with mortality risk, the risk increasing in parallel with the degree of cognitive impairment (Hazard ratio, HR: 1.18 in the ‘mild’ degree of impairment; HR: 1.29 in the ‘moderate’ degree; and HR: 2.08 in the ‘severe’ degree). The PAF of mortality due to severe cognitive impairment was 3.49%.
A gradient of increased mortality-risk associated with severity of cognitive impairment was observed. The results support the claim that routine assessment of cognitive function in older adults should be considered in clinical practice.
The subgenual anterior cingulate cortex (sgACC) is considered to be an important site of abnormality in major depressive disorder. However, structural alterations in this region have not been a consistent finding and functional imaging studies have also implicated additional areas.
A total of 32 patients with major depressive disorder, currently depressed, and 64 controls underwent structural imaging with MRI. Also, 26 patients and 52 controls were examined using functional magnetic resonance imaging (fMRI) during performance of the n-back working memory task. Structural and functional changes were evaluated using whole-brain, voxel-based methods.
The depressed patients showed volume reductions in the sgACC and orbitofrontal cortex bilaterally, plus in both temporal poles and the hippocampus/parahippocampal gyrus on the left. Functional imaging revealed task-related hypoactivation in the left lateral prefrontal cortex and other regions, as well as failure of deactivation in a subcallosal medial frontal cortical area which included the sgACC.
Whole-brain, voxel-based analysis finds evidence of both structural and functional abnormality in the sgACC in major depressive disorder. The fact that the functional changes in this area took the form of failure of deactivation adds to previous findings of default mode network dysfunction in the disorder.
Cognitive–behavioural therapy (CBT) is considered to be effective for the symptoms of schizophrenia. However, this view is based mainly on meta-analysis, whose findings can be influenced by failure to consider sources of bias.
To conduct a systematic review and meta-analysis of the effectiveness of CBT for schizophrenic symptoms that includes an examination of potential sources of bias.
Data were pooled from randomised trials providing end-of-study data on overall, positive and negative symptoms. The moderating effects of randomisation, masking of outcome assessments, incompleteness of outcome data and use of a control intervention were examined. Publication bias was also investigated.
Pooled effect sizes were −0.33 (95% CI −0.47 to −0.19) in 34 studies of overall symptoms, −0.25 (95% CI −0.37 to −0.13) in 33 studies of positive symptoms and −0.13 (95% CI −0.25 to −0.01) in 34 studies of negative symptoms. Masking significantly moderated effect size in the meta-analyses of overall symptoms (effect sizes −0.62 (95% CI −0.88 to −0.35) v. −0.15 (95% CI −0.27 to −0.03), P = 0.001) and positive symptoms (effect sizes −0.57 (95% CI −0.76 to −0.39) v. −0.08 (95% CI −0.18 to 0.03), P<0.001). Use of a control intervention did not moderate effect size in any of the analyses. There was no consistent evidence of publication bias across different analyses.
Cognitive–behavioural therapy has a therapeutic effect on schizophrenic symptoms in the ‘small’ range. This reduces further when sources of bias, particularly masking, are controlled for.
Mesoporous materials have typical average pore diameters in the range 20 – 500 Å, which are usually accompanied by high specific surface area (ABET) and large pore volume (Vp) with narrow pore size distributions. These features are very attractive for potential application as catalysts and adsorbents. Mesoporous materials are usually prepared by soft templating or nanocasting process. The latter approach is based on the replication of hard-templates, such as mesoporous silica (e.g. SBA-15), being a very flexible and suitable method to obtain stable and predictable pore mesostructures. However, the chemical compatibility between the template and the precursors must be ensured.
Schizo-affective disorder has not been studied to any significant extent using functional imaging. The aim of this study was to examine patterns of brain activation and deactivation in patients meeting strict diagnostic criteria for the disorder.
Thirty-two patients meeting Research Diagnostic Criteria (RDC) for schizo-affective disorder (16 schizomanic and 16 schizodepressive) and 32 matched healthy controls underwent functional magnetic resonance imaging (fMRI) during performance of the n-back task. Linear models were used to obtain maps of activations and deactivations in the groups.
Controls showed activation in a network of frontal and other areas and also deactivation in the medial frontal cortex, the precuneus and the parietal cortex. Schizo-affective patients activated significantly less in prefrontal, parietal and temporal regions than the controls, and also showed failure of deactivation in the medial frontal cortex. When task performance was controlled for, the reduced activation in the dorsolateral prefrontal cortex (DLPFC) and the failure of deactivation of the medial frontal cortex remained significant.
Schizo-affective disorder shows a similar pattern of reduced frontal activation to schizophrenia. The disorder is also characterized by failure of deactivation suggestive of default mode network dysfunction.
Deficits in memory and executive performance are well-established features of bipolar disorder and schizophrenia. By contrast, data on cognitive impairment in schizoaffective disorder are scarce and the findings are conflicting.
We used the Wechsler Memory Scale (WMS-III) and the Behavioural Assessment of the Dysexecutive Syndrome (BADS) to test memory and executive function in 45 schizophrenic patients, 26 schizomanic patients and 51 manic bipolar patients in comparison to 65 healthy controls. The patients were tested when acutely ill.
All three patient groups performed significantly more poorly than the controls on global measures of memory and executive functioning, but there were no differences among the patient groups. There were few differences in memory and executive function subtest scores within the patient groups. There were no differences in any test scores between manic patients with and without psychotic symptoms.
Schizophrenic, schizomanic and manic patients show a broadly similar degree of executive and memory deficits in the acute phase of illness. Our results do not support a categorical differentiation across different psychotic categories with regard to neuropsychological deficits.
It is not known whether first-episode psychosis is characterized by the same prefrontal cortex functional imaging abnormalities as chronic schizophrenia.
Thirty patients with a first episode of non-affective functional psychosis and 28 healthy controls underwent functional magnetic resonance imaging (fMRI) during performance of the n-back working memory task. Voxel-based analyses of brain activations and deactivations were carried out and compared between groups. The connectivity of regions of significant difference between the patients and controls was also examined.
The first-episode patients did not show significant prefrontal hypo- or hyperactivation compared to controls. However, they showed failure of deactivation in the medial frontal cortex. This area showed high levels of connectivity with the posterior cingulate gyrus/precuneus and parts of the parietal cortex bilaterally. Failure of deactivation was significantly greater in first-episode patients who had or went on to acquire a DSM-IV diagnosis of schizophrenia than in those who did not, and in those who met RDC criteria for schizophrenia compared to those who did not.
First-episode psychosis is not characterized by hypo- or hyperfrontality but instead by a failure of deactivation in the medial frontal cortex. The location and connectivity of this area suggest that it is part of the default mode network. The failure of deactivation seems to be particularly marked in first-episode patients who have, or progress to, schizophrenia.