[Show abstract][Hide abstract] ABSTRACT: Sensory processing abnormalities are common in autism spectrum disorders (ASD), and now form part of the Diagnostic and Statistical Manual 5th Edition (DSM-5) diagnostic criteria, but it is unclear whether they characterize the 'broader phenotype' of the disorder. We recruited adults (n = 772) with and without an ASD and administered the Autism Quotient (AQ) along with the Adult/Adolescent Sensory Profile (AASP), the Cardiff Anomalous Perceptions Scale (CAPS), and the Glasgow Sensory Questionnaire (GSQ), all questionnaire measures of abnormal sensory responsivity. Autism traits were significantly correlated with scores on all three sensory scales (AQ/GSQ r = 0.478; AQ/AASP r = 0.344; AQ/CAPS r = 0.333; all p < 0.001). This relationship was linear across the whole range of AQ scores and was true both in those with, and without, an ASD diagnosis. It survived correction for anxiety trait scores, and other potential confounds such as mental illness and migraine.
Journal of Autism and Developmental Disorders 12/2013;
[Show abstract][Hide abstract] ABSTRACT: Emotion, memories and behaviour depend on the coordinated activities of regions connected by the limbic system. Here, we propose an update of the limbic model based on the seminal work of Papez, Yakovlev and MacLean. In the revised model we identify three distinct but partially overlapping networks: i) the hippocampal-diencephalic-retrosplenial network dedicated to memory and spatial orientation; ii) The temporo-amygdala-orbitofrontal network for the integration of visceral sensation and emotion with semantic memory and behaviour; iii) the default-mode network involved in autobiographical memories and introspective self-directed thinking. The three networks share cortical nodes that are emerging as principal hubs in connectomic analysis. This revised network model of the limbic system reconciles recent functional imaging findings with anatomical accounts of clinical disorders commonly associated with limbic pathology.
Limbic system, tractography, white matter connections, brain networks, emotion, memory, amnesia, dementia, antisocial behaviour, schizophrenia, depression, bipolar disorder, obsessive-compulsive disorder, autism spectrum disorder.
[Show abstract][Hide abstract] ABSTRACT: The frontal aslant tract is a direct pathway connecting Broca's region with the anterior cingulate and pre-supplementary motor area. This tract is left lateralized in right-handed subjects, suggesting a possible role in language. However, there are no previous studies that have reported an involvement of this tract in language disorders. In this study we used diffusion tractography to define the anatomy of the frontal aslant tract in relation to verbal fluency and grammar impairment in primary progressive aphasia. Thirty-five patients with primary progressive aphasia and 29 control subjects were recruited. Tractography was used to obtain indirect indices of microstructural organization of the frontal aslant tract. In addition, tractography analysis of the uncinate fasciculus, a tract associated with semantic processing deficits, was performed. Damage to the frontal aslant tract correlated with performance in verbal fluency as assessed by the Cinderella story test. Conversely, damage to the uncinate fasciculus correlated with deficits in semantic processing as assessed by the Peabody Picture Vocabulary Test. Neither tract correlated with grammatical or repetition deficits. Significant group differences were found in the frontal aslant tract of patients with the non-fluent/agrammatic variant and in the uncinate fasciculus of patients with the semantic variant. These findings indicate that degeneration of the frontal aslant tract underlies verbal fluency deficits in primary progressive aphasia and further confirm the role of the uncinate fasciculus in semantic processing. The lack of correlation between damage to the frontal aslant tract and grammar deficits suggests that verbal fluency and grammar processing rely on distinct anatomical networks.
[Show abstract][Hide abstract] ABSTRACT: Dysfunctional glutamatergic neurotransmission has been implicated in autism spectrum disorder (ASD). However, relatively few studies have directly measured brain glutamate in ASD adults, or related variation in glutamate to clinical phenotype. We therefore set out to investigate brain glutamate levels in adults with an ASD, comparing these to healthy controls and also comparing results between individuals at different points on the spectrum of symptom severity. We recruited 28 adults with ASD and 14 matched healthy controls. Of those with ASD, 15 fulfilled the 'narrowly' defined criteria for typical autism, whereas 13 met the 'broader phenotype'. We measured the concentration of the combined glutamate and glutamine signal (Glx), and other important metabolites, using proton magnetic resonance spectroscopy in two brain regions implicated in ASD-the basal ganglia (including the head of caudate and the anterior putamen) and the dorsolateral prefrontal cortex-as well as in a parietal cortex 'control' region. Individuals with ASD had a significant decrease (P<0.001) in concentration of Glx in the basal ganglia, and this was true in both the 'narrow' and 'broader' phenotype. Also, within the ASD sample, reduced basal ganglia Glx was significantly correlated with increased impairment in social communication (P=0.013). In addition, there was a significant reduction in the concentration of other metabolites such as choline, creatine (Cr) and N-acetylaspartate (NAA) in the basal ganglia. In the dorsolateral prefrontal cortex, Cr and NAA were reduced (P<0.05), although Glx was not. There were no detectable differences in Glx, or any other metabolite, in the parietal lobe control region. There were no significant between-group differences in age, gender, IQ, voxel composition or data quality. In conclusion, individuals across the spectrum of ASD have regionally specific abnormalities in subcortical glutamatergic neurotransmission that are associated with variation in social development.
[Show abstract][Hide abstract] ABSTRACT: In responding to high levels of psychiatric morbidity amongst prisoners and recognising earlier poor quality prison mental health care, prison mental health in-reach teams have been established in England and Wales over the last decade. They are mostly provided by the National Health Service (NHS), which provides the majority of UK healthcare services. Over the same period, the prison population has grown to record levels, such that prisons in England and Wales now contain almost 90,000 of the world's overall prison population of over 10million people (roughly the size of Paris or Istanbul). This study provides an overview of mental health in-reach services in prisons in England and Wales, including variations between them, through a telephone survey of senior staff in all prisons and young offender institutions in England and Wales. 73% of prisons took part; of them 13% had no in-reach team at all (usually low security establishments) and the majority of services were run by NHS teams, usually according to a generic community mental health team (CMHT) model rather than other specialist models. Team size was unrelated to prison size. Each nurse covered around 500 prisoners, each doctor over 3700. Many provided few or no healthcare cells and 24-h psychiatric cover (including on-call cover) was uncommon. Despite developments in recent years, mental health in-reach services still fall short of community equivalence and there is wide variation in service arrangements that cannot be explained by prison size or function. The aim of community equivalence has not yet been reached in prison healthcare and a more sophisticated measure of service improvement and standardisation would now be useful to drive and monitor future development.
International Journal of Law and Psychiatry 05/2013;
[Show abstract][Hide abstract] ABSTRACT: Borderline personality disorder (BPD) is a common, debilitating disorder for which the evidence base for treatment is modest. This case series aimed to explore preliminary evidence of clozapine's effectiveness for patients with severe BPD.
We examined the case notes of 22 female inpatients with a primary diagnosis of BPD who had started treatment with clozapine. Baseline routine clinical data were extracted from the records and at 6 monthly intervals thereafter, up to a maximum of 18 months after starting treatment. Patients also were interviewed about their experiences.
We found evidence for a beneficial effect of clozapine across several clinical domains. Symptom severity, need for enhanced observations, use of additional medication, and the number of aggressive incidents all significantly improved after clozapine. The greatest improvements appeared within the first 6 months of initiating treatment. There also was a significant increase in weight.
The results suggest that clozapine, with suitable health monitoring, may be beneficial for this clinical population. Larger, randomized, blinded, and controlled prospective studies are needed to confirm these findings.
Annals of Clinical Psychiatry 05/2013; 25(2):125-34.
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