Publications by authors named "Fiona Toal"

It has been suggested that the restricted, stereotyped and repetitive behaviours typically found in autism are underpinned by deficits of inhibitory control. The biological basis of this is unknown but may include differences in the modulatory role of neurotransmitters, such as serotonin, which are implicated in the condition. However, this has never been tested directly.

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Context: People with autism spectrum disorders (ASDs) have lifelong deficits in social behavior and differences in behavioral as well as neural responses to facial expressions of emotion. The biological basis to this is incompletely understood, but it may include differences in the role of neurotransmitters such as serotonin, which modulate facial emotion processing in health. While some individuals with ASD have significant differences in the serotonin system, to our knowledge, no one has investigated its role during facial emotion processing in adults with ASD and control subjects using acute tryptophan depletion (ATD) and functional magnetic resonance imaging.

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Fragile X Syndrome (FraX) is caused by the expansion of a single trinucleotide gene sequence (CGG) on the X chromosome, and is a leading cause of learning disability (mental retardation) worldwide. Relatively few studies, however, have examined the neuroanatomical abnormalities associated with FraX. Of those that are available many included mixed gender populations, combined FraX children and adults into one sample, and employed manual tracing techniques which measures bulk volume of particular regions.

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Introduction: Acute tryptophan depletion (ATD) temporarily lowers brain serotonin (5-HT) synthesis, and behavioral studies have shown that this alters the processing of facial expressions of emotion.

Materials And Methods: The neural basis for these alterations is not known. Therefore, we employed ATD and event-related functional magnetic resonance imaging (fMRI) to examine neural responses during incidental processing of fearful, happy, sad, and disgusted facial expressions.

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People with obsessive-compulsive disorder (OCD) have abnormalities in cognitive and motor inhibition, and it has been proposed that these are related to dysfunction of fronto-striatal circuits. However, nobody has investigated neuro-functional abnormalities during a range of inhibition tasks in adults with OCD. The aims of the study were to compare brain activation of people with OCD and controls during three tasks of inhibitory control.

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Background: Autism-spectrum disorder is increasingly recognised, with recent studies estimating that 1% of children in South London are affected. However, the biology of comorbid mental health problems in people with autism-spectrum disorder is poorly understood.

Aims: To investigate the brain anatomy of people with autism-spectrum disorder with and without psychosis.

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Background: We investigated structural brain morphology of intellectually disabled children with Williams (WS) syndrome and its relationship to the behavioural phenotype.

Methods: We compared the neuroanatomy of 15 children (mean age:13+/-2) with WS and 15 age/gender-matched healthy children using a manual region-of-interest analysis to measure bulk (white+grey) tissue volumes and unbiased fully-automated voxel-based morphometry to assess differences in grey/white matter throughout the brain. Ratings of abnormal behaviours were correlated with brain structure.

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Background: 22q11.2 deletion syndrome (22q11DS) is associated with intellectual disability, poor social interaction and a high prevalence of psychosis. However, to date there have been no studies comparing cognition and neuroanatomical characteristics of 22q11DS with other syndromes to investigate if the cognitive strengths and difficulties and neuroanatomical differences associated with 22q11DS are specific to the syndrome.

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Background: Our understanding of anatomical differences in people with autistic-spectrum disorder, is based on mixed-gender or male samples.

Aims: To study regional grey-matter and white-matter differences in the brains of women with autistic-spectrum disorder.

Method: We compared the brain anatomy of 14 adult women with autistic-spectrum disorder with 19 controls using volumetric magnetic resonance imaging and voxel-based morphometry.

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Background: People with Asperger syndrome (AS) have life-long deficits in social behavior. The biological basis of this is unknown, but most likely includes impaired processing of facial emotion. Human social communication involves processing different facial emotions, and at different intensities.

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Objective: The neural basis for autistic spectrum disorders is unclear, but abnormalities in the development of limbic areas and of glutamate have been suggested. Proton magnetic resonance spectroscopy ((1)H-MRS) can be used to measure the concentration of brain metabolites. However, the concentration of glutamate/glutamine in brain regions implicated in autistic spectrum disorders has not yet been examined in vivo.

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In people with velo-cardio-facial syndrome [or 22q11.2 deletion syndrome (22qDS)], a single interstitial deletion of chromosome 22q11.2 causes a wide spectrum of cognitive deficits ranging from global learning difficulties to specific cognitive deficits.

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Autistic-spectrum disorder is approximately half as common as schizophrenia but its cause remains unknown. Recent studies have begun to clarify the underlying neuroanatomical abnormalities and brain-behaviour relationships in autism. In the past decade, great advances have been made in our understanding of the neurobiological basis of autism.

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