Tardive dyskinesia (TD) is a persistent hyperkinetic movement disorder associated with dopamine receptor blocking agents including antipsychotic medications. Although uncertainty and concern about this drug side effect have vacillated since its initial recognition 60 years ago, recent commercial interest in developing effective treatments has rekindled scientific and clinical interest after a protracted period of neglect. Although substantial research has advanced knowledge of the clinical features and epidemiology of TD, many fundamental questions raised by early investigators remain unresolved.
View Article and Find Full Text PDFIntroduction: The study aim was to describe behaviours associated with autistic traits.
Methods: The Childhood Behaviour Checklist (CBCL) and Social Communication Questionnaire (SCQ) were used as measures of behaviour and autistic traits respectively in 331 adolescents receiving educational support. CBCL scores were compared between three groups defined by SCQ score: autism, pervasive developmental disorder (PDD) and non-PDD.
Background: Existing studies of brain structural changes before the onset of schizophrenia have considered individuals with either familial risk factors or prodromal symptomatology. We aimed to determine whether findings from these studies are also applicable to those at enhanced risk of developing schizophrenia for another reason-intellectual impairment.
Methods: Participants with intellectual impairment (mean IQ: 78.
Am J Med Genet B Neuropsychiatr Genet
December 2010
A single nucleotide polymorphism (val66met) in the brain derived neurotrophic factor (BDNF) gene has been shown to be a risk factor for a number of psychiatric disorders, including schizophrenia. This polymorphism has also been shown to have effects on prefrontal brain morphology and function. This study aims to clarify the effects of the val66met polymorphism on prefrontal brain function in a population at high genetic risk for schizophrenia.
View Article and Find Full Text PDFMultiple strands of evidence suggest a role for Brain Derived Neurotrophic Factor (BDNF) in the pathophysiology of schizophrenia. It is not yet clear, however, how BDNF may contribute to altered brain function seen in the disorder, or in those at high genetic risk. The current study examines functional imaging correlates of the BDNF val66met polymorphism in a population at high genetic risk of schizophrenia.
View Article and Find Full Text PDFNRG1, encoding neuregulin 1, is a susceptibility gene for schizophrenia, but no functional mutation causally related to the disorder has yet been identified. Here we investigate the effects of a variant in the human NRG1 promoter region in subjects at high risk of schizophrenia. We show that this variant is associated with (i) decreased activation of frontal and temporal lobe regions, (ii) increased development of psychotic symptoms and (iii) decreased premorbid IQ.
View Article and Find Full Text PDFTheory of Mind (ToM) is the ability to correctly determine the intentions and behaviours of others. It is known that this capability is compromised in individuals with schizophrenia. It is has not been fully elucidated whether this observed phenomenon is of a state or trait nature.
View Article and Find Full Text PDFBackground: There is evidence that groups of people with schizophrenia have deficits in Theory of Mind (ToM) capabilities. Previous studies have found these to be linked to psychotic symptoms (or psychotic symptom severity) particularly the presence of delusions and hallucinations.
Methods: A visual joke ToM paradigm was employed where subjects were asked to describe two types of cartoon images, those of a purely Physical nature and those requiring inferences of mental states for interpretation, and to grade them for humour and difficulty.
Neuropsychological assessments were compared among individuals at enhanced genetic risk of schizophrenia (n = 157) and controls (n = 34). The relationship between cognitive impairments and the presence of psychotic symptoms and measures of genetic risk was explored in the high-risk subjects. Neuropsychological differences were identified in many areas of function and were not accounted for by the presence of psychotic symptoms.
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