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A 38-year-old professional is brought in by police extremely distressed and in pain. She reports intense feelings of contamination over her arms and torso and fears that this is spreading and killing other people or animals. She has tried neutralising this contamination by applying concentrated sodium hydroxide (figure 1). She was taken to various emergency departments (ED) 39 times in the last 8 months and has a history of serious overdoses requiring intensive care unit admission. She says she did …

Human voices play a fundamental role in social communication, and areas of the adult "social brain" show specialization for processing voices and their emotional content (superior temporal sulcus, inferior prefrontal cortex, premotor cortical regions, amygdala, and insula) [ [1], [2], [3], [4], [5], [6], [7] and [8]]. However, it is unclear when this specialization develops. Functional magnetic resonance (fMRI) studies suggest that the infant temporal cortex does not differentiate speech from music or backward speech [ [9] and [10]], but a prior study with functional near-infrared spectroscopy revealed preferential activation for human voices in 7-month-olds, in a more posterior location of the temporal cortex than in adults [11]. However, the brain networks involved in processing nonspeech human vocalizations in early development are still unknown. To address this issue, in the present fMRI study, 3- to 7-month-olds were presented with adult nonspeech vocalizations (emotionally neutral, emotionally positive, and emotionally negative) and nonvocal environmental sounds. Infants displayed significant differential activation in the anterior portion of the temporal cortex, similarly to adults [1]. Moreover, sad vocalizations modulated the activity of brain regions involved in processing affective stimuli such as the orbitofrontal cortex [12] and insula [ [7] and [8]]. These results suggest remarkably early functional specialization for processing human voice and negative emotions.

The aim of this study was to derive a causal model of age-related grey matter atrophy across the cortex on the basis of cortical thickness measures using surface reconstruction of structural magnetic resonance images. Using confirmatory factor analysis, it was shown that the observed interregional correlations matrix between thickness measures could most accurately be accounted for by a single common age-related mechanism. This common factor did not predict cortical thickness directly, but exerted differential effects on individual region through independent lobe-specific systems. This model reconciles two seemingly mutually exclusive hypotheses, namely, the existence of different decay functions being caused by the same underlying mechanism.

BACKGROUND Attention-deficit hyperactivity disorder (ADHD) is increasingly recognised as occurring in people with intellectual disability (ID), although treatment of ADHD in this population has not been tested widely. Amfetamine has been used to treat ADHD in people with and without ID, although the evidence for its efficacy in people with ID is unclear. OBJECTIVES To examine the effectiveness of amfetamine for the treatment of attention deficit hyperactivity disorder in people with intellectual disabilities. SEARCH STRATEGY MEDLINE, PsycINFO, EMBASE, AMED, ISI Web of Science and WorldCat Dissertations were searched using an extensive list of synonyms for ADHD and ID. CENTRAL, Current Controlled Trials meta-register (mRCT), CenterWatch, NHS National Research Register, clinicaltrials.gov were searched in August 2007. Pharmaceutical companies and experts in the field were contacted. Reference lists of review articles were examined and citation searches were performed in ISI Web of Knowledge. SELECTION CRITERIA All randomised controlled studies, both published and unpublished, in any language, in which children or adults with ADHD and ID were treated with amfetamine. DATA COLLECTION AND ANALYSIS Data were extracted independently by two reviewers using a standardised extraction sheet. Risk of bias was assessed by two authors using a standardised framework. Meta-analyses were planned but were not performed due to a lack of suitable studies. MAIN RESULTS Only one study was suitable for inclusion. This was a cross-over study in 15 children with ADHD, ID and Fragile X syndrome. Duration of treatment was only one week. No significant difference was reported between amfetamine and placebo for any of the ADHD measures, but significantly more side effects were reported while taking amfetamine, mainly mood lability and irritability. AUTHORS' CONCLUSIONS There is very little evidence for the effectiveness of amfetamine for ADHD in people with ID . Prescribing in this population is based on extrapolation of research in people without ID. More research into effectiveness and tolerability is urgently needed.