Gilbert SJ, Bird G, Brindley R, et al. Atypical recruitment of medial prefrontal cortex in autism spectrum disorders: an fMRI study of two executive function tasks

Institute of Cognitive Neuroscience and Department of Psychology, University College London, London, UK.
Neuropsychologia (Impact Factor: 3.3). 02/2008; 46(9):2281-91. DOI: 10.1016/j.neuropsychologia.2008.03.025
Source: PubMed


Recent studies have suggested an uneven profile of executive dysfunction in autism spectrum disorders (ASD). For example, some authors have reported deficits on newly developed tests of executive function sensitive to rostral prefrontal function, despite spared, or even superior, performance on other tests. We investigated the performance of a group of high-functioning participants with ASD (N=15) and an age- and IQ-matched control group (N=18) on two executive function tests, whilst undergoing functional magnetic resonance imaging (fMRI). Behaviourally, there were no significant differences between the two groups. In a classical test of executive function (random response generation), BOLD signal differed between the groups in the cerebellum but not in the frontal lobes. However, on a new test of executive function (selection between stimulus-oriented and stimulus-independent thought), the ASD group exhibited significantly greater signal-change in medial rostral prefrontal cortex (especially Brodmann Area 10) in the comparison of stimulus-oriented versus stimulus-independent attention. In addition, the new test (but not the classical test) provided evidence for abnormal functional organisation of medial prefrontal cortex in ASD. These results underline the heterogeneity of different tests of executive function, and suggest that executive functioning in ASD is associated with task-specific functional change.

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    • "It is also important to note that the paradigm used in this study was not designed to elicit global differences in executive function, as both the primary and control conditions (i.e., attend-face and attend-house) necessitated some working memory (i.e., a one-back task). Recent research on frontal lobe function in ASD shows variable results, with some executive function tasks eliciting normal or increased activation patterns (Dichter et al. 2009; Gilbert et al. 2008). Findings for DLPFC in fact parallel those of Dichter and colleagues (Dichter et al. 2009), who reported increased activation of dorsal anterior cingulate and medial prefrontal cortices in ASD during a target detection task. "
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    • "This might indicate that the behavioral effects reported in Karvat and Kimchi (2013) arise by restoring medial prefrontal acetylcholine availability ; i.e., restoring precision dynamics at higher cortical levels such that sensory precision is no longer (relatively) high. However, while there are many reports of abnormal medial prefrontal cortex function in autism (Gilbert et al., 2008; Watanabe et al., 2012), there is, at present, little neurochemical evidence for low brain acetylcholine levels in human autism. Furthermore, acetylcholine is not only involved in " attentionlike " (Feldman and Friston, 2010) modulation of perception, but is also implicated in widespread facilitation of many cognitive processes, including novelty processing (Pepeu and Giovannini, 2004), conscious awareness and sleep states (Perry et al., 1999) and interacts with other monoaminergic neurotransmitter systems . "
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    • "Data were shown as mean ± SE. **p < 0.01. as hippocampus pathological changes have also been reported in autism patients (Courchesne et al., 2011; Gilbert et al., 2008; Nicolson et al., 2006; Raymond et al., 1996; Rojas et al., 2004; Saitoh et al., 2001; Schumann et al., 2004; Wallace et al., 2012). Therefore, Hippocampus, termporal cortex and prefrontal cortex were evaluated for histopathological assays. "
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