Parietal abnormalities detected with MR in patients with autism

Department of Neurosciences, School of Medicine, University of California, San Diego, La Jolla 92093.
American Journal of Roentgenology (Impact Factor: 2.73). 03/1993; 160(2):387-93. DOI: 10.2214/ajr.160.2.8424359
Source: PubMed


Infantile autism is a neurologic disorder that severely disrupts the development of many higher cognitive functions. The most consistent abnormal neuroanatomic findings in autism are loss of Purkinje neurons in the posterior cerebellum as detected by autopsy studies and hypoplasia of the posterior cerebellar vermis and hemispheres as detected by in vivo neuroimaging. Evidence of developmental arrest has also been detected in limbic structures in autopsy studies of autistic patients with mental retardation. Neither in vivo neuroimaging nor autopsy studies of autistic persons have reported abnormalities in the cerebrum. Because the cerebrum mediates many higher cognitive functions, such as social communication, language, abstract reasoning, planning, and organization, that are known to be deficient in patients with autism, a closer examination of the neuroanatomy of the cerebrum in infantile autism is warranted.
MR images of 21 healthy autistic patients (6-32 years old) were mixed with MR images of control subjects and reviewed on four separate occasions by a neuroradiologist for any neuroanatomic abnormalities. Autism was diagnosed on the basis of criteria for autism as defined by the Diagnostic and Statistical Manual of Mental Disorders, and the autistic patients did not have any other concurrent neurologic disorders. To control for systematic bias in judging the type and location of abnormalities in the autistic population, three control groups were used: a normal control group of 12 subjects, a control group of 23 nonautistic patients with a variety of brain abnormalities for the first review, and another control group of 17 nonautistic patients for the second review. Control patients with brain abnormalities were selected from patients' files on the basis of MR findings of a variety of brain abnormalities. All MR images were coded for anonymity, randomly mixed, and examined by a neuroradiologist blinded to the purpose of the study and to the group membership of each subject. All normal and abnormal findings seen on the MR images of each subject were described on a standard form listing all major brain structures to ensure an examination of each structure in turn. To test for reliability, three subsequent reviews were performed by the same neuroradiologist.
Parietal lobes were abnormal in appearance in 43% (9/21) of autistic patients. Cortical volume loss in the parietal lobes was seen in seven autistic patients; in four of these cases, cortical volume loss extended either into the adjacent superior frontal or occipital lobe. Additional abnormalities detected with MR in these nine patients included white matter volume loss in the parietal lobes (three patients) and thinning of the corpus callosum, especially along the posterior body (two patients). Abnormalities were bilateral. The mesial, lateral, and orbital regions of the frontal lobes; temporal lobes; limbic structures; basal ganglia; diencephalon; and brainstem were normal in all autistic patients. No abnormalities were found in the 12 normal control subjects. The control subjects with neurologic abnormalities had various abnormal findings consistent with their medical conditions.
Our results indicate that the parietal lobes are reduced in volume in a portion of the autistic population. Possible origins for this localized cerebral abnormality include early-onset altered development and late-onset progressive atrophy.

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    • "Our results, which show atypical information processing in these networks in ASD, are reminiscent of previous literature, which has demonstrated widespread patterns of hypo-and hyperactivation in ASD (Belger et al. 2011; Philip et al. 2012), as well as disrupted structural and functional connectivity (Anagnostou et al. 2011). Many of these regions have previously been implicated in ASD, including cuneus and extrastriate cortex (Bonilha et al. 2008; Wong et al. 2008), precuneus and posterior cingulate (Wang et al. 2004; Cherkassky et al. 2006; Kennedy et al. 2006; Oblak et al. 2011), inferior parietal lobule (Koshino et al. 2005), superior parietal cortex and paracentral lobule (Courchesne et al. 1993; Belmonte and Yurgelun-Todd 2003; Hadjikhani et al. 2006), hippocampal formation (Raymond et al. 1995; Aylward et al. 1999; Schumann et al. 2004), anterior cingulate (Haznedar et al. 1997; Mundy 2003; Thakkar et al. 2008), and inferior frontal gyrus (Dapretto et al. 2005; Villalobos et al. 2005). Our data are consistent with the recent literature because they demonstrate that ASD does not affect any one region or pathway, but ensembles of regions, supporting the view that disruptions of integrated network functions may play an important role in the pathophysiology of ASD. "
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    ABSTRACT: Autism spectrum disorder (ASD) includes deficits in social cognition, communication, and executive function. Recent neuroimaging studies suggest that ASD disrupts the structural and functional organization of brain networks and, presumably, how they generate information. Here, we relate deficits in an aspect of cognitive control to network-level disturbances in information processing. We recorded magnetoencephalography while children with ASD and typically developing controls performed a set-shifting task designed to test mental flexibility. We used multiscale entropy (MSE) to estimate the rate at which information was generated in a set of sources distributed across the brain. Multivariate partial least-squares analysis revealed 2 distributed networks, operating at fast and slow time scales, that respond completely differently to set shifting in ASD compared with control children, indicating disrupted temporal organization within these networks. Moreover, when typically developing children engaged these networks, they achieved faster reaction times. When children with ASD engaged these networks, there was no improvement in performance, suggesting that the networks were ineffective in children with ASD. Our data demonstrate that the coordination and temporal organization of large-scale neural assemblies during the performance of cognitive control tasks is disrupted in children with ASD, contributing to executive function deficits in this group.
    Cerebral Cortex 04/2014; 25(9). DOI:10.1093/cercor/bhu082 · 8.67 Impact Factor
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    • "The cerebellum is also known to play a critical role in the development and maturation of the sensory integration processes, including visuo-motor integration (Glickstein, 1998). Underlying abnormalities within the cerebellum, commonly present in individuals with ASD (Courchesne et al., 1993; Bauman, 1996; Courchesne, 1997), may therefore emerge as potential problems with sensory integration resulting in a lack of perception-action coupling. This is further supported by evidence for cerebellar hyperactivity in PD, compensating for hypoactivity of the basal ganglia (Yu et al., 2007). "
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    ABSTRACT: Despite being largely characterized as a social and cognitive disorder, strong evidence indicates the presence of significant sensory-motor problems in Autism Spectrum Disorder (ASD). This paper outlines our progression from initial, broad assessment using the Movement Assessment Battery for Children (M-ABC2) to subsequent targeted kinematic assessment. In particular, pronounced ASD impairment seen in the broad categories of manual dexterity and ball skills was found to be routed in specific difficulties on isolated tasks, which were translated into focused experimental assessment. Kinematic results from both subsequent studies highlight impaired use of perception-action coupling to guide, adapt and tailor movement to task demands, resulting in inflexible and rigid motor profiles. In particular difficulties with the use of temporal adaption are shown, with "hyperdexterity" witnessed in ballistic movement profiles, often at the cost of spatial accuracy and task performance. By linearly progressing from the use of a standardized assessment tool to targeted kinematic assessment, clear and defined links are drawn between measureable difficulties and underlying sensory-motor assessment. Results are specifically viewed in-light of perception-action coupling and its role in early infant development suggesting that rather than being "secondary" level impairment, sensory-motor problems may be fundamental in the progression of ASD. This logical and systematic process thus allows a further understanding into the potential root of observable motor problems in ASD; a vital step if underlying motor problems are to be considered a fundamental aspect of autism and allow a route of non-invasive preliminary diagnosis.
    Frontiers in Integrative Neuroscience 07/2013; 7:51. DOI:10.3389/fnint.2013.00051
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    • "It is thought that this difference in growth rates during the first years of life disrupts development of neural circuitry essential for higher order social, language and cognitive functions [18]. Of particular interest to the current study is the discovery of corpus callosum thinning in people with ASC [20,21]. According to previous investigations [22-24] white matter density appears to be decreased in the genu, rostrum and splenium of the corpus callosum in people with ASC, reflecting decreased interhemispheric structural connectivity in this group, relative to typically developing individuals. "
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    ABSTRACT: Autism Spectrum Conditions (ASC) are a set of pervasive neurodevelopmental conditions characterized by a wide range of lifelong signs and symptoms. Recent explanatory models of autism propose abnormal neural connectivity and are supported by studies showing decreased interhemispheric coherence in individuals with ASC. The first aim of this study was to test the hypothesis of reduced interhemispheric coherence in ASC, and secondly to investigate specific effects of task performance on interhemispheric coherence in ASC. We analyzed electroencephalography (EEG) data from 15 participants with ASC and 15 typical controls, using Wavelet Transform Coherence (WTC) to calculate interhemispheric coherence during face and chair matching tasks, for EEG frequencies from 5 to 40 Hz and during the first 400 ms post-stimulus onset. Results demonstrate a reduction of interhemispheric coherence in the ASC group, relative to the control group, in both tasks and for all electrode pairs studied. For both tasks, group differences were generally observed after around 150 ms and at frequencies lower than 13 Hz. Regarding within-group task comparisons, while the control group presented differences in interhemispheric coherence between faces and chairs tasks at various electrode pairs (FT7-FT8, TP7-TP8, P7-P8), such differences were only seen for one electrode pair in the ASC group (T7-T8). No significant differences in EEG power spectra were observed between groups. Interhemispheric coherence is reduced in people with ASC, in a time and frequency specific manner, during visual perception and categorization of both social and inanimate stimuli and this reduction in coherence is widely dispersed across the brain. Results of within-group task comparisons may reflect an impairment in task differentiation in people with ASC relative to typically developing individuals. Overall, the results of this research support the value of WTC in examining the time-frequency microstructure of task-related interhemispheric EEG coherence in people with ASC.
    Molecular Autism 01/2013; 4(1):1. DOI:10.1186/2040-2392-4-1 · 5.41 Impact Factor
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