Article

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: 2.74). 03/1993; 160(2):387-93. DOI: 10.2214/ajr.160.2.8424359
Source: PubMed

ABSTRACT 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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    Cerebral Cortex 04/2014; DOI:10.1093/cercor/bhu082 · 8.67 Impact Factor
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    • "Increased head circumference; higher rates of macrocephaly Anatomical measurements [143] Increases in cerebral volume Magnetic resonance imaging (MRI) [144] [145] [146] Increases in frontal and temporal gray matter volume MRI [147] Increased neuron counts and brain weight in prefrontal cortex Post-mortem anatomical analysis [148] Gray matter increases in regions related to social cognition, communication, and repetitive behaviors, as well as auditory and visual perception MRI [149] Decreases in parietal lobe volume MRI [150] Lack of asymmetry in planum temporale volume MRI [151] Increased cortical thickness in temporal and parietal lobes [152] Decreases in gray matter density in ventromedial aspects of the temporal cortex MRI [147] Cortical thinning in regions related to the mirror neuron system, emotional recognition, and social cognition MRI [82] Increases in local density and computation in cortical minicolumns Post-mortem anatomical analysis [153] Increased white matter growth, especially in the prefrontal cortex and cerebellum MRI [144] [145] Increases in the cerebral white matter specifically in the parietal, occipital, and frontal lobes Transverse relaxation time imaging [154] Decreases in corpus callosum volume MRI, Diffusion tensor imaging (DTI) [155] [156] Reduced fractional anisotropy in a variety of white matter regions, especially corpus callosum, frontal, and temporal regions DTI [34–36,157–159] Mean diffusion increases in various regions including corpus callosum, arcuate fasciculus, and temporal areas DTI [33] [34] [36] Increased connectivity volume between the superior temporal sulcus and amygdala fMRI, DTI [160] trajectories and impaired connectivity.'' To bring some level of reconciliation among these various studies, several investigators have proposed a local overconnectivity-long range underconnectivity hypothesis [32] that is supported by noisy local processing in minicolumns [32] and reduced integrity in extensive white matter tracts [33] [34] [35] [36]. "
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    • "Pathological studies have revealed an association between autistic symptoms and certain pathological changes in brain structure and cellularity (reviewed in (Bauman & Kemper, 2005). Postmortem autopsy of autistic brains revealed alterations in neuronal anatomy within frontal (Bailey et al., 1998), temporal (Bachevalier, 1994), parietal (Courchesne et al., 1993), limbic (Bauman, 1991), brainstem and cerebellar (Kemper & Bauman, 1998) regions. The few cross-sectional studies that examined age-related changes revealed a complex pattern of growth abnormalities in the cerebellum, cortex, amygdala, and hippocampus (Courchesne, 2004; Hashimoto et al., 1995; Schumann et al., 2004; Schumann et al., 2010). "
    Autism - A Neurodevelopmental Journey from Genes to Behaviour, 08/2011; , ISBN: 978-953-307-493-1
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