Imaging data in autism: From structure to malfunction

Acosta, Maria T.; Pearl, Phillip L.

doi:10.1016/j.spen.2004.07.004

Cited by 37 publications

(26 citation statements)

References 74 publications

Supporting

Mentioning

Contrasting

Unclassified

Order By: Relevance

“…A relationship between the Purkinje cell abnormality and neuroimaging findings has not been established (Lee et al, 2002). Neuroimaging studies of the cerebellum in autism have been inconsistent (Acosta & Pearl, 2004). Some researchers have found smaller cerebellar measurements, particularly in the vermis (Courchesne, 1991(Courchesne, , 1997(Courchesne, , 1999Courchesne et al, 2001;Courchesne et al, 1989;Courchesne et al, 1994Courchesne et al, , 1995Hashimoto et al, 1993;Murakami et al, 1989;Schaefer et al, 1996).…”

Section: Hb Cleavinger Et Almentioning

confidence: 99%

Quantitative magnetic resonance image analysis of the cerebellum in macrocephalic and normocephalic children and adults with autism

Cleavinger

Bigler

Johnson

et al. 2008

J Inter Neuropsych Soc

View full text Add to dashboard Cite

A detailed morphometric analysis of the cerebellum in autism with and without macrocephaly. Four subject groups (N 5 65; male; IQs Ն 65; age 7 to 26 years) were studied with quantitative MRI; normocephalic and macrocephalic individuals with autism without mental retardation were compared to normocephalic and benign macrocephalic typically developing individuals. Total cerebellum volumes and surface areas of four lobular midsagittal groups were measured. Independent t-tests between autism and control subjects matched for head size revealed no significant differences. Multivariate analyses of variance were also performed, using the diagnostic group as the fixed factor, cerebellar measures as the dependent variables and total intracranial volume, total brain volume, age, verbal IQ, and performance IQ as covariates. No significant differences were found; however, a trend was noted in which macrocephalic individuals with autism consistently exhibited slightly smaller cerebellar volume or surface area when compared to individuals with benign macrocephaly. In autism, with and without macrocephaly, cerebellar structures were found to be proportional to head size and did not differ from typically developing subjects. (JINS, 2008, 14, 401-413.)

show abstract

Section: Hb Cleavinger Et Almentioning

confidence: 99%

Quantitative magnetic resonance image analysis of the cerebellum in macrocephalic and normocephalic children and adults with autism

Cleavinger

Bigler

Johnson

et al. 2008

J Inter Neuropsych Soc

View full text Add to dashboard Cite

show abstract

“…The prevalence of ASD is considered to be approximately 4 to 5 per 1000, but numbers differ according to criteria used for diagnosis [1].…”

Section: Introductionmentioning

confidence: 99%

“…Besides the well-known morphological and functional abnormalities, there are also many paths which have begun to be explored by current imaging techniques. When we consider cerebellum as the common source of the pathology in ASD and Cerebellar Mutism (CM), it could be said that three major neuropathologic findings have been described: (1) curtailed development of neurons in the forebrain limbic system (anterior cingulate gyrus, hippocampus, subiculum, etorhinal cortex, and mamillary body (2) decreased number of Purkinje cells in the cerebellum (3) age-related differences in cell size and neuronal number in the cerebellar and the inferior olivary nuclei, suggesting an evolving process and disturbance in the synaptic relationships of these structures. Typically brain development is comprised of several stages, including proliferation and migration of neurons, creation of dendritic arbors and synaptic connections, and eventually dendritic pruning and programmed cell death.…”

Section: Introductionmentioning

confidence: 99%

See 1 more Smart Citation

Autism and Cerebellar Mutism: A Review of the Neuroanatomical Findings

Kaya¹

2012

Autism

View full text Add to dashboard Cite

Autistic Spectrum Disorder (ASD) is behaviorally defined syndrome characterized by atypical social interaction, disordered verbal and non-verbal communication, restricted areas of interest and limited imaginative play. The prevalence of ASD is considered to be approximately 4 to 5 per 1000, but numbers differ according to criteria used for diagnosis [1].Individuals with ASD have three core features; 1. Impairments of reciprocal social interactions, 2. Abnormal development and use of language and 3. Repetitive and ritualized behaviors and a narrow range of interests. In addition to the core features of autism, there are common co-morbid neurological disorders. The prevalence of mental retardation in the autism spectrum is approximately 30%. Epilepsy prevalence associated with autism varies from 5% to 44%. Anxiety and mood disorders are also very common in autism.There is heterogeneity in the onset of autism. Although some children have signs of development delays between 0-18 months of life, up to 40% of children with ASD initially demonstrate the near-normal development until 18-24 months.As Brunelle et al. says: All the results are converging toward the description of anatomical and functional anomalies in the regions of the so-called "social brain" [2]. Several brain regions such as frontal lobe, the superior temporal cortex, the parietal cortex, and amygdala have been implicated in social behavior. But the recent developments make us think more about the role of cerebellum in ASD. This review presents an overview of the neuroanatomical abnormalities that occur within ASD. We discuss the findings that have advanced our understanding of cerebellar organization in ASD.

show abstract

“…The frontal lobe is the region of the brain associated with executive control and planning, including functions such as response inhibition, working memory and motivational aspects of behavior and high-order motor control (Alvarez and Emory 2006;Ashe, et al 2006;Graziano and Aflalo 2007;Tekin and Cummings 2002). Due to this wide range of complex brain functions, abnormalities in frontal lobe structure and function have been hypothesized to contribute to many neuropsychiatric disorders, including obsessive-compulsive disorder (OCD) (Tekin and Cummings 2002), depression and bipolar disorder (Tekin and Cummings 2002), schizophrenia (Shad, et al 2006;Suzuki, et al 2005;Yamasue, et al 2004), Down syndrome (Pinter, et al 2001;Porter, et al 2007), Rett syndrome (Carter, et al 2008), fragile X syndrome (Gothelf, et al 2008;Kates, et al 2002a), idiopathic autism (Acosta and Pearl 2004;Courchesne, et al 2007), Tourette syndrome (Fredericksen, et al 2002;Marsh, et al 2007) and Attention-Deficit/Hyperactivity disorder (ADHD) (Kelly, et al 2007;Nigg and Casey 2005;Shaw, et al 2007;Shaw, et al 2006;Sowell, et al 2003). In view of the size and functional heterogeneity of the frontal lobe (Fuster 1997), it is likely that abnormalities in distinct functional regions are preferentially associated with a particular disorder or with a specific aspect of that disorder.…”

mentioning

confidence: 99%