Our research will continue to use a multidisciplinary approach to establish neurophysiological, neuroanatomical, and neurobehavioral markers that differentiate autism from other developmental disorders of communication. (1) Neurophysiological markers will continue to be established by the identification of aberrant sensory and cognitive ERPs in autism and developmental dysphasia. We will determine whether neurophysiological abnormalities in autism occur predominantly in attentional and cognitive, as opposed to sensory, ERPs; whereas in dysphasia, neurophysiological abnormalities occur throughout sensory and cognitive stages of auditory, but not in visual and somatosensory, information processing. (2) Neuroanatomical markers will continue to be established by identifying abnormal neuroanatomical structures using MRI (magnetic resonance imaging) technology. In particular, we will determine whether the distinctive hypoplasia of the cerebellar vermis, which we have found in several non-retarded autistic people, is also present in retarded autistic people, but not in dysphasic and mentally retarded non-autistic people. (3) Neurobehavioral markers will be sought by evaluating the long-term habituation of the acoustic startle response, a potentially distinctive neurobehavioral marker which, heretofore, has not been fully researched in autism. Recent basic research with animals shows that the cerebellar vermis is central to systems which mediate one form of memory -- the long-term habitation of the acoustic startle response. Since our preliminary MRI data has shown that this neuroanatomical structure is abnormal in some autistic people, we will determine whether autistic people have a deficit in the long-term habituation of this response. Neurologic symptoms and signs of cerebellar disorder, such as dysarthria and nystagmus, will be clinically evaluated.

Agency
National Institute of Health (NIH)
Institute
National Institute of Neurological Disorders and Stroke (NINDS)
Type
Research Project (R01)
Project #
5R01NS019855-06
Application #
3399942
Study Section
Neurology A Study Section (NEUA)
Project Start
1983-09-10
Project End
1990-03-31
Budget Start
1989-04-01
Budget End
1990-03-31
Support Year
6
Fiscal Year
1989
Total Cost
Indirect Cost
Name
Rady Children's Hospital-San Diego
Department
Type
DUNS #
City
San Diego
State
CA
Country
United States
Zip Code
92123
Courchesne, Eric; Campbell, Kathleen; Solso, Stephanie (2011) Brain growth across the life span in autism: age-specific changes in anatomical pathology. Brain Res 1380:138-45
Schumann, Cynthia M; Bloss, Cinnamon S; Barnes, Cynthia Carter et al. (2010) Longitudinal magnetic resonance imaging study of cortical development through early childhood in autism. J Neurosci 30:4419-27
Schumann, Cynthia Mills; Barnes, Cynthia Carter; Lord, Catherine et al. (2009) Amygdala enlargement in toddlers with autism related to severity of social and communication impairments. Biol Psychiatry 66:942-9
Akshoomoff, Natacha; Farid, Nikdokht; Courchesne, Eric et al. (2007) Abnormalities on the neurological examination and EEG in young children with pervasive developmental disorders. J Autism Dev Disord 37:887-93
Redcay, Elizabeth; Kennedy, Daniel P; Courchesne, Eric (2007) fMRI during natural sleep as a method to study brain function during early childhood. Neuroimage 38:696-707
Bloss, Cinnamon S; Courchesne, Eric (2007) MRI neuroanatomy in young girls with autism: a preliminary study. J Am Acad Child Adolesc Psychiatry 46:515-23
Akshoomoff, Natacha (2006) Use of the Mullen Scales of Early Learning for the assessment of young children with Autism Spectrum Disorders. Child Neuropsychol 12:269-77
Belmonte, Matthew K; Carper, Ruth A (2006) Monozygotic twins with Asperger syndrome: differences in behaviour reflect variations in brain structure and function. Brain Cogn 61:110-21
Redcay, Elizabeth; Courchesne, Eric (2005) When is the brain enlarged in autism? A meta-analysis of all brain size reports. Biol Psychiatry 58:1-9
Courchesne, Eric; Pierce, Karen (2005) Why the frontal cortex in autism might be talking only to itself: local over-connectivity but long-distance disconnection. Curr Opin Neurobiol 15:225-30

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