{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2026,10,19]],"date-time":"2026-10-19T23:18:14Z","timestamp":1792451894849,"version":"4.5.0"},"reference-count":109,"publisher":"Cambridge University Press (CUP)","issue":"3","license":[{"start":{"date-parts":[[2005,11,1]],"date-time":"2005-11-01T00:00:00Z","timestamp":1130803200000},"content-version":"unspecified","delay-in-days":61,"URL":"https:\/\/www.cambridge.org\/core\/terms"}],"content-domain":{"domain":[],"crossmark-restriction":false},"short-container-title":["Dev Psychopathol"],"published-print":{"date-parts":[[2005,9]]},"abstract":"<jats:p>\n                    Autistic symptoms begin in the first years of life, and recent \nmagnetic resonance imaging studies have discovered brain growth \nabnormalities that precede and overlap with the onset of these symptoms. \nRecent postmortem studies of the autistic brain provide evidence of \ncellular abnormalities and processes that may underlie the recently \ndiscovered early brain overgrowth and arrest of growth that marks the \nfirst years of life in autism. Alternative origins and time tables for \nthese cellular defects and processes are discussed. These cellular and \ngrowth abnormalities are most pronounced in frontal, cerebellar, and \ntemporal structures that normally mediate the development of those same \nhigher order social, emotional, speech, language, speech, attention, and \ncognitive functions that characterize autism. Cellular and growth \npathologies are milder and perhaps nonexistent in other structures (e.g., \noccipital cortex), which are known to mediate functions that are often \neither mildly affected or entirely unaffected in autistic patients. It is \nargued that in autism, higher order functions largely fail to develop \nnormally in the first place because frontal, cerebellar, and temporal \ncellular and growth pathologies occur prior to and during the critical \nperiod when these higher order neural systems first begin to form their \ncircuitry. It is hypothesized that microstructural maldevelopment results \nin local and short distance overconnectivity in frontal cortex that is \nlargely ineffective and in a failure of long-distance \ncortical\u2013cortical coupling, and thus a reduction in \nfrontal\u2013posterior reciprocal connectivity. This altered circuitry \nimpairs the essential role of frontal cortex in integrating information \nfrom diverse functional systems (emotional, sensory, autonomic, memory, \netc.) and providing context-based and goal-directed feedback to lower \nlevel systems.\n                    <jats:fn>\n                      <jats:p>The authors were supported by \nfunds from the National Institute of Mental Health (2-ROI-MH36840) and \nNational Institute of Neurological Disorders and Stroke (2-ROI-NS19855) \nawarded to Eric Courchesne.<\/jats:p>\n                    <\/jats:fn>\n                  <\/jats:p>","DOI":"10.1017\/s0954579405050285","type":"journal-article","created":{"date-parts":[[2008,6,6]],"date-time":"2008-06-06T06:18:00Z","timestamp":1212733080000},"page":"577-597","source":"Crossref","is-referenced-by-count":155,"title":["Autism at the beginning: Microstructural and growth abnormalities \nunderlying the cognitive and behavioral phenotype of autism"],"prefix":"10.1017","volume":"17","author":[{"given":"ERIC","family":"COURCHESNE","sequence":"first","affiliation":[{"name":"University of California, San Diego"},{"name":"Children's Hospital Research Center"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"ELIZABETH","family":"REDCAY","sequence":"additional","affiliation":[{"name":"University of California, San Diego"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"JOHN T.","family":"MORGAN","sequence":"additional","affiliation":[{"name":"University of California, San Diego"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"DANIEL P.","family":"KENNEDY","sequence":"additional","affiliation":[{"name":"University of California, San Diego"}],"role":[{"vocabulary":"crossref","role":"author"}]}],"member":"56","published-online":{"date-parts":[[2005,11,1]]},"reference":[{"key":"S0954579405050285_ref095","doi-asserted-by":"crossref","unstructured":"Rubenstein, J. 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