Biochemical Studies on Autism

  • A. Yuwiler
  • E. Geller
  • E. Ritvo


Like many contemporary clinical designations, the term early infantile autism refers to a clinical syndrome and not an etiologically homogeneous disease. This is a distinction of some importance in evaluating the existing literature on the syndrome and in devising strategies for its biochemical elucidation. The term was coined by Kanner1 in 1944 to identify a syndrome of four key symptoms: the early onset of profound disturbances in relating to others; great difficulty or inability in developing communicative speech; displays of stereotypic motor behavior; and insistence on a stable environment. While Kanner’s clinical descriptions were clear, whether they defined a distinct clinical entity was open to debate.2–6 Currently defined as a syndrome of disturbances in perception, developmental rate, relating, language, and motility, and sanctified by inclusion in the American Psychiatric Association’s Diagnostic and Statistical Manual of Mental Disorders (DMS-III), the question of whether the syndrome should be considered a distinct “disease” is unresolved. What is clear, however, is that the syndrome can be associated with, and may be secondary to, a number of etiologies. Autistic behavior occurs in a significant number of phenylketonurics7 and in about 8% of the cases of maternal rubella.8 It has been found associated with tuberous sclerosis,9 Hurler’s disease, congenital hypothyroidism,10 and some cases of fragile x syndrome.11,12


Autistic Child Child Psychiatry Congenital Hypothyroidism Pyridoxal Phosphate Enterochromaffin Cell 


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© Plenum Press, New York 1985

Authors and Affiliations

  • A. Yuwiler
    • 1
    • 2
  • E. Geller
    • 1
    • 2
  • E. Ritvo
    • 2
  1. 1.Neurobiochemistry LaboratoryVeterans Administration Medical CenterLos AngelesUSA
  2. 2.Department of PsychiatryUniversity of CaliforniaLos AngelesUSA

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