Autoimmune Dysfunction in Neurodevelopmental Disorders of Childhood

Abstract

The syndrome of autism is characterized by a failure to develop normal age-appropriate social relationships, with disturbances of motor, social, adaptive, and cognitive abilities. Etiologic heterogeneity is assumed by most investigators because of the occurrence of autistic syndromes in persons with a variety of disorders (e.g., viral or genetic). As yet, no specific biochemical markers or deviations have been demonstrated. Abnormal responses to sensory stimuli (e.g., auditory, vestibular, visual, tactile, olfactory, and proprioceptive) have been described. Whether these features are due to emotional disturbances or to organic lesion is still controversial. Neurological syndromes such as phenylketonuria (PKU), hypsarrhythmia, and encephalitis caused by fetal rubella infection that may result in autistic features, as well as other brain dysfunctions, raise the possibility that autism is associated with an organic brain lesion(s). Extensive neurological examinations, including EEGs, demonstrated that signs of neurological dysfunction appear more frequently in autistic children than in normal children.^{1, 2} Damasio and Maurer³ suggested a neural bilateral dysfunction of the ring of mesolimbic cortex (located in the medial, frontal, and temporal lobes), the neostriatum, and the anterior and medial thalamic nuclei as a result of perinatal viral infection or genetically determined neurochemical abnormalities.