Acquired Reversible Autistic Syndrome in Acute Encephalopathic Illness in Children

JAMA Neurology (Impact Factor: 7.42). 04/1981; 38(3):191-4. DOI: 10.1001/archneur.1981.00510030085013
Source: PubMed


In seeking the neurologic substrate of the autistic syndrome of childhood, previous studies have implicated the medial temporal lobe or the ring of mesolimbic cortex located in the mesial frontal and temporal lobes. During an acute encephalopathic illness, a clinical picture developed in three children that was consistent with infantile autism. This development was reversible. It was differentiated from acquired epileptic aphasia, and the language disorder was differentiated aphasia. One child has rises in serum herpes simplex titers, and a computerized tomographic (CT) scan revealed an extensive lesion of the temporal lobes, predominantly on the left. The other two, with similar clinical syndromes, had normal CT scans, and no etiologic agent was defined. These cases are examples of an acquired and reversible autistic syndrome in childhood, emphasizing the clinical similarities to bilateral medial temporal lobe disease as described in man, including the Klüver-Bucy syndrome seen in postencephalitic as well as postsurgical states.

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    • "In addition to the above cases, other sources regarding unconventional ages of ASD onset have emerge in the form of rare case reports describing the onset of autism in late childhood [43,44] and adolescence [45]. There have even been reports of adulthood onset autism [46]; however, regardless of age, these late onset presentations are typically associated with herpes encephalitis infections. "
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    ABSTRACT: This article examines the most significant, contradictory evidence pertaining to autism. The first section of the article includes reports of recovery from autism, data obtained from studies involving oxytocin, early deprivation, autism in preterm children, late-onset autism, and symptom overlap among ASD, social phobias and personality disorders. In the second section of the article, we offer a model that better incorporates current findings and address controversies that continue to surround ASD. We propose an umbrella term "social inhibition disorders" which integrates autism spectrum disorders and social phobias, as well as schizoid, schizotypal, and obsessive-compulsive personality disorders. It would also include "quasi-autism," which has been found in early deprivation studies, autism in preterm children, and cases of late-onset autism presenting after herpes encephalitis infection. Finally, we discuss suggestions for further research and clinical perspectives.
    Child and Adolescent Psychiatry and Mental Health 03/2013; 7(1):9. DOI:10.1186/1753-2000-7-9
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    • "Infections/infectious agents that appear to be causally related to the development of autistic behavior include encephalitis caused by measles, congenital rubella, herpes simplex virus, mumps, varicella, cytomegalovirus, and Stealth virus (Chess, 1971; DeLong et al., 1981; Libbey et al., 2005). Rubella virus was the first known cause of autism (Chess, 1971; Ziring, 2001). "
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    ABSTRACT: Autism, a member of the pervasive developmental disorders (PDDs), has been increasing dramatically since its description by Leo Kanner in 1943. First estimated to occur in 4 to 5 per 10,000 children, the incidence of autism is now 1 per 110 in the United States, and 1 per 64 in the United Kingdom, with similar incidences throughout the world. Searching information from 1943 to the present in PubMed and Ovid Medline databases, this review summarizes results that correlate the timing of changes in incidence with environmental changes. Autism could result from more than one cause, with different manifestations in different individuals that share common symptoms. Documented causes of autism include genetic mutations and/or deletions, viral infections, and encephalitis following vaccination. Therefore, autism is the result of genetic defects and/or inflammation of the brain. The inflammation could be caused by a defective placenta, immature blood-brain barrier, the immune response of the mother to infection while pregnant, a premature birth, encephalitis in the child after birth, or a toxic environment.
    Journal of Immunotoxicology 02/2011; 8(1):68-79. DOI:10.3109/1547691X.2010.545086 · 2.05 Impact Factor
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    • "The implication of viruses in mental disorders is supported by several lines of epidemiological evidence. Prenatal or perinatal viral infections are risk factors for schizophrenia and autism-spectrum disorders [12] [13]. Numerous epidemiological surveys have also documented a birth excess of schizophrenia and bipolar patients in winter and spring [14– 17] or seasonal correlations between incidence of autismspectrum disorders and viral outbreaks [18] [19] [20] [21] [22]. "
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    ABSTRACT: Converging lines of clinical and epidemiological evidence suggest that viral infections in early developmental stages may be a causal factor in neuropsychiatric disorders such as schizophrenia, bipolar disorder, and autism-spectrum disorders. This etiological link, however, remains controversial in view of the lack of consistent and reproducible associations between viruses and mental illness. Animal models of virus-induced neurobehavioral disturbances afford powerful tools to test etiological hypotheses and explore pathophysiological mechanisms. Prenatal or neonatal inoculations of neurotropic agents (such as herpes-, influenza-, and retroviruses) in rodents result in a broad spectrum of long-term alterations reminiscent of psychiatric abnormalities. Nevertheless, the complexity of these sequelae often poses methodological and interpretational challenges and thwarts their characterization. The recent conceptual advancements in psychiatric nosology and behavioral science may help determine new heuristic criteria to enhance the translational value of these models. A particularly critical issue is the identification of intermediate phenotypes, defined as quantifiable factors representing single neurochemical, neuropsychological, or neuroanatomical aspects of a diagnostic category. In this paper, we examine how the employment of these novel concepts may lead to new methodological refinements in the study of virus-induced neurobehavioral sequelae through animal models.
    Interdisciplinary Perspectives on Infectious Diseases 05/2010; 2010(1687-708X):380456. DOI:10.1155/2010/380456
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