Journal article
Does bilateral damage to the human amygdala produce autistic symptoms?
Journal of neurodevelopmental disorders, Vol.2(3), pp.165-173
09/2010
DOI: 10.1007/s11689-010-9056-1
PMCID: PMC2914867
PMID: 20700516
Abstract
A leading neurological hypothesis for autism postulates amygdala dysfunction. This hypothesis has considerable support from anatomical and neuroimaging studies. Individuals with bilateral amygdala lesions show impairments in some aspects of social cognition. These impairments bear intriguing similarity to those reported in people with autism, such as impaired recognition of emotion in faces, impaired theory of mind abilities, failure to fixate eyes in faces, and difficulties in regulating personal space distance to others. Yet such neurological cases have never before been assessed directly to see if they meet criteria for autism spectrum disorders (ASD). Here we undertook such an investigation in two rare participants with developmental-onset bilateral amygdala lesions. We administered a comprehensive clinical examination, as well as the Autism Diagnostic Observation Schedule (ADOS), the Social Responsiveness Scale (SRS), together with several other standardized questionnaires. Results from the two individuals with amygdala lesions were compared with published norms from both healthy populations as well as from people with ASD. Neither participant with amygdala lesions showed any evidence of autism across the array of different measures. The findings demonstrate that amygdala lesions in isolation are not sufficient for producing autistic symptoms. We suggest instead that it may be abnormal connectivity between the amygdala and other structures that contributes to autistic symptoms at a network level.
Details
- Title: Subtitle
- Does bilateral damage to the human amygdala produce autistic symptoms?
- Creators
- Lynn K Paul - Division of Humanities and Social Sciences, California Institute of Technology, Pasadena, CA 91125 USAChristina Corsello - Rady Children’s Hospital, San Diego, CA USADaniel Tranel - Department of Neurology, University of Iowa, Iowa City, IA USARalph Adolphs - Division of Humanities and Social Sciences, California Institute of Technology, Pasadena, CA 91125 USA
- Resource Type
- Journal article
- Publication Details
- Journal of neurodevelopmental disorders, Vol.2(3), pp.165-173
- DOI
- 10.1007/s11689-010-9056-1
- PMID
- 20700516
- PMCID
- PMC2914867
- NLM abbreviation
- J Neurodev Disord
- ISSN
- 1866-1947
- eISSN
- 1866-1955
- Publisher
- Springer US; Boston
- Language
- English
- Date published
- 09/2010
- Academic Unit
- Neurology; Psychological and Brain Sciences; Iowa Neuroscience Institute
- Record Identifier
- 9984002303002771
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