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Does bilateral damage to the human amygdala produce autistic symptoms?

Paul LK, Corsello C, Tranel D, Adolphs R - J Neurodev Disord (2010)

Bottom Line: Here we undertook such an investigation in two rare participants with developmental-onset bilateral amygdala lesions.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.

View Article: PubMed Central - PubMed

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.

No MeSH data available.


Related in: MedlinePlus

Neuroanatomy of the two subjects from T1-weighted MRI scans. Both show focal, bilateral lesions of the amygdala (arrows) in horizontal MR scans of the medial temporal lobe
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Fig1: Neuroanatomy of the two subjects from T1-weighted MRI scans. Both show focal, bilateral lesions of the amygdala (arrows) in horizontal MR scans of the medial temporal lobe

Mentions: Participants We tested two women with bilateral damage to the amygdala who have IQ, language, perceptual and motor functions all in the normal range (Buchanan et al. 2009). Both patients have bilateral developmental amygdala lesions resulting from Urbach-Wiethe disease. Subject SM is a 43-year-old woman with a high-school education (full-scale IQ = 88), whose lesions encompass the entire amygdala plus subjacent white matter and anterior entorhinal cortex. Subject AP is a 23-year-old woman with a college education (full-scale IQ = 98). Her lesions are entirely confined to the amygdala, and occupy roughly 50% of each amygdala’s volume (Fig. 1).Fig. 1


Does bilateral damage to the human amygdala produce autistic symptoms?

Paul LK, Corsello C, Tranel D, Adolphs R - J Neurodev Disord (2010)

Neuroanatomy of the two subjects from T1-weighted MRI scans. Both show focal, bilateral lesions of the amygdala (arrows) in horizontal MR scans of the medial temporal lobe
© Copyright Policy
Related In: Results  -  Collection

Show All Figures
getmorefigures.php?uid=PMC2914867&req=5

Fig1: Neuroanatomy of the two subjects from T1-weighted MRI scans. Both show focal, bilateral lesions of the amygdala (arrows) in horizontal MR scans of the medial temporal lobe
Mentions: Participants We tested two women with bilateral damage to the amygdala who have IQ, language, perceptual and motor functions all in the normal range (Buchanan et al. 2009). Both patients have bilateral developmental amygdala lesions resulting from Urbach-Wiethe disease. Subject SM is a 43-year-old woman with a high-school education (full-scale IQ = 88), whose lesions encompass the entire amygdala plus subjacent white matter and anterior entorhinal cortex. Subject AP is a 23-year-old woman with a college education (full-scale IQ = 98). Her lesions are entirely confined to the amygdala, and occupy roughly 50% of each amygdala’s volume (Fig. 1).Fig. 1

Bottom Line: Here we undertook such an investigation in two rare participants with developmental-onset bilateral amygdala lesions.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.

View Article: PubMed Central - PubMed

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.

No MeSH data available.


Related in: MedlinePlus