The Amygdala Is Enlarged in Children But Not Adolescents with Autism; the Hippocampus Is Enlarged at All Ages
By C. Schumann, J. Hamstra, B. Goodlin-Jones, L. Lotspeich, H. Kwon, Michael H. Buonocore, C. Lammers, Allan L. Reiss, D. Amaral. Journal of Neuroscience, 2004
859 citations recorded by the source corpus.
Autism is a neurodevelopmental disorder characterized by impairments in reciprocal social interaction, deficits in verbal and nonverbal communication, and a restricted repertoire of activities or interests. We performed a magnetic resonance imaging study to better define the neuropathology of autistic spectrum disorders. Here we report findings on the amygdala and the hippocampal formation. Borders of the amygdala, hippocampus, and cerebrum were defined, and their volumes were measured in male children (7.5-18.5 years of age) in four diagnostic groups: autism with mental retardation, autism without mental retardation, Asperger syndrome, and age-matched typically developing controls. Although there were no differences between groups in terms of total cerebral volume, children with autism (7.5-12.5 years of age) had larger right and left amygdala volumes than control children. There were no differences in amygdala volume between the adolescent groups (12.75-18.5 years of age). Interestingly, the amygdala in typically developing children increases substantially in volume from 7.5 to 18.5 years of age. Thus, the amygdala in children with autism is initially larger, but does not undergo the age-related increase observed in typically developing children. Children with autism, with and without mental retardation, also had a larger right hippocampal volume than typically developing controls, even after controlling for total cerebral volume. Children with autism but without mental retardation also had a larger left hippocampal volume relative to controls. These cross-sectional findings indicate an abnormal program of early amygdala development in autism and an abnormal pattern of hippocampal development that persists through adolescence. The cause of amygdala and hippocampal abnormalities in autism is currently unknown.
Subfields: Cognitive Neuroscience, Genetics
View Paper: https://www.semanticscholar.org/paper/93586eb2c9139d4a766a6f54d4da9e543b8b082b
How researchers see this paper
The researchers whose trusted networks rank it highest, strongest advocate first. Every researcher gets a different order.
In Cognitive Neuroscience
- Olaf Sporns
- Jessica R. Andrews-Hanna
- Daniel L. Schacter
- Randy L. Buckner
- R. Quian Quiroga
- Stephen Waydo
- Bhismadev Chakrabarti
- Andreas Meyer-Lindenberg
In Genetics
- Bhismadev Chakrabarti
- Michael V. Lombardo
- Bonnie Auyeung
- Andreas Meyer-Lindenberg
- Daniel R. Weinberger
- Rebecca C. Knickmeyer
- R. J. Kelleher
- Mark F. Bear
Citations in the corpus
- Neuroscience and education: from research to practice? (2006, background): “Children, too, show amygdala activity to fearful expressions, and children with autism (who have impaired social cognition) have significantly increased amygdala volum”
- The eye contact effect: mechanisms and development. (2009, neutral): “could result from the structural impairment in sub-cortical structures that underlies the eye contact effect, such as the amygdala [ 71 ]”
- Pten regulates neuronal arborization and social interaction in mice. (2006, background): “Similarly, enlarged amygdala in children and enlarged hippocampus in children and adolescents have been associated with ASD (Schumann et al., 2004).”
- The autistic neuron: troubled translation? (2008, background): “Neuropathological studies have reported minor and inconsistent abnormalities in the autistic brain, but recent morphometric analysis has demonstrated enlargement of the hippocampus and amygdala (Schumann et al., 2004).”
- A Review of Adversity, The Amygdala and the Hippocampus: A Consideration of Developmental Timing (2009, neutral): “…amygdala neurons eventually leads to neuronal atrophy or cell death by adulthood (Teicher et al., 2003), a pattern identifi ed in other populations (e.g., autism spectrum disorders) who demonstrate amygdala hypertrophy in childhood followed by smaller volumes in adulthood (Schumann et al., 2004).”
- Facial Emotion Recognition in Autism Spectrum Disorders: A Review of Behavioral and Neuroimaging Studies (2010, result): “Abnormal structural development of the amygdala has been found in ASD (Howard et al. 2000; Schumann et al. 2004), and two other structural MRI studies, although not related to FER, found that a larger amygdala volume at 3 years of age was associated with more social and communication problems at age”
- A common allele in the oxytocin receptor gene (OXTR) impacts prosocial temperament and human hypothalamic-limbic structure and function (2010, result): “Again, the evidenced negative correlation between amygdala volume and prosocial temperament scores argued for the behavioral relevance of this finding, as do prior neuroimaging studies that have shown increased amygdala volume in autism (43, 81).”
- Sparse Representation in the Human Medial Temporal Lobe (2006, methodology): “Given the number of stimuli we present and the number of neurons from which we record, we used probabilistic reasoning to explore these issues.”
- The Brain's Default Network (2008, background): “A further consistent observation has been that the amygdala is increased in volume in children with ASD (e.g., Abell et al. 1999, Schumann et al. 2004), perhaps as a reflection of abnormal regulation of brain growth (Courchesne et al. 2001).”
- Mapping early brain development in autism. (2007, neutral): “On MRI, the amygdala in autism is reported to be either similar to (Schumann et al., 2004) or smaller than (Nacewicz et al., 2006; Pierce et al., 2004) normal adolescents and adults.”
- Why Are Autism Spectrum Conditions More Prevalent in Males? (2011, background): “Amgydala 3 [22–25,144–150].”
- A time of change: behavioral and neural correlates of adolescent sensitivity to appetitive and aversive environmental cues. (2010, background): “Sexual dimorphisms have been reported in both global changes in brain structure (Giedd, Castellanos, Rajapakse, Vaituzis, & Rapoport, 1997) as well as differing trajectories for maturation of the amygdala and striatum (Caviness, Kennedy, Richelme, Rademacher, & Filipek, 1996; Giedd et al., 1997; Sch”