International Meeting for Autism Research: Amygdala, Hippocampus, and Delayed Memory Impairments in Autism

Amygdala, Hippocampus, and Delayed Memory Impairments in Autism

Friday, May 21, 2010
Franklin Hall B Level 4 (Philadelphia Marriott Downtown)
10:00 AM
J. S. Southwick , Department of Psychology, Brigham Young University, Provo, UT
E. D. Bigler , Psychology & Neuroscience, Brigham Young University, Provo, UT
M. B. DuBray , Interdepartmental Program in Neuroscience, University of Utah, Salt Lake City, UT
A. Froelich , University of Utah, Salt Lake City, UT
A. L. Alexander , Department of Medical Physics, Department of Psychiatry, Waisman Laboratory for Brain Imaging & Behavior, University of Wisconsin, Madison, WI
N. Lange , Departments of Psychiatry and Biostatistics, Harvard University, Belmont, MA
J. E. Lainhart , Psychiatry, University of Utah, Salt Lake City, UT
Background: Impaired cognitive functioning including memory is frequently associated with autism spectrum disorder. Little is known about potential anatomical differences that may be associated with the cognitive deficits observed in autism as compared to typical developing individuals. Several studies have demonstrated that individuals with autism exhibit particular memory deficits, especially delayed retention, for tasks involving complex information, such as the memorization of stories or pictures that they are not intrinsically interested in. Because of the purported role of the hippocampus and amygdala in both memory and autism it is hypothesized that differences in the relationship of these medial temporal lobe structures to memory exists between autism and typical developing controls.
Objectives: Determine the relationship between amygdala and hippocampus volume and delayed memory performance in autism and typical development.
Methods: High functioning, all male participants with autism (n = 46) and typically developing controls (n = 28) ages 5 to 19 completed a delayed verbal recall task, Memory for Stories, and a delayed nonverbal recognition task, Facial Memory, from the Test of Memory and Learning (TOMAL). Memory tests were individually administered as part of a larger battery of neuropsychological measures, including assessment of intellectual ability. To maximize on the potential for the greatest differences in memory performance,  only the 30 minute delayed recall component was examined.  All subjects underwent magnetic resonance imaging (MRI) with image quantification being performed by the FreeSurfer automated image analysis program. 
Results: Groups were matched for Performance IQ (autism, 106.15; controls 111.71) and age (autism, 11.6 yrs.; controls, 11.9 yrs.), and did not differ in head size, handedness, or hippocampal or amygdala volumes. As expected, significant differences were found for Verbal IQ (autism, 93.15; controls, 111.71; p <.001), Memory for Stories-Delayed (autism, 6.93; controls, 11.32; p <.001), and Facial Memory-Delayed (autism, 7.83; controls, 10.04; p <.001).
Partial correlations, controlling for intracranial volume, revealed group differences in amygdalo-hippocampal memory relationships. All correlations for controls were significant for Memory for Stories-Delayed (.40 to .45; p < .05 to .02); both left (.42, p < .04) and total hippocampal volumes (.35; p <.09) related to Facial Memory. Amygdala volume did not significantly correlate with Facial Memory. No significant correlations were found for participants with autism for either memory variable or amygdalo-hippocampal measurement (-.11 to .20; all p values >.20).
Conclusions: The volume of medial temporal lobe structures was found to relate to complex, delayed memory performance in typically developing controls but not individuals with autism. Although participants with autism were equated to controls in terms of non-verbal IQ and there were no differences in age, intracranial volume nor amygdala and hippocampal volumes, distinct differences were observed in memory performance for delayed retention of content information for stories and recollection of observed faces. The absence of significant correlations in the autism group suggests a disconnection in the typical associations observed with medial temporal lobe structures and memory function. This likely has implications for atypical medial temporal lobe connectivity that may be related to the expression of autism and associated cognitive deficits.
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