Neuronal Density and Architecture (Gray Level Index) in the Brains of Autistic Patients
Abstract
Although neuropathologic studies have centered on small samples, it is accepted that brains of autistic individuals tend to be large, on average. Knowledge regarding the cause of this macrocephaly is limited. Postmortem studies reveal little in terms of cortical dysplasia. Some of these studies suggest increased cell-packing density in subcortical structures. These neuronomorphometric studies have been subjective or based their conclusions on measures of neuronal density. Our study sought the possible presence of increased cell-packing density by using the Gray Level Index. The Gray Level Index is defined as the ratio of the area covered by Nissl-stained elements to unstained area in postmortem samples. Analyzed images included Brodmann's cortical areas 9, 21, and 22 of 9 autistic patients (7 males, 2 females; mean age of 12 years, with a range of 5 to 28 years) and 11 normal controls (7 males, 4 females; mean age of 14 years, with a range of 3 to 25 years). The overall multivariate test revealed significant differences both between autistic patients and controls (P = .001) and between hemispheres (P = .025). Follow-up univariate tests showed significant diagnosis-dependent effects in feature distance (P = .005), the standard deviation in distance (P = .016), and feature amplitude (P = .001). The overall mean Gray Level Index was 19.4% in controls and 18.7% in autism (P = .724). In autism, an increased number of minicolumns, combined with fewer cells per column (or their greater dispersion), results in no global difference in neuronal density. (J Child Neurol 2002;17:515-521).
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ASD patients have smaller and more numerous minicolumns with more dispersed neurons in Brodmann areas 9, 21, and 22, while Asperger's syndrome patients have smaller, less compact minicolumns in the temporal neocortex.
“Patients with ASD have smaller and more numerous minicolumns with more dispersed neurons in Brodmann’s areas 9, 21, and 22 [57, 58], and patients with Asperger’s syndrome have smaller, less compact minicolumns in the temporal neocortex [56].”
From Autism spectrum disorder: neuropathology and animal models (2017) · cites this paper as [58]
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- Authors
- Casanova, M. F., Buxhoeveden, D. P., Switala, A. E., & Roy, E.
- Affiliations
- Augusta University (US)
- Downtown VA Medical Center, Augusta, Georgia
- Venue
- Journal of Child Neurology
- Publisher
- SAGE Publications
- Published
- 2002-07
- Volume
- 17
- Issue
- 7
- Pages
- 515-521
- ISSN
- 0883-0738 (ISSN-L)
- 1708-8283
- OpenAlex
- W2025090265
- Cited by
- 121
- References
- 80
- Citations by year
- 2025: 1 · 2023: 2 · 2022: 2 · 2021: 4 · 2019: 1 · 2018: 2 · 2017: 6 · 2016: 5 · 2015: 13 · 2014: 7 · 2013: 9 · 2012: 10
- FWCI
- 2.19
- Type
- journal article
- Language
- en
- Open access
- closed
- Locations
- Journal of Child Neurology (publishedVersion)
- PubMed (publishedVersion)
- Topics
- Life Sciences › Neuroscience › Cognitive Neuroscience › Autism Spectrum Disorder Research
- Life Sciences › Biochemistry, Genetics and Molecular Biology › Genetics › Genetics and Neurodevelopmental Disorders
- Health Sciences › Medicine › Psychiatry and Mental health › Child Nutrition and Feeding Issues
- Keywords
- autism spectrum disorder, neuronal density, Nissl staining, macrocephaly, hemispheric lateralization, postmortem brain, cortical dysplasia
- MeSH terms
- Adolescent, Adult, Autistic Disorder, Brain, Cell Count, Child, Child, Preschool, Female, Humans, Image Processing, Computer-Assisted, Male, Neurons, Case-Control Studies
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