Neuronal density and architecture (Gray Level Index) in the brains of autistic patients

被引:72
作者
Casanova, MF
Buxhoeveden, DP
Switala, AE
Roy, E
机构
[1] Downtown VA Med Ctr, Dept Psychiat, Augusta, GA 30904 USA
[2] Med Coll Georgia, Dept Psychiat, Augusta, GA 30912 USA
[3] Med Coll Georgia, Dept Neurol, Augusta, GA 30912 USA
关键词
D O I
10.1177/088307380201700708
中图分类号
R74 [神经病学与精神病学];
学科分类号
摘要
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 =.0 16), 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.
引用
收藏
页码:515 / 521
页数:7
相关论文
共 90 条
[1]  
Afifi AK., 1998, FUNCTIONAL NEUROANAT
[2]  
Allman J., 1990, Cerebral Cortex, V8A, P269
[3]  
Allman J., 1977, PROGR PSYCHOBIOLOGY, V7, P1
[4]   Postnatal development of interhemispheric asymmetry in the cytoarchitectuve of human area 4 [J].
Amunts, K ;
SchmidtPassos, F ;
Schleicher, A ;
Zilles, K .
ANATOMY AND EMBRYOLOGY, 1997, 196 (05) :393-402
[5]  
[Anonymous], 1981, ORG SOMATOSENSORY CO
[6]   Autism: Towards an integration of clinical, genetic, neuropsychological, and neurobiological perspectives [J].
Bailey, A ;
Phillips, W ;
Rutter, M .
JOURNAL OF CHILD PSYCHOLOGY AND PSYCHIATRY, 1996, 37 (01) :89-126
[7]   AUTISM AND MEGALENCEPHALY [J].
BAILEY, A ;
LUTHERT, P ;
BOLTON, P ;
LECOUTEUR, A ;
RUTTER, M ;
HARDING, B .
LANCET, 1993, 341 (8854) :1225-1226
[8]   A clinicopathological study of autism [J].
Bailey, A ;
Luthert, P ;
Dean, A ;
Harding, B ;
Janota, I ;
Montgomery, M ;
Rutter, M ;
Lantos, P .
BRAIN, 1998, 121 :889-905
[9]   HISTOANATOMIC OBSERVATIONS OF THE BRAIN IN EARLY INFANTILE-AUTISM [J].
BAUMAN, M ;
KEMPER, TL .
NEUROLOGY, 1985, 35 (06) :866-874
[10]  
Bauman M.L., 1996, NEUROBIOLOGY AUTISM, P119