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ARTICLES: H. Petropoulos, S. D. Friedman, D.W.W. Shaw, A. A. Artru, G. Dawson, and S. R. Dager Gray matter abnormalities in autism spectrum disorder revealed by T2 relaxation Neurology 2006; 67: 632-636 [Abstract] [Full text] [PDF]

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Gray matter abnormalities in autism spectrum disorder revealed by T2 relaxation

Silvio Loddo   (9 November 2006)

Reply from the Authors

Stephen R. Dager, MD, Helen Petropoulos, Seth D. Friedman, Dennis W.W. Shaw   (9 November 2006)

Gray matter abnormalities in autism spectrum disorder revealed by T2 relaxation 9 November 2006
Silvio Loddo, Neuropsichiatria dell'Età Evolutiva AUSL n. 5 Oristano, Piazza S. Martino, 09170 Oristano, Italy Send Correspondence to journal: Re: Gray matter abnormalities in autism spectrum disorder revealed by T2 relaxation svloddo{at}tiscali.it Silvio Loddo	Petropoulos et al’s findings about gray matter abnormalities in autism [1] suggest a possible underdevelopment or a dysfunction of a particular subset of neurons in this disorder and that white matter abnormalities might appear late in development. Recent studies on autism have detected reduced coordination between cortical areas involved in the execution of complex tasks. [2] A reduced synchronization in the gamma band [3] has been suggested as the cause of the weak central coherence and executive dysfunction in this disorder. Interneurons are considered to play a crucial role in the generation of brain rhythms which coincide with the performance of cognitive tasks [4] so that a neurobiological account of autism should take into consideration an interneuronal deficit. An account on autism as a disorder of interneurons would be parsimonious and exhaustive. It would imply that in physiological conditions, a system of coordination of mental functions would have an in-built relais in every single minicolumn and that this system would be distributed all over the cortex. This system would be capable of rapid adjustments in the gating of impulses toward the correct neuronal groups and away from those which are not involved in the processing of a particular category of stimuli. This putative interneuronal activity might receive bottom-up signals from lower cortical areas. For example, when optical stimuli pertaining to a facial configuration must be preferentially transmitted to holistic processing areas of the cortex such as the fusiform gyrus, or top-down modulations from higher cortical centers. For example, when the amygdala is reached by upstream signals from emotionally laden elements in the environment, it consequently directs attentional resources toward those elements. If correct, this account of autism would immediately generate the next question: In which class(es) or particular cellular structures and processes of interneurons would the dysfunction reside? References 1. Petropoulos H, Friedman SD, Shaw DWW, Artru AA, Dawson G, Dager SR. Gray matter abnormalities in autism spectrum disorders revealed by T2 relaxation. Neurology 2006;67;632-636. 2. Bertone A, Mottron L, Jelenic P, Faubert J. Enhanced and diminished visuo-spatial information processing in autism depends on stimulus complexity. Brain 2005;128:2430-2441. 3. Brock J, Brown CC, Boucher J, Rippon G. The temporal binding deficit hypothesis of autism. Development and Psychopathology 2002;14:209–224. 4. Whittington MA, Traub RD. Interneuron diversity series: inhibitory interneurons and network oscillations in vitro. Trends Neurosci. 2003;26:676-82. Disclosure: The authors report no conflicts of interest.
Reply from the Authors 9 November 2006
Stephen R. Dager, MD, University of Washington 1100 NE 45th, Suite 555, Seattle, WA 98105, Helen Petropoulos, Seth D. Friedman, Dennis W.W. Shaw Send Correspondence to journal: Re: Reply from the Authors srd{at}u.washington.edu Stephen R. Dager, MD, et al.	Dr Loddo’s letter presents an interesting perspective in response to our findings. [1] Theories of disrupted interneuron development and unbalanced excitatory and inhibitory interneuron connectivity in autism are intriguing. [5] In particular, models of reduced inhibitory GABAergic interneurons [6] in conjunction with altered minicolumn organization observed in autism [7] are consistent with our findings of abnormal gray matter structure evidenced by prolonged cortical grey matter T2 relaxation in this population. Additional regional analyses of T2 relaxation differences may help to further elucidate general abnormalities of cytoarchitecture in autism. Direct insight into abnormal interneuron connectivity, and for a particular subset of neurons, will require more targeted research strategies for in vivo assessment. References 5. Gustafsson, L. Excessive lateral feedback synaptic inhibition may cause autistic characteristics. J Autism Dev Disord 1997; 27:219-220. 6. Levitt, P. Disruption of interneuron development. Epilepsia 2005;46 Suppl 7:22-28. 7. Casanova MF, Buxhoeveden DP, Switala AE, Roy E. Minicolumnar pathology in autism. Neurology. 2002; 12;58:428-432. Disclosure: The authors report no conflicts of interest.