Hughes John R
Department of Neurology, University of Illinois Medical Center at Chicago, 912 South Wood Street, Chicago, IL 60612, USA.
Epilepsy Behav. 2007 Aug;11(1):20-4. doi: 10.1016/j.yebeh.2007.03.010. Epub 2007 May 24.
In January 2005, J.R. Hughes and M. Melyn published an electroencephalographic study on autistic children and found 46% with seizures and also a relatively high prevalence of 20% with epileptiform discharges but without any clinical seizures (Clin EEG Neurosci 2005;36:15-20). Because the discharges have always been viewed as focal events and the clinical seizures as requiring spread, the conclusion from these data was that children with autism may have a deficiency of corticocortical fibers. Since that time many MRI and functional MRI studies have been published confirming that one of the first findings in this devastating condition is underconnectivity. Specific findings are the thinning of the corpus callosum and the reduced connectivity, especially with the frontal areas and also the fusiform face area. Other studies involving positron emission tomography scans, magnetoencephalography, and perception have added to the evidence of underconnectivity. One final point is the initial overgrowth of white matter in the first 2 years of life in autistic children, followed later by arrested growth, resulting in aberrant connectivity; myelination of white matter will likely be significant in the etiology of autism.
2005年1月,J.R. 休斯和M. 梅林发表了一项关于自闭症儿童的脑电图研究,发现46%的自闭症儿童患有癫痫,还有20%的儿童有癫痫样放电但无任何临床癫痫发作,这一比例相对较高(《临床脑电图与神经科学》2005年;36:15 - 20)。由于这些放电一直被视为局灶性事件,而临床癫痫发作被认为需要扩散,因此从这些数据得出的结论是,自闭症儿童可能存在皮质皮质纤维缺陷。从那时起,许多磁共振成像(MRI)和功能磁共振成像(fMRI)研究已经发表,证实了在这种毁灭性疾病中最早发现的一个现象是连接不足。具体表现为胼胝体变薄以及连接减少,尤其是与额叶区域以及梭状面孔区的连接减少。其他涉及正电子发射断层扫描、脑磁图和感知的研究进一步补充了连接不足的证据。最后一点是,自闭症儿童在生命的头两年白质最初过度生长,随后生长停滞,导致连接异常;白质髓鞘形成可能在自闭症病因中起重要作用。