Gage Nicole M, Siegel Bryna, Callen Melanie, Roberts Timothy P L
Biomagnetic Imaging Laboratory, Department of Radiology, University of California, Irvine, CA 92697-5100, USA.
Neuroreport. 2003 Nov 14;14(16):2047-51. doi: 10.1097/00001756-200311140-00008.
Previous work investigating frequency encoding mechanisms in human auditory cortex has provided evidence that latency of the auditory evoked M100 is strongly proportional to frequency, with low frequency (100-200 Hz) tones associated with approximately 30 ms longer latencies than mid-range frequency (1-2 kHz) tones. Motivated by pervasive speech and auditory perception deficits observed in autism spectrum disorder, we evaluated M100 frequency dependence in children with autism disorder and typically developing controls. Results indicate that for control children, the dynamic range of frequency modulation was similar to previous reports for healthy adults. Children with autism had a much reduced range of modulation in right hemisphere sites. Findings indicate that frequency encoding mechanisms may follow a differential maturational path in autism spectrum disorder.
先前研究人类听觉皮层频率编码机制的工作已提供证据表明，听觉诱发M100的潜伏期与频率密切相关，低频（100 - 200赫兹）音调的潜伏期比中频（1 - 2千赫兹）音调长约30毫秒。受自闭症谱系障碍中普遍存在的言语和听觉感知缺陷的影响，我们评估了自闭症谱系障碍儿童和正常发育对照组儿童M100对频率的依赖性。结果表明，对于对照组儿童，频率调制的动态范围与先前关于健康成年人的报告相似。自闭症儿童右半球区域的调制范围明显减小。研究结果表明，频率编码机制在自闭症谱系障碍中可能遵循不同的成熟路径。
