Department of Psychiatry, National Taiwan University Hospital and College of Medicine, Taipei, Taiwan.
Department of Psychiatry, National Taiwan University Hospital and College of Medicine, Taipei, Taiwan; Graduate Institute of Clinical Medicine, College of Medicine, National Taiwan University, Taipei, Taiwan; Graduate Institute of Brain and Mind Sciences, and Graduate Institute of Epidemiology and Preventive Medicine, College of Medicine, National Taiwan University, Taipei, Taiwan.
Prog Neuropsychopharmacol Biol Psychiatry. 2019 Dec 20;95:109683. doi: 10.1016/j.pnpbp.2019.109683. Epub 2019 Jun 28.
Sensory symptoms are common in individuals with autism spectrum disorder (ASD). Altered sensory gating may cause sensory overload. However, whether ASD individuals have P50 gating deficits is controversial in childhood and lacks evidence in adulthood. Beyond P50, fewer studies have examined N100 or P200, although N100 is considered to be more reliable than P50. Also, the clinical correlates of these parameters are mostly unknown. This study aimed to investigate P50, N100, and P200 sensory gating in adolescents and young adults with ASD and examine their clinical correlates. In a sample of 34 ASD participants (mean age 20.6 ± 4.1, female 5.9%) and 34 sex- and age-matched typically-developing controls (TDC, mean age 20.4 ± 3.1), we investigated P50, N100, and P200 sensory gating by a paired-click paradigm, which generated the data of S1 amplitude after the first click and S2 amplitude after the second click. We found that compared to TDC, ASD participants had significant N100 suppression deficits reflected by a larger N100 S2 amplitude, smaller N100 ratio of S2 over S1, and the difference between the two amplitudes. N100 S2 amplitude was significantly associated with sensory sensitivity independent of the diagnosis. Although there was no group difference in P50 suppression, S1 amplitude was negatively associated with social deficits in ASD. P200 gating parameters were correlated with attention switching difficulty. Our findings suggest N100 gating deficit in adolescents and young adults with ASD. The relationships between P50 S1 and social deficits and between N100 S2 and sensory sensitivity warrant further investigation.
感觉症状在自闭症谱系障碍（ASD）个体中很常见。感觉门控的改变可能导致感觉过载。然而，在儿童时期，ASD 个体是否存在 P50 门控缺陷存在争议，并且在成年期缺乏证据。除了 P50，较少的研究检查了 N100 或 P200，尽管 N100 被认为比 P50 更可靠。此外，这些参数的临床相关性大多未知。本研究旨在调查 ASD 青少年和年轻成人的 P50、N100 和 P200 感觉门控，并研究其临床相关性。在 34 名 ASD 参与者（平均年龄 20.6±4.1，女性 5.9%）和 34 名性别和年龄匹配的正常发育对照者（TDC，平均年龄 20.4±3.1）的样本中，我们通过配对点击范式研究了 P50、N100 和 P200 感觉门控，该范式生成了第一个点击后的 S1 幅度数据和第二个点击后的 S2 幅度数据。我们发现，与 TDC 相比，ASD 参与者的 N100 抑制缺陷显著，表现为 N100 S2 幅度较大、N100 S2 与 S1 的比值较小以及两个幅度之间的差异。N100 S2 幅度与感觉敏感性显著相关，与诊断无关。尽管 P50 抑制没有组间差异，但 S1 幅度与 ASD 中的社交缺陷呈负相关。P200 门控参数与注意转换困难相关。我们的发现表明，ASD 青少年和年轻成人存在 N100 门控缺陷。P50 S1 与社交缺陷之间的关系以及 N100 S2 与感觉敏感性之间的关系值得进一步研究。
