Department of Psychology, University of Turku, 20014, Finland; Turku Brain and Mind Centre, University of Turku, 20014, Finland.
Department of Psychology, University of Turku, 20014, Finland; Turku Brain and Mind Centre, University of Turku, 20014, Finland.
Neuroimage. 2019 Jan 15;185:313-321. doi: 10.1016/j.neuroimage.2018.10.058. Epub 2018 Oct 23.
The study of blindsight has revealed a seminal dissociation between conscious vision and visually guided behavior: some patients who are blind due to V1 lesions seem to be able to employ unconscious visual information in their behavior. The standard assumption is that these findings generalize to the neurologically healthy. We tested whether unconscious processing of motion is possible without the contribution of V1 in neurologically healthy participants by disturbing activity in V1 using transcranial magnetic stimulation (TMS). Unconscious processing was measured with redundant target effect (RTE), a phenomenon where participants respond faster to two stimuli than to one stimulus, when the task is just to respond as fast as possible when one stimulus or two simultaneous stimuli are presented. We measured the RTE caused by a motion stimulus. V1 activity was interfered with different stimulus onset asynchronies (SOA) to test whether TMS delivered in a specific time window suppresses conscious perception (participant reports seeing only one of the two stimuli) but does not affect unconscious processing (RTE). We observed that at each SOA, when TMS suppressed conscious perception of the stimulus, the RTE was also eliminated. However, when visibility of the redundant target was suppressed with a visual mask, we found unconscious processing of motion. This suggests that unconscious processing of motion depends on V1 in neurologically healthy humans. We conclude that the neural mechanisms that enable motion processing in blindsight are modulated by neuroplastic changes in connectivity between subcortical areas and the visual cortex after the V1 lesion. Neurologically healthy observers cannot process motion unconsciously without functioning of V1.
一些由于 V1 损伤而失明的患者似乎能够在行为中利用无意识的视觉信息。标准假设是,这些发现适用于神经健康的人。我们通过经颅磁刺激(TMS)干扰 V1 的活动来测试在神经健康的参与者中,是否可以在没有 V1 贡献的情况下无意识地处理运动,使用冗余目标效应(RTE)来测量无意识处理,当任务只是尽可能快地对一个刺激或两个同时刺激做出反应时,参与者对两个刺激的反应比一个刺激更快的现象。我们测量了运动刺激引起的 RTE。用不同的刺激起始时间间隔(SOA)干扰 V1 活动,以测试 TMS 是否在特定的时间窗口内抑制意识感知(参与者报告只看到两个刺激中的一个),但不影响无意识处理(RTE)。我们发现,在每个 SOA 下,当 TMS 抑制对刺激的意识感知时,RTE 也被消除。然而,当用视觉掩蔽抑制冗余目标的可见性时,我们发现了运动的无意识处理。这表明,在神经健康的人类中,无意识处理运动依赖于 V1。我们得出结论,使盲视中的运动处理成为可能的神经机制是通过 V1 损伤后皮质下区域和视皮层之间的连接的神经可塑性变化来调节的。神经健康的观察者如果没有 V1 的功能,就无法无意识地处理运动。