Ramachandran V S
Center for Research on Brain and Cognition, University of California, San Diego, La Jolla 92093-0109, USA.
Conscious Cogn. 1995 Mar;4(1):22-51. doi: 10.1006/ccog.1995.1002.
Patients with right parietal lesions often deny their paralysis (anosognosia), but do they have "tacit" knowledge of their paralysis? I devised three novel tests to explore this. First, the patients were given a choice between a bimanual task (e.g., tying shoe laces) vs a unimanual one (e.g., threading a bolt). They chose the former on 17 of 18 trials and, surprisingly, showed no frustration or learning despite repeated failed attempts. I conclude that they have no tacit knowledge of paralysis (or, if such knowledge exists, it is not available for this particular task). Second, I used a "virtual reality box" to convey the optical illusion to the patient that she was moving her paralyzed left hand up and down to the rhythm of a metronome, and yet she showed no sign of surprise. Third, I irrigated patient BM's left ear canal with cold water, a procedure that is known to shift that patient's spatial frame of reference by stimulating the vestibular system. Surprisingly, this allowed her "repressed" memory of the paralysis to come to the surface; she said she had been paralyzed continuously for several days. I suggest that the vestibular stimulation produces these remarkable effects by mimicking REM sleep. These patients also employ a whole arsenal of grossly exaggerated Freudian "defense mechanisms" to account for their paralysis. To explain this, I propose that in normal individuals the left hemisphere ordinarily deals with small, local anomalies by trying to impose consistency but, when the anomaly exceeds threshold, an interaction with the right hemisphere forces a "paradigm shift." A failure of this process, in patients with right hemisphere damage, might partially account for anosognosia. Finally, I present a new conceptual framework that may help link several psychological and neurological phenomena such as Freudian defense mechanisms, vestibular stimulation, anosognosia, memory repression, visual illusions, anterograde amnesia, REM sleep, dreaming, and humor.
右侧顶叶病变的患者常常否认自己瘫痪(疾病感缺失),但他们对自己的瘫痪是否有“隐性”认知呢?我设计了三项新颖的测试来探究这一问题。首先,让患者在一项双手任务(如系鞋带)和一项单手任务(如拧螺栓)之间做出选择。在18次试验中,他们有17次选择了前者,令人惊讶的是,尽管多次尝试失败,他们并未表现出沮丧或学习的迹象。我得出结论,他们对瘫痪没有隐性认知(或者说,如果存在这种认知,在这项特定任务中无法体现出来)。其次,我使用一个“虚拟现实盒子”向患者传达视觉错觉,让她觉得自己瘫痪的左手正随着节拍器的节奏上下移动,但她并未表现出惊讶的迹象。第三,我用冷水冲洗患者BM的左耳耳道,这一操作已知会通过刺激前庭系统来改变该患者的空间参照系。令人惊讶的是,这使得她对瘫痪的“被压抑”记忆浮出水面;她说自己已经连续瘫痪了好几天。我认为前庭刺激通过模拟快速眼动睡眠产生了这些显著效果。这些患者还运用了一整套极度夸张的弗洛伊德式“防御机制”来解释自己的瘫痪。为了解释这一点,我提出在正常个体中,左半球通常通过试图强加一致性来处理小的局部异常情况,但当异常超过阈值时,与右半球的相互作用会迫使发生“范式转变”。在右半球受损的患者中,这一过程的失败可能部分解释了疾病感缺失。最后,我提出了一个新的概念框架,它可能有助于将几种心理和神经现象联系起来,比如弗洛伊德式防御机制、前庭刺激、疾病感缺失、记忆压抑、视觉错觉、顺行性遗忘、快速眼动睡眠、做梦和幽默。