Levine D N
Neurology Services, Spaulding Rehabilitation Hospital, Boston, MA 02114.
Brain Cogn. 1990 Jul;13(2):233-81. doi: 10.1016/0278-2626(90)90052-p.
A theory is proposed to account for unawareness of blindness, hemianopsia, and hemiplegia, and for phantom limb after amputation. It is assumed that interruption of a sensory pathway at any level--from peripheral nerve to primary sensory cortex--is not associated with any immediate sensory experience that uniquely specifies the defect. Instead the sensory loss must be discovered by a process of self-observation and inference. Discovery is easy for defects that create major functional disability, such as total blindness. Hence unawareness of total blindness occurs only in association with severe intellectual impairment, precluding the required self-observation and inference. In contrast, hemianopsia is difficult to discover because several mechanisms automatically compensate the defect effectively. Thus unawareness of hemianopsia is common, even in intellectually normal individuals. Insensate fields are often the source of suggested (false) percepts, because no information from such a field specifies the absence of a sensory stimulus. The most powerful source of suggestion is sensory activity in uninvolved portions of the affected sensory field. Thus hemianopsics may perceive complete geometric forms when only incomplete forms are shown and the missing portion falls in the hemianopsic fields. Such perceptual completion also occurs in hemianesthetic hemiplegics, creating the illusion that there are normally functioning limbs on the affected side. This perceptual completion increases the difficulty of discovery of hemianesthetic hemiplegia, but the disability is still sufficiently obvious that some additional cognitive impairment is invariably present in patients with lasting unawareness of hemiplegia. Phantom limb after amputation is the product of perceptual completion without associated cognitive impairment. The patient with phantom limb is thus aware of the illusory quality of his phantom. Some insight into the neural basis of perceptual completion and of unawareness of sensory loss may derive from considering sensory systems and associative cortex as parallel-distributed processing mechanisms.
本文提出了一种理论,用以解释失明、偏盲和偏瘫患者的不自知现象,以及截肢后的幻肢现象。我们假设,从外周神经到初级感觉皮层的任何水平的感觉通路中断,都不会立即产生能唯一确定缺陷的感觉体验。相反,感觉丧失必须通过自我观察和推理的过程才能被发现。对于造成严重功能残疾的缺陷,如完全失明,发现起来很容易。因此,只有在伴有严重智力障碍,无法进行必要的自我观察和推理时,才会出现对完全失明的不自知。相比之下,偏盲很难被发现,因为有几种机制能有效地自动补偿这种缺陷。因此,即使在智力正常的个体中,偏盲不自知也很常见。无感觉区域常常是引发(错误)感知的源头,因为来自该区域的信息无法表明没有感觉刺激。最强大的引发因素是受影响感觉区域未受影响部分的感觉活动。因此,当只展示不完整的几何图形,且缺失部分落在偏盲区域时,偏盲患者可能会感知到完整的几何图形。这种感知完整性也会出现在偏身感觉缺失的偏瘫患者身上,产生患侧肢体功能正常的错觉。这种感知完整性增加了发现偏身感觉缺失性偏瘫的难度,但残疾仍然足够明显,以至于持续不自知偏瘫的患者总是伴有一定程度的认知障碍。截肢后的幻肢是没有相关认知障碍的感知完整性的产物。因此,幻肢患者能意识到其幻肢的虚幻性质。通过将感觉系统和联合皮层视为并行分布式处理机制,或许能对感知完整性和感觉丧失不自知的神经基础有一些深入了解。