Gallagher S, Butterworth G E, Lew A, Cole J
Department of Philosophy, Canisius College. Buffalo, NY, USA.
Brain Cogn. 1998 Oct;38(1):53-65. doi: 10.1006/brcg.1998.1020.
Studies of phantom limb in cases of congenital (aplasic) absence of limb have provided inadequate evidence concerning the innate neurological substrate responsible for the phantom. In this study we review evidence from ultrasonic and behavioral studies of hand-mouth coordination in utero and in early infancy, neurobiological studies in primates, and studies of neural reorganization following amputation. We suggest two complementary hypotheses to explain aplasic phantoms. First, aplasic phantoms are based on the existence of specific neural circuitry associated with innate motor schemas, such as the neural matrix responsible for early hand-mouth coordination. Second, aplasic phantoms are modified by mechanisms that involve a reorganization of neural representations of the missing limb within a complex network involving both cortical and subcortical structures.
对于先天性（发育不全性）肢体缺失病例中幻肢现象的研究，尚未提供充分证据来证明负责幻肢的先天性神经学基质。在本研究中，我们回顾了来自以下方面的证据：关于子宫内和婴儿早期手口协调的超声和行为研究、灵长类动物的神经生物学研究以及截肢后神经重组的研究。我们提出两个互补的假说来解释发育不全性幻肢。第一，发育不全性幻肢基于与先天性运动模式相关的特定神经回路的存在，例如负责早期手口协调的神经基质。第二，发育不全性幻肢通过涉及在一个包含皮层和皮层下结构的复杂网络内对缺失肢体的神经表征进行重组的机制而被改变。
