PubMed · 5209974
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J M Little. 1971-10-01. An immediate prosthesis.. https://pubmed.ncbi.nlm.nih.gov/5209974/
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This study presents a review of the literature on the attributes and potential mechanisms involved in phantom limb pain, encompassing studies describing pain in the residual limb, phantom sensation and phantom limb pain, and the difficulties that may arise when making these distinctions. A variety of theories have been proposed to explain causal mechanisms for phantom limb pain. Conceptually, research into phantom limb pain is informed by the particular theory of chronic pain that is dominant at the time the research is undertaken. For example, early physiological theories on the etiology of phantom limb pain were grounded in specificity or pattern theories of pain. Later physiological research was based on the framework provided by Gate Control Theory and focused on identifying peripheral, spinal, and central neural mechanisms. Psychological explanations were grounded in psychoanalytic or personality theories of chronic pain which propose that phantom limb pain results from pre-amputation psychological disturbance. Despite numerous studies examining phantom limb pain, much of this research has both conceptual and methodological shortcomings. As such, the application of these research findings to clinical practice has limited utility.
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Formation of a regeneration blastema following limb amputation is believed to occur through a process of dedifferentiation. It has been suggested, however, that the cells contributed to the blastema by the stump muscle are satellite-like cells, rather than cells originated by dedifferentiation. We have previously shown that simple epithelial keratins 8 and 18 are expressed in the mesenchymal progenitor cells of the regenerating amphibian limb and in cultured cells with myogenic potential, and that their expression appears to be causally related to changes in proliferation and differentiation. We show here that retinoic acid (RA) affects the expression of these keratins differently in myogenic cells originated from normal limb and limb blastema. Furthermore, we find that the effects of RA on proliferation, myogenic differentiation and adhesion of these cells also differ. In fact, whereas RA does not affect keratin expression, proliferation or myogenic differentiation in blastemal cells, it does decrease keratin levels and thymidine incorporation and increase myogenesis in cells from normal limb. Conversely, RA increases cell adhesion only in blastemal cells. Significantly, these effects of RA on cultured cells are consistent with those observed in vivo. Overall the results presented here suggest that in the urodele limb there are two distinct cell populations with myogenic potential, one originating from dedifferentiation and one equivalent to the satellite cells of the mammalian muscle, which are likely to be primarily involved in blastema formation and muscle repair, respectively.