THE NATURE OF THE SYMPTOM AND ITS RELEVANCE FOR NEUROPSYCHOLOGY
Jason W. Brown, Maria Pąchalska
New York University Krakowskie Centrum Rehabilitacji
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摘要与影响
The origin of the error or symptom, understood as an unexpected deviation from normal behavior, remains one of the fundamental problems in neuropsychology. Luria regarded a theory of the symptom as a sine qua non for neuropsychology, but he did not have a definitive theory; rather, he applied the insights of various authors in different situations, including Pavlov, Wernicke, Vygotsky, and Goldstein. In microgenetic theory, the symptom is a link from the pathological to the normal, a piece of preliminary behavior that becomes a momentary terminus. In both normal and pathological behavior, microgeny deposits a cognition in the same way that phylogeny and ontogeny deposit the human mind/brain. There is progressive zeroing in on the target over growth planes in brain evolution, moving generally from whole to part, context to item, depth to surface. The microgenetic approach reconsiders the regression hypothesis advanced in a different form by such earlier thinkers as Hughlings Jackson and Roman Jakobson. In contrast to the prevailing assumption that brain function is dynamic and structure is static, the process of structural growth (morphogenesis) and behavior turns out to be one and the same process, reiterated over time, such that behavior is four-dimensional morphology. In order to understand the morphogenesis of brain and behavior, it is necessary to consider the role of two concepts: parcellation and heterochrony. Parcellation is the achievement of specification from the sculpting of exuberant initial growth. Heterochrony refers to the timing of development. In particular, neoteny (the prolongation of an early phase of development) creates the potential for new behavioral possibilities, adaptive or maladaptive. A symptom occurs when a lesion delays a segment of process (neoteny) with incomplete specification (parcellation). The regression hypothesis is reformulated thus: pathology does not expose stages in the reverse of the acquisitional sequence, but rather the process leading to the stages. Further evidence that symptoms undergo a coherent, rather than piecemeal transition is provided by observation of the recovery of function after brain damage. Some aspects of the theory can provide a motivation for research and a strategy for treatment.
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