Commentary on THOMAS

Abstract: 88 words
Main Text: 685 words
References: 110 words
Total Text: 963 words

Encapsulating Architecture and Encapulating Processes

Abstract

Thomas and Karmiloff-Smith raise the excellent, and in retrospect, obvious, point that in a dynamic learning environment where feedback is possible, we should expect networks to adapt to damage by altering details of their behavior. We should therefore not expect that developmental disorders should result in "normal" modules. The implications of this point go much further, since interprocess dependency in the brain does not rely only on learned neural connections. This argues strongly against behavioral and process-related definitions, as opposed to structural and architecture-related definitions, of mental modularity.

One mark of a good scientific paper is that it raises new issues. By this standard, Thomas and Karmiloff-Smith have written an excellent paper. The issue of "Residual Normality" should be crucial to any analysis where neuroplasticity or development is an issue. In a dynamic and complex system, one expects damage, alterations or perturbations to one facet of the system to be reflected in changed behavior of both the sytem as a whole and of other facets -- this is part of the fundamentals of complexity (Nichols & Prigogine, 1989). Within broad limits, neural tissue can adapt itself to changes in its environment, including changes in the surrounding tissue. And although researchers can comfortably expect lifetime employment in teasing out exactly what those limits are, we have no reason a priori to believe that the components of a system fully adapted to an unusual environment will behave ``normally.''

However, it remains an open question what time-scale is necessary for this sort of adaptation. Specifically, the notion of "Residual Normality" assumes a very strong version of mental modularity, a theoretical position at best controversial (Juola & Plunkett, 1998, Dunn & Kirsner, in press). Mental modules are assumed to be encapsulated to a degree that it is possible to damage a single module without affecting others at all. Not even an automobile displays this level of modularity --- bad alignment of the front tires will immediately drop the fuel efficiency, and will probably even result in the radio volume increasing. These are the result of a complex feedback system : the poor alignment makes increased tire noise, causing the human driver to turn up the radio to drown it out. The radio doesn't behave ``normally'' in the presence of faulty alignment.

This sort of feedback and recovery is explicit in the experimental setup of simulation 2; although a damaged module such as the indirect route may not directly interact with the direct route, the learning mechanism will compensate for errors by adjusting the weights in the undamaged module. However, the performance of the undamaged route will only be "normal," if there is no feedback at all in the system to alter performance. Three factors assure this in the connectionist system under discussion. First, the topology of the network makes it impossible for changes in indirect representation to affect direct representation, so that there is no immediate effect of a lesion to the indirect route on the weights of the direct route. Second, no further learning/change can occur after insult; in the case of the connectionist model, only "endstate" damage will result normality, while in the case of a human, we assume that the neuroplasticity of an adult approximates zero. Third, the inflectional module itself is sufficiently encapsulated that it can be modelled in isolation from the rest of cognition.

Unfortunately, it's not clear, and perhaps not even likely, that any of these three conditions hold in vivo. The human brain appears to be deeply interconnected, to the point that the stress of hospitalization (Bates et al., 1987) or of unrelated cognitive processing (Blackwell & Bates, 1995) can produce symptoms similar to the loss of a neural module. This dependence on cognitive resources provides an immediate pathway for cognitive change in unrelated modules immediately after insult, and shows the dependence of these hypothesized "modules" on the rest of the brain.

Common sense and the new experimental findings both support the idea that the brain can compensate for its own failure to develop correct processes by altering other processes in the brain. Bates et al. have shown that the correctness of processes in normal adults is subject to variation. Within this framework, the idea of mental modules as encapsulated "processes" is an increasingly difficult one to support. Our strongest evidence for modules within the system built by Thomas and Karmiloff-Smith is architectural: the topology of the network. Arguments from localization of brain function and neural mappings can produce the same evidence for architectural modularity in the brain, evidence that behavioral studies cannot duplicate. The issues raised by Thomas and Karmiloff-Smith are yet another reason to distrust behavioral evidence.

References

Bates, E., Friederici, A. & Wulfeck, B. (1987). Comprehension in aphasia : A Cross-Linguistic Study. Brain and Language, 32, 19-37.

Blackwell, A. & Bates, E. (1995). Inducing agrammatic profiles in normals: Evidence for the selective vulnerability of morphology under cognitive resource limitation. Journal of Cognitive Neuroscience, 7(2), 228-257.

Dunn, J. & Kirsner, K. (in press). What can we infer from double dissociations? Cortex.

Juola, P. & Plunkett, K. (1998) Why double dissociations don't mean much. Proceedings of the 20th Annual Conference of the Cognitive Science Society. 561-566.

Nichols, G. & Prigogine, I. (1989) Exploring Complexity : An Introdution. New York : W. H. Freeman & Co.