There has evolved a conventional approach to analysis of the effect of brain dysfunction, induced by anatomical damage or chemical disruption, on learning and memory. The results have indicated that brain dysfunction impairs some instances of learning and memory, but not all. Given verification that the sensory detection of events to be learned is not impaired, the conventional conclusion has been that brain dysfunction can disrupt the operation of some systems of learning and memory but leave others quite intact.
The clear and often dramatic dissociation between how the CNS is impaired and what aspects of learning and memory are impaired has had an appropriately forceful impact that has shaped this conventional analysis. Yet this analysis, and the general case for separate memory systems, is weakened by an often-overlooked consequence of brain dysfunction: the enhancement of learning and memory that sometimes occurs. Some instances of this enhancement are dismissible as method-specific artifacts that are relatively uninteresting, such as lesion-induced increases in activity imposed on learning that is especially indicated by high levels of activity. Yet the number and variety of enhancement examples argue for their serious consideration and for the reality of enhanced memory function as one consequence of brain dysfunction.
One could conceivably deal with this in terms of a multiple-memory-systems approach, but new and untested assumptions would be necessary. A much simpler form of explanation is possible. Perhaps it is not so much entire memory systems that are affected by brain damage, but subprocesses of the one (or perhaps more) memory system(s). We have in mind subprocesses such as orienting, attention, encoding and retrieval, with present emphasis on changes in encoding that lead to corresponding changes in what is learned and remembered. How might the array of memory changes induced by brain dysfunction be accounted for in these terms? Considerations of recent studies of the ontogeny of learning and memory provide a guide.
Similar to the case of brain dysfunction and memory (although by no means directly analogous), animals and people with a relatively immature brain during the early phases of ontogeny typically have been less effective in learning and memory than are those in later stages of ontogeny. This, too, has been explained by some theorists in terms of the differential availability of certain memory systems; the notion is that early in ontogeny, the critical memory systems needed for effective learning and memory have not yet developed. Like the case of general memory dysfunction, however, this interpretation is complicated by a variety of instances of more effective learning early in ontogeny than later on. An alternative interpretation focusing on ontogenetic changes in encoding and stimulus selection has proven useful. Perhaps it would be equally useful to consider similarly the encoding changes that result from general brain dysfunction.