Introduction

It has been known for more than 100 years that brain damage can impair memory in a relatively selective fashion. In the past 50 years, it has also become clear that damage to different brain regions selectively disrupts some kinds of memory, but leaves other kinds of memory intact. Since the 1970s, it has become increasingly possible to scan the brains of living memory-impaired subjects to better identify the location of damage that causes specific kinds of memory deficit. In the 1990s, research exploring the effects of differently located brain lesions on memory was complemented by neuroimaging studies that have explored the brain regions that are activated when particular memory processes are engaged. These neuroimaging studies have helped clarify the normal role of brain structures that when damaged cause different kinds of memory disorder.

Memory depends on encoding (processing and representing) different kinds of information, which are then stored and later retrieved. The occurrence of selective memory disorders has several implications about the way in which the brain mediates these processes. First, the existence of selective memory disorders is surprising because it means that memory loss occurs although the information for which memory is impaired is still being processed (and hence encoded) relatively normally. This challenges a widely held assumption that information is stored in the same neural network that represents it during encoding because if the assumption is correct, then brain lesions that damage such networks should disturb not only storage but also the ability to process and represent the information. In other words, the assumption seems difficult to reconcile with the occurrence of selective memory deficits for particular kinds of information that are still processed normally at input. Because retrieval and encoding involve many overlapping processes, the assumption is still problematic even if it was postulated that a memory deficit was caused by a retrieval deficit. Therefore, care must be taken to determine the selectivity of memory disorders.

Second, the existence of different kinds of memory disorders is consistent with growing evidence that the whole central nervous system is, to varying degrees, plastic and thus capable of storing memories. The spinal cord, as well as the brain, should be regarded as a storer as well as a processor of information. That different kinds of memory should be disrupted by lesions in different brain areas should not be surprising because it is known that different kinds of information are processed and represented in different parts of the central nervous system.

Third, the existence of several different kinds of selective memory disorders caused by lesions in distinct brain regions has resulted in the view that there are several systems of memory organized in a hierarchical fashion. Memory systems differ from each other not only because they are mediated by distinct systems of neurons but also because they involve qualitatively distinct kinds of memory processes. Memory systems are organized hierarchically to the extent that certain kinds of memory share more qualitatively similar kinds of processes with each other than they do with other kinds of memory.

What is known about the range of short- and long-term memory disorders caused by brain damage and the selectivity of these disorders to memory are outlined before briefly considering what this reveals about how the brain mediates memory.

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