Some of the brain structures involved in amnesia (indicated by asterisks). Figure from "Clinical symptoms, neuropathology and etiology" by Nelson Butters and Laird S.Cermak in Alcoholic Korsakoff's syndrome: An information-processing approach to amnesia. Copyright © 1980 by Academic Press, reproduced by permission of the publisher.

misleading; both groups have damage to the same functional system.The proposed hippocampal-diencephalic system is required for the encoding of episodic information, permitting the information to be set in its spatial and temporal context." They argued that there is a second system involving the perirhinal cortex of the temporal lobe and the medial dorsal nucleus of the thalamus which is involved in making familiarity judgements on tests of recognition memory. It is difficult to find patients with damage to only one system because, "in the large majority of amnesic cases both the hippocampal-anterior thalamic and the perirhinal-medial dorsal thalamic systems are compromised, leading to severe deficits in both recall and recognition." Various views on this theory are provided in the commentaries that immediately followed the Aggleton and Brown (1999) article in Behavioral and Brain Sciences.

So far there have been relatively few attempts to move beyond the broad notion of an amnesic syndrome. However, the development of increasingly sophisticated brain-scanning techniques (see Chapter 1) means we can now identify the precise regions of brain damage in amnesics more accurately than before. It is likely in the future that theorists will begin to propose various specific categories of amnesia linked to particular damaged brain areas.

Retrograde amnesia

Retrograde amnesia is the Cinderella of amnesia research, in that it has not received anything like the attention paid to anterograde amnesia. The characteristics of retrograde amnesia vary considerably from patient to patient, sometimes involving severe retrieval problems for memories formed several years before the onset of amnesia, and sometimes involving minor retrieval problems for memories covering a much shorter period. However, there is generally a temporal gradient, with retrieval problems being greater for memories acquired closer to the onset of the amnesia than those acquired longer ago.

Most amnesic patients show evidence of both retrograde and anterograde amnesia, which might suggest that they depend on damage to the same brain structures. The evidence from postmortem analyses indicates that the extent of both retro-grade and anterograde amnesia depends on the amount of damage to medialtemporal structures in the brain. In addition, both forms of amnesia share features, such as impaired recall and recognition of factual information (e.g., public events) and of autobiographical information.

There are also important differences between retrograde and anterograde amnesia. Damage restricted to a small part of the hippocampal region known as the CA1 field produces only anterograde amnesia (Gabrieli, 1998). Perhaps as a result, the severity of retrograde amnesia often correlates poorly with the severity of anterograde amnesia. Some patients have focal retrograde amnesia, in which the main deficit is retrograde rather than anterograde. Such patients generally have damage to the anterior temporal lobe, or the posterior temporal lobe, or the frontal lobe. The important point is that these areas are not thought to be directly associated with the amnesic syndrome.

Evidence supporting the involvement of the temporal lobe in producing retrograde amnesia was reported by Reed and Squire (1998) in a study of four amnesic patients. MRI examinations indicated that all four had hippocampal damage, but only two also had temporal lobe damage. The two patients with temporal lobe damage had severe anterograde amnesia for facts and events, whereas the other two patients had limited anterograde amnesia covering only a few years. These findings led Reed and Squire (1998, p. 3953) to conclude: "RA [retrograde amnesia] can be quite limited or very extensive, depending on whether the damage is restricted to the hippocampal formation or also involves additional temporal cortex."

The precise relationship between retrograde and anterograde amnesia remains unclear. The present state of play was summarised by Mayes and Downes (1997, p. 30): "The evidence is certainly strong enough to suggest that substantial components of AA [anterograde amnesia] and RA [retrograde amnesia] dissociate from one another, but it is still far from conclusively favouring either dissociation or its opposite."

Korsakoff patients

Many studies on amnesia have made use almost exclusively of Korsakoff patients. How suitable are such patients for understanding the processes underlying amnesia? There are two main problems posed by Korsakoff patients. First, the amnesia usually has a gradual onset. It is caused by an increasing deficiency of the vitamin thiamine, which is associated with chronic alcoholism. As a result, it is often hard to know whether past events occurred before or after the onset of amnesia. Second, brain damage in Korsakoff patients is often rather widespread. Structures within the diencephalon, such as the hippocampus and amygdala, are usually damaged, and these structures seem to be of vital significance to memory. In addition, there is very often damage to the frontal lobes. This may produce a range of cognitive deficits that are not specific to the memory system, but which have indirect effects on memory performance. It would be easier to make coherent sense of findings from Korsakoff patients if the brain damage were more limited.

Residual learning ability

If we are to understand amnesia, it is important to consider which aspects of learning and memory remain fairly intact in amnesic patients. These aspects are commonly referred to as "residual learning ability". It would be useful to draw up lists of those memory abilities impaired and not impaired in amnesia. By comparing the two lists, it might be possible to identify those processes and/or memory structures that are affected in amnesic patients. Theoretical accounts could then proceed on a solid foundation of knowledge. The available evidence is less extensive than would be desirable, but we will consider it in some detail.

Short-term memory

Amnesic patients have a fairly intact short-term memory system, but a severely deficient long-term memory system. Korsakoff patients perform almost as well as normals on the digit-span task (e.g., Butters & Cermak, 1980). Similar results have also been found in non-Korsakoff patients. NA became amnesic as a result of having a fencing foil forced up his nostril and into his brain. This caused widespread diencephalic and medial temporal damage. Teuber, Milner, and Vaughan (1968) found that he performed at the normal level on span measures. HM had an operation that damaged the temporal lobes, together with partial removal of the hippocampus and amygdala, He had intact short-term memory as indexed by immediate span (Wickelgren, 1968).

Span measures are not the only way in which short-term memory can be assessed. Baddeley and Warrington (1970) observed normal performance by amnesic patients on various measures of short-term memory (e.g., recency effect in free recall).

Skill learning

Skill learning in amnesics can be divided into sensori-motor and perceptual skills. So far as sensori-motor skills are concerned, amnesics have been shown to have normal rates of learning for the pursuit rotor, serial reaction time, and mirror tracing (see Gabrieli, 1998). Each of these skills will be considered in turn.

Corkin (1968) reported that the amnesic patient HM was able to learn mirror drawing and the pursuit rotor, which involves manual tracking of a moving target. His rate of learning was slower than that of normals on the pursuit rotor. In contrast, Cermak et al. (1973) found that Korsakoff patients learned the pursuit rotor as fast as normals. However, the amnesic patients were slower than normals at learning a finger maze.

The typical form of the serial reaction time task involves presenting visual targets in one of four horizontal locations, with the task being to press the closest key as rapidly as possible. The sequence of targets is sometimes repeated over 10 or 12 trials, and skill learning is shown by improved performance on these repeated sequences. This skill learning is generally intact in amnesics (e.g., Nissen & Bullemer, 1987).

Mirror tracing involves tracing a figure with a stylus, with the figure to be traced being seen reflected in a mirror. Performance on this task improves with practice in normals, and the same is true of amnesic patients (e.g., Milner, 1962).

Which brain areas are involved in the acquisition of sensori-motor skills? Sensori-motor skill learning is often impaired in patients with damage to the basal ganglia caused by various diseases (e.g., Parkinson's disease; Huntington's disease; Gilles de la Tourette's syndrome). In addition, patients with cerebellar

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