amnesia We forget almost everything that we have, at some time, briefly remembered. Think of all the telephone numbers you have kept in mind between looking in the directory and dialling the number; of all the people and places you once knew for a few minutes but have now mostly forgotten; of every meal that you have eaten, which you could have described in detail the same day, but could not possibly remember now. Given the overwhelming flood of information that pours into our brains each day, forgetting most things is just as important as remembering some.
On the other hand, forgetfulness can become an illness, an incapacitating inability to remember things, which is called amnesia. Amnesia occurs in many situations — after head injuries, in Alzheimer's disease, and, to some extent, in all old people. But it has mainly been studied in particular patients with profound impairments of
memory, despite otherwise normal cognitive ability and intelligence. These patients are said to have the amnesic syndrome, whose characteristics include: (i)
severe anterograde amnesia: poor retention of new information, exhibited by difficulty in spontaneously recalling words and objects, in recognizing faces (unless they are very familiar), and in learning associations between words or things; (ii)
retrograde amnesia: poor recollection of previously established memories (such as knowledge of one's childhood, and even such things as one's own name). In general, the retrograde component of clinical amnesia is less severe than the anterograde, and may be limited to a period of months or years prior to the onset of the amnesia. In some way, ancient memories are more robust than newer ones, and can persist even when new, conscious long-term memories cannot be formed.
Despite these defects in long-term memory, patients with clinical amnesia have relatively normal short-term memory span (as measured by the ability immediately to recall a list of digits). Indeed, amnesic patients are able to engage in normal conversation and recall current information so long as it is continually ‘rehearsed’. But after just a few seconds of distraction, they may forget not only what has been said but even whether they have met the person they were talking to moments before.
Not all forms of long-term learning are impaired. Motor skills (such as typing on a keyboard or driving a car) learnt prior to the onset of the illness are unaffected, and patients show residual abilities to learn new motor skills (even though they are not consciously aware of having done the motor task before). Other simple forms of memory also persist, including classical conditioning (the kind of simple learning shown by
Pavlov's dogs when they salivated to the sound of a bell after it had been rung a few times before the presentation of food). The common denominator between the forms of learning still exhibited by amnesic patients is that they can all be mediated without the need for recollection of past experience: they involve what has been called
procedural learning (the learning of skills) or
implicit learning (unconscious learning).
The vast majority of amnesic patients are chronic alcoholics, suffering from
Korsakoff's syndrome. This is due to diffuse brain damage, predominately to lower parts of the cerebral hemispheres (principally the mamillary bodies and dorso-medial nucleus of the
thalamus), although there is also frequently degeneration of the frontal lobes of the
cerebral cortex. The gradual deterioration of mental function is probably due to the toxic effects of alcohol, combined with thiamine deficiency. In addition to profound memory impairments, Korsakoff patients also exhibit a range of impairments shared by patients with damage to the frontal lobes, such as lack of insight into their own deficits, confabulation (inventing explanations for their difficulties), and impairments on tests of card sorting. Due to the multiple sites of damage and the diffuse nature of the brain damage it is hard to draw firm conclusions from Korsakoff patients about which particular structures in the brain contribute to memory.
Discrete damage to the brain, especially to parts of the interior surface of the temporal lobes of the cerebral hemispheres, can also cause profound anterograde amnesia. The classical example of this devastating condition is the patient known by his initials, H. M., who underwent surgery to remove the inner parts of the temporal lobe on both sides, to relieve intractable epilepsy, and has subsequently suffered deep amnesia for decades. This part of the brain includes specialized regions of cerebral cortex called the hippocampus and the amygdala, which are thought to be involved in the laying down of memories. Unfortunately this vital part of the brain seems to be particularly vulnerable: it is relatively easily damaged by hypoxia (for instance during surgical operations in which blood supply to the brain is compromised), by the degenerative changes that occur in Alzheimer's disease, and by infection in herpes simplex encephalitis. All of these conditions can produce pronounced amnesia.
Although intensively studied and extensively documented in a small group of select patients, the classical amnesic syndrome may not be completely typical of most people with amnesia. The extent of retrograde amnesia for personal recollections of the past is particularly hard to assess in the absence of any independent verification. The amount of retrograde amnesia in H. M., for example, may have been grossly underestimated. It has even been argued that there may not be a single amnesic syndrome, since patients with temporal lobe damage tend to forget information rapidly, whereas Korsakoff patients, given enough training, are able to retain information over longer periods of time.
Because of the complexity of clinical syndromes, most of our present understanding of which neural systems contribute to normal learning and memory have come from the study of animals, especially of animal ‘models’ of human amnesia. It was initially believed that combined damage to the hippocampus and amygdala was necessary to produce severe anterograde amnesia, and the hippocampus in particular became the supposed seat of ‘episodic’ (personal, conscious) memory. However, this view has been challenged by the discovery that damage to a neighbouring region, the rhinal cortex, which underlies the hippocampus and amygdala, was necessary and sufficient to produce memory impairments.
Behavioural studies on monkeys, analysing the effect of circumscribed damage to specific regions in the inner part of the temporal lobe, have identified several dissociable, interacting memory structures. Much research effort is presently focused on ascertaining the role of these different components. For example, current research has called into question the traditionally accepted role of the hippocampus in episodic memory and suggests instead that this structure may play a more restricted role in the memory of places, which then contributes to a broader neural memory system. Other components of this system include the amygdala, now believed to be involved in remembering whether particular stimuli are associated with rewarding or punishing events. Another important nearby structure is the perirhinal cortex, which appears to be specialized for processing knowledge about objects. The nerve fibres of the white matter within the temporal lobe, known as the temporal stem, have also been implicated in memory. However the temporal lobe is by no means the only structure involved in human learning and memory. Communication between the temporal lobe and the frontal lobe is also important and this interaction occurs via multiple routes. In fact, neither the hippocampus, amygdala, perirhinal cortex, temporal stem, nor any other single structure in the temporal lobe when damaged on its own results in dense amnesia. But this does occur when the majority of the routes by which the temporal lobe can interact with the frontal lobe are interrupted.
Detailed structural imaging of the brain of H.M., through magnetic resonance imaging (MRI), has recently confirmed the extent of bilateral damage sustained by each of the temporal lobe structures in H. M., and this has been interpreted in terms of the understanding gained from the study of animals. The damage in H. M. is entirely consistent with the predictions from animal studies — one indication of the usefulness of these models in understanding the neural systems underlying normal human learning and memory.
Mark Buckley
Bibliography
Bolhuis, J. J. (2000). Brain, perception, memory: advances in cognitive neuroscience. Oxford University Press, Oxford.
Eysenck, M. W. (1995). Cognitive psychology: a student's handbook, (3rd edn). Erlbaum, Hove.
See also
brain;
cerebral cortex;
hypothalamus;
limbic system;
memory.
