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Through the study of amnesic patients, cognitive neuroscience has advanced our understanding of the processes that underlie learning and remembering. Memory is now understood to be a collection of functional systems, with each contributing uniquely to the storage and retrieval of information. The study of neurological populations with lesions that interfere with the function of specific components of memory has revealed distinct roles for these memory systems. This understanding has provided the theoretical foundation for evidence-based treatment approaches.
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- The Contribution of Patient H.M.
- Impaired Memory in Amnesia: Declarative Memory
- Preserved Aspects of Memory in Amnesia: Nondeclarative Memory
- Amnesic Syndromes
- Neuropathology of Amnesia
- Approaches to Treatment of Amnesic Disorders
In 1606, Shakespeare’s Lady Macbeth described memory as ‘‘the warder of the brain,’’ as a function that somehow stands apart from the brain’s other cognitions while bearing witness to them. She made this reference while planning to induce a temporary amnesia in the king’s attendants by getting them drunk. Her aim in doing so was to ensure that the attendants would not recall the events surrounding her husband’s intended murder of the king. She knew that after the deed was done and their alcohol-induced stupor passed off, they would be left witness to a blank, to a discontinuity in their experience, and not to the murder. For memory to be capable of keeping an account of the swift interplay of sensations, perceptions, and thoughts that make up events and thereby give experience its continuity, memory must itself have an underlying continuity. If it did not, there would be nothing for people to ‘‘go back to’’ that would allow them to witness an earlier event again, and Lady Macbeth would have had nothing to fear from any witnesses to her husband’s intended crime. Now, four centuries later, modern cognitive neuroscience is going beyond description. It investigates how memory enables people to actively bring the past into the present moment, thereby allowing them to experience their personal persistence through time.
The fact that memory can fail has been known for millennia, but its failure was not specifically called ‘‘amnesia’’ (from the Greek for forgetfulness) until relatively recently in 1786. In current common use, amnesia refers loosely and interchangeably to either one of two quite different states or to both of them. First, it refers to a state in which memories that were available for recall in the past have been lost and are no longer available in the present. Second, it refers to a state in which current experiences are not being kept account of and duly recorded, with the result that they will not be available for recall in the future. The first usage is reflected in the Oxford English dictionary definition of amnesia as ‘‘loss of memory’’ and roughly coincides with retrograde amnesia, whereas the second usage is reflected in the Merriam–Webster dictionary definition as ‘‘forgetfulness’’ and roughly coincides with anterograde amnesia. The loss of previously consolidated memories, on the one hand, and the inability to create and retain new memories, on the other, are states that can occur separately. However, more often than not, both occur together in the same individual following a single event, hence the tendency to refer to either or both of them without distinction by means of the same term ‘‘amnesia.’’
In addition to its common meaning, the term ‘‘amnesia’’ has both a general sense and a specific sense in current scientific literature. In general, it refers to any pathological loss of the ability to acquire or recall information. In that sense, it encompasses psychogenic amnesia, posttraumatic amnesia following closed head injury, memory loss that occurs along with other major cognitive impairments in progressive degenerative neurological disorders such as Alzheimer’s disease, and isolated global memory loss that characterizes the amnesic syndromes. In its more restricted use, it refers specifically to these latter syndromes, and it is in this sense that the term is used in what follows.
Early investigation of the amnesic syndromes proceeded both by means of clinical case descriptions and through the correlation of lesion analyses with deficits found through neuropsychological investigations. The most widely known of the early case studies was of the patient ‘‘H.M.,’’ and it is through studies of his memory function that the current understanding of amnesia began to unfold.
2. The Contribution Of Patient H.M.
At 9 years of age, H.M. suffered a head injury followed by seizures that became more frequent and more severe over the subsequent 18 years. In 1953, as a treatment of last resort, he underwent an experimental neurosurgical operation in which a large portion of the medial temporal region of his brain was removed bilaterally. That extensive resection was successful in reducing his seizures, but it left him with an unexpected devastating memory loss.
One striking finding that came to light in the early studies of H.M.’s memory loss was that his profound forgetfulness and loss of personal memories had occurred without any damage to his general intellectual ability, attention, and language. This discovery established that normal medial temporal lobe functioning is necessary for the accumulation of memories. However, the fact that its dysfunction does not interfere with the attention, thoughts, and perceptions that give rise to experiences in the first place suggests that memory is specifically linked to the function of the medial temporal lobe. Further studies of H.M.’s memory impairment led to the current understanding of the characteristics of hippocampal amnesia. They also revealed that memory, rather than being a unitary capacity, is composed of several functional systems, not all of which are impaired in amnesia. Those systems fall into two major classes. The first group involves nondeclarative memory, that is, the form of memory that functions without awareness. The second group involves declarative memory, that is, the form of memory that supports conscious retrieval of experiences. It is the latter form of memory that is impaired in amnesia.
3. Impaired Memory in Amnesia: Declarative Memory
After H.M.’s operation, it became apparent that he had suffered damage to the memory system that supports the conscious (intentional) retrieval of experiences. Not only did he fail to remember the events of his then current day-to-day life, but he also could not recall memories he had accumulated over much of his life prior to the onset of his amnesia. This clinical profile of severe anterograde amnesia together with an extensive retrograde memory impairment is typical of hippocampal amnesia.
3.1. Retrograde Amnesia
H.M.’s inability to recall memories that he had formed prior to the onset of his amnesia extended back approximately 11 years. The density of his retrograde amnesia followed Ribot’s law, a semi quantitative description offered in 1881 that states that the ‘‘loss of memory is … inversely [related to] the time that has elapsed between any given incident and the fall (injury). … The new dies before the old.’’ H.M. showed just such a temporal gradient. His inability to recall autobiographical and public events from shortly before his operation was total, but his amnesia was found to be less dense as testing probed further back in time and he was able to remember more and more.
Investigation of patients with a variety of amnesic syndromes has demonstrated that such a temporally graded retrograde amnesia is common and that its severity and duration tend to vary with the size of the brain lesion. Retrograde amnesia can affect both the recall of autobiographical and public events (episodic memory) and the retrieval of facts and concepts (semantic memory) that were known before the onset of amnesia. However, episodic and semantic memory are differentially affected across syndromes. For example, some patients have severe retrograde amnesia for events together with relatively preserved memory for facts and concepts, whereas others show the opposite pattern with severely impaired semantic memory but relatively preserved episodic remote memory.
The finding of a graded decrease in the density of memory loss as probing moves backward through time starting from the onset of amnesia establishes two important facts regarding how memories are stored and retrieved. First, it establishes that a functional medial temporal region is required for permanent learning of new information. Second, it indicates that the medial temporal lobe is not the ultimate repository of long-term memories given that long-established memories can survive and be available for recall despite the presence of medial temporal damage. It has since been found that long-term memories are stored in the neocortex, specifically in the lateral temporal regions. This is confirmed by the fact that in patients with lesions in these areas, even old memories can be permanently lost, so that their retrograde amnesia is not temporally graded. Thus, the medial temporal lobes and neocortical areas make unique contributions to information storage. When an event is originally experienced, separate aspects of the event, such as its perceptual characteristics, emotional connotations, and associated thoughts, are processed in initially unconnected sites throughout the cortex, as determined by the functional specialization of various parts of the brain. The medial temporal lobes, and especially the hippocampus, provide the glue that allows these diverse aspects to be linked together into a single representation. When a part of any event is recalled again, the hippocampus is engaged, and it simultaneously reactivates the spatially separated cortical traces that together make up the brain’s representation of the whole event. With repeated activation over time, links are established among the involved neocortical sites. Eventually, these separate neocortical sites that collectively represent a single event become interlinked to the extent that hippocampal activation is no longer necessary for recall of the event as a whole. It is at that point that the consolidated memory can survive medial temporal lobe damage.
3.2. Anterograde Amnesia
The nature of the impact of H.M.’s neurosurgery on his cognition gradually became apparent when it was noticed that H.M. consistently failed to recall having eaten a meal and that he failed to develop any ability to get to know the people who provided his daily care. This anterograde amnesia was so pervasive that he could hold onto new information for only a few seconds and then only if there was no distraction. If his attention was diverted, the information faded away and was not available for recall. As was noted earlier, the normal functioning of the hippocampus and surrounding medial temporal lobe structures is crucial for forming and storing new memories. In general, the severity of anterograde amnesia is proportional to the extent of damage to medial temporal structures. Furthermore, because the hippocampus receives input from a variety of neocortical regions that process information in the various sensory modalities, such anterograde loss is invariably global; that is, it involves both verbal and nonverbal information in all possible modalities of presentation. Such dense global anterograde memory impairment is the hallmark of medial temporal lobe amnesia.
Anterograde amnesia is evaluated in the clinic through tasks that measure recall and recognition of information to which the individual is exposed during a testing session. Recall tasks require that recently learned information be consciously and deliberately retrieved in response to a question, whereas recognition tasks require that previously encountered information be distinguished from, and so recognized among, foils. The recognition format is generally easier for normal individuals because it requires less retrieval effort than does recall. Recognition is thought to be easier for individuals with intact memories because recall depends on conscious and effortful recollection, whereas recognition can be supported not only by recollection but also by familiarity. Familiarity refers to the sense of knowing that arises when a stimulus is processed with ease. Recollection and familiarity can be distinguished from one another experientially. For example, consider the situation where a man hears his name being called out while he is in a crowd. He turns and sees the woman who called his name and has a short conversation with her. The woman is familiar to the man, but he cannot recall any context that accounts for that familiarity. Several days later, the man receives a telephone call from the woman in which she identifies her place of work and, at that moment, he knows who she is and is flooded with memories of details and events. Sudden recollection replaces felt familiarity. In the laboratory, patients with amnesia secondary to medial temporal lobe damage generally show impairments on both recall and recognition tasks, suggesting that familiarity and recollection both are impaired. However, some amnesic patients show relatively preserved recognition memory, and this may reflect their residual ability to use familiarity as a basis for remembering.
Patients with lesions involving the frontal lobes, either directly or indirectly, can also have severe deficits in memory. However, although their performance is impaired on tasks of free recall, they show normal performance on tasks that require the recognition of previously learned information. This performance disparity between recall and recognition is due to the distinct roles of the medial temporal lobes and the frontal lobes. The medial temporal lobes contribute to the encoding, storage, and retention of newly learned information, whereas the frontal lobes support the organizational and strategic aspects of memory necessary for developing encoding and retrieval strategies, monitoring and verifying memory output, and setting order within the recalled memories.
4. Preserved Aspects Of Memory In Amnesia: Nondeclarative Memory
H.M.’s severe amnesia notwithstanding, some aspects of his memory functioning were found to be intact following his surgery. In contrast to his inability to consciously retrieve information acquired before and after onset of his amnesia, it was found that H.M. showed evidence of learning on tasks that did not require his awareness of the learning episode.
4.1. Procedural Memory
Careful experimental study brought to light that H.M. was able to acquire specific perceptual–motor skills as well as do normal individuals. One such motor task involved his tracing the outline of a star with a stylus while gaining feedback of his ongoing performance through the reflection of his performance in a mirror. H.M. improved with repetition exactly as did normal individuals. But for him, each trial was experienced as if it were his first trial, despite his steady improvement. He had no way of knowing that he was getting better at it, as normal people did. This finding was one of the first to show that procedural memory (i.e., the ability to know how) is distinct from declarative memory (i.e., the ability to know that something occurred). It also established that procedural memory does not depend on the integrity of the medial temporal lobes. Procedural memory develops gradually through repetition without any requisite awareness that the skill is being learned.
4.2. Repetition Priming
Priming is another form of learning that occurs without conscious awareness. It is defined as a bias or facilitation in identifying or responding to certain information to which one has been exposed previously. In contrast to procedural learning, the effect of priming can be seen following a single exposure. In a typical priming task, an individual is asked to view a list of words or pictures. The individual is then asked to perform a seemingly unrelated task such as naming words or identifying degraded pictures. Unbeknownst to the individual, some of the stimuli in the second task were part of the list of stimuli that were seen in the first task, whereas others are presented for the first time. Priming is in evidence when naming or identification of previously seen stimuli occurs faster or more accurately than does identification of stimuli not seen previously. Amnesic patients show intact priming across a broad variety of tasks. Sometimes priming reflects facilitation of the processes that support the perception of stimuli, whereas other times priming reflects the facilitation of processes that support conceptual analysis (i.e., meaningful interpretation) of stimuli. Both perceptual priming and conceptual priming are independent of medial temporal structures, and both depend on distinct neocortical regions.
5. Amnesic Syndromes
Amnesia can result from a variety of etiologies that cause damage to various regions of the brain. For example, diencephalic amnesia, the memory disorder of patients with Korsakoff’s syndrome, arises from damage to structures that make up the diencephalon, particularly the mammillary bodies, the anterior thalamic nuclei, and the medial dorsal thalamic nucleus. Basal forebrain amnesia, in contrast, arises in patients with a history of rupture and repair of an anterior communicating artery (ACoA) aneurysm and is caused by damage to structures of the basal forebrain, the septum, and frontal brain regions. The following is an overview of the clinical characteristics of five of the more common amnesic syndromes.
5.1. Herpes Simplex Encephalitis
Herpes simplex encephalitis (HSE) is an acute inflammation of the brain caused by a herpes simplex virus infection. Some patients recover fully following infection, but most are left with a cluster of cognitive deficits that include a memory disorder. The heterogeneous pattern of these cognitive impairments reflects the extent and variability of damage to the brain. Among those patients who recover, a small number are left with a circumscribed amnesic syndrome similar to that of H.M. The fact that these two forms of amnesia share a clinical profile is not surprising given that the herpes simplex virus preferentially affects medial temporal brain structures, including the hippocampus and adjacent entorhinal, perirhinal, and parahippocampal cortices. In all post encephalitic patients, the extent of any anterograde memory impairment is proportional to the amount of damage to the medial temporal lobes. Although some patients are incapable of any new learning, others can learn and can benefit from increased study time, external cues, and/or repeated exposure. Because the herpes virus can affect the brain asymmetrically, the pattern of anterograde memory loss will also depend on the laterality of damage. The greater the damage to the right temporal region, the greater the difficulty in performing nonverbal/ visual memory tasks (e.g., memory for faces), whereas the greater the damage to the left temporal region, the greater the deficit in verbal memory.
Postencephalitic patients with damage extending to the lateral temporal lobes, the region where memories are permanently stored, will have dense retrograde amnesia for autobiographical and public information with little or no temporal gradient. Damage to the right anterior temporal region interferes primarily with retrieval of autobiographical memories, whereas damage to the left temporal cortex impairs semantic memory.
Amnesia can result from damage to, or death of, brain tissue due to a lack of oxygen supply to the brain. This can be caused either by reduced blood flow, such as in cardiac arrest or strangulation, or by normal perfusion with hypoxic blood secondary to respiratory distress or carbon monoxide poisoning. When the oxygen supply to brain tissue is disrupted, compensatory mechanisms that maintain cerebral homeostasis are triggered immediately. These protective autoregulatory mechanisms, although effective in adjusting for sudden short-lived changes, will eventually fail in the face of sustained oxygen deprivation. Oxygen deprivation for 3 to 8 minutes will trigger the release of excitatory neurotransmitters that can result in damage to the hippocampus. Shorter events may also damage regions that are perfused by terminal vascular branches or that lie in the watershed regions because these areas are deprived of oxygen early on. Longer lasting events will result in neuronal damage that extends to the cerebellum, the basal ganglia, the thalamus, and neocortical areas. The outcome following an anoxic event depends on many factors, including the cause and duration of the event as well as the age and health status of the individual.
Therefore, it is not surprising to find variability in the clinical profiles associated with anoxic events. Most individuals who have suffered an anoxic brain injury experience a memory disorder along with other cognitive impairments. On occasion, an isolated amnesic syndrome is documented secondary to a lesion in the hippocampus. When the lesion is limited to the CA1 area of the hippocampus, there is moderately severe anterograde amnesia together with very mild retrograde loss. When the lesion extends beyond the CA1 area of the hippocampus but remains limited to the hippocampal formation, there is severe anterograde memory impairment and more robust retrograde memory impairment that can extend back more than 15 years. More commonly, however, anoxic patients have a memory impairment that is akin to that seen in patients with damage to the frontal brain region due to disruption of frontal–subcortical circuits as a result of damage to watershed zones in the cerebral cortex. Rather than encoding, storage, and retention deficits, these patients demonstrate impairments at the level of the organizational and strategic aspects of memory.
5.2.1. Anterior Communicating Artery Aneurysm
Memory deficits, along with associated behavioral disorders, frequently follow rupture and surgical repair of an ACoA aneurysm. Such deficits vary from a very mild impairment to a severe amnesic disorder called basal forebrain amnesia. This wide variability reflects the fact that the ACoA perfuses a broad anatomical brain region, all of which is vulnerable in the event of rupture to damage from infarction, either directly or secondary to subarachnoid hemorrhage, vasospasm, or hematoma formation. Basal forebrain amnesia is usually due to damage to the septal nucleus and the subcallosal area. Disruption of hippocampal functioning may play a role in the amnesia of at least some patients with ACoA aneurysm because several basal forebrain nuclei contain a large number of cholinergic neurons that innervate the hippocampus as well as large neocortical regions. Disruption of frontal network systems can occur and may also contribute to the quality of the memory deficit seen in some ACoA aneurysm-related forms of amnesia. The severe deficit in recall found in basal forebrain amnesia shares superficial similarities with the anterograde memory impairment that characterizes medial temporal lobe amnesia. However, the deficit in basal forebrain amnesia is due to inefficient encoding and not to the failure of consolidation that characterizes
medial temporal amnesia. As a result, ACoA patients will benefit from the use of encoding strategies, whereas patients with medial temporal lobe damage will not. Another difference is found in the performance of ACoA patients on recognition tasks, where they are found to succeed more often than their medial temporal lobe counterparts. This recall–recognition disparity is attributed to the frontal executive component of the amnesia that follows ACoA aneurysm, particularly the disruption of strategic effortful search processes that give access to information stored in memory. Another executive contribution to the disorder is the tendency of some ACoA patients to score many false positives on recognition tasks, a finding that suggests an additional impairment in the ability to monitor the outcome of a memory search. Retrograde memory is nearly always impaired in amnesia secondary to ACoA aneurysm, and it invariably shows a temporal gradient. However, patients do appear to benefit substantially more from cueing than do other amnesic groups, suggesting that impaired retrieval efficiency contributes to both the anterograde and retrograde aspects of their amnesia.
Amnesia is a common consequence of infarction of the posterior cerebral artery (PCA). It results from neural tissue damage caused by the interruption of blood flow to a large part of the medial temporal lobes, particularly the posterior two-thirds of the hippocampus, the parahippocampal gyrus, and other critical pathways that connect the hippocampus to surrounding brain areas. A more posterior extension of the lesion will result in other neuropsychological deficits in addition to the memory disturbance, for example, visual field defects and other visual disturbances that may affect reading and cause problems with color identification, space perception, and/or object naming. The typical memory disturbance associated with bilateral PCA infarction is an inability to establish new memories in the presence of preserved intelligence and attention. Retrograde memory problems are also often present. There have been several reported cases of bilateral PCA infarction that spared the medial temporal lobes proper but that involved the occipital lobes bilaterally as well as the deep white matter of both the occipital and temporal lobes. These patients present with a visual amnesic syndrome that results from the disconnection between occipital cortices involved in visual processing and temporal brain regions supporting memory. There have been other reported cases in which the PCA infarction was unilateral. Patients with infarction of the left PCA present with a selective verbal memory deficit, whereas patients with infarction of the right PCA have preserved verbal memory but impaired visual processing skills and impaired visual memory.
Amnesia can also be caused by thalamic infarction. In such cases, the severity of the memory impairment is related to the site of damage within the thalamus. Lesions that damage the mammillo–thalamic tract, in particular, have been associated with severe anterograde amnesia. Infarction of the medial dorsal thalamic nuclei has also been associated with memory impairments, but it appears that the damage must extend beyond the medial dorsal nucleus to include the mammillo–thalamic tract or anterior nucleus for the development of a severe amnesic disorder. Because the thalamus has rich connections with the frontal lobes, this anterograde amnesia is also accompanied by an increased sensitivity to interference and by impairments in executive functioning. As with other amnesic syndromes, left-sided lesions result in impairments on tasks of verbal learning, whereas right-sided lesions result in nonverbal/visual memory impairments. Retrograde memory deficits following thalamic infarction are variable; some patients are found to have little impairment in remote memory, whereas others demonstrate severe long-term memory impairments.
5.2.3. Wernicke–Korsakoff Syndrome
Wernicke–Korsakoff syndrome (WKS) is seen in patients with a history of long-term alcohol abuse in association with poor nutrition and a lack of Vitamin B1 (thiamine). In acute Wernicke’s encephalopathy, patients exhibit confusion, a gait disorder (ataxia), and abnormal eye movements (oculomotor palsy). Treatment with large doses of thiamine may result in improvement in, or even reversal of, some of these symptoms. However, most patients are left with a permanent dense amnesic disorder referred to as Korsakoff’s syndrome. This amnesic syndrome arises from damage to the thalamic nuclei, the mammillary bodies, and the frontal system.
Patients with WKS suffer from both anterograde and retrograde amnesia. Several explanations have been proposed to account for their episodic memory impairment. Although early models emphasized their superficial and deficient encoding strategies or their failure to inhibit competition from irrelevant material at the time of retrieval, current views agree that an explanation of their learning deficits is best accounted for by a theory that integrates both encoding and retrieval processes.
The retrograde amnesia in WKS has a steeper temporal gradient than that found in medial temporal lobe amnesia. The concomitant presence of frontal dysfunction in Korsakoff’s patients is believed to account for their poorer performance on remote memory tests. Intelligence is usually preserved in Korsakoff’s patients, but there are often associated cognitive and neurobehavioral deficits that are unique to this patient population. In particular, some combination of impaired planning and initiation, passivity, apathy, confabulation, and limited insight is nearly always found. These symptoms are thought to arise from associated frontal dysfunction.
6. Neuropathology Of Amnesia
For centuries, any lapse in the functioning of the warder of the brain’s cognitions was described, and eventually defined, as simple forgetfulness. During the first half of the 20th century, it was thought that memory, as the cognition that keeps account of other cognitions, was not dependent on the activity of a circumscribed brain region (as are those other cognitions) but rather was directly dependent on the functioning of the whole brain. There also emerged an opposing view that held that memory function was localized in the brain. There was no conclusive experimental evidence for either view until, at midcentury, the consequences of H.M.’s surgical resection decided the matter in favor of a localized brain representation for declarative memory. Later evidence similarly established distinct localizations for priming and procedural learning, two forms of nondeclarative memory. Cognitive neuroscience has since clarified the nature of those localizations in substantial detail.
6.1. Declarative Memory
Declarative memory is mediated by a group of interconnected structures that are part of the extended limbic system. Within the limbic system, two interacting memory circuits can be identified: the Papez circuit and the basolateral circuit. The Papez circuit is composed of the hippocampus, the fornix, mammillary bodies, the anterior thalamus, and the posterior cingulate gyrus (with additional connections to the basal forebrain via the fornix). The basolateral circuit is composed of the amygdala and surrounding perirhinal cortex, the dorsomedial thalamus, and the prefrontal cortex. Although damage to any part of either circuit in isolation will impair memory function, damage to both circuits will result in a profound amnesic disorder. The contribution that each circuit makes to memory function remains a matter of active debate. On one side of the discussion are those who believe that both circuits are involved in all aspects of declarative memory. Lesions affecting both circuits would, therefore, be expected to result in more severe amnesia simply because more of the relevant neural tissue would be dysfunctional. Others suggest that the two circuits make qualitatively different contributions to memory. In particular, they suggest that the hippocampus and related structures in the Papez circuit support the recollection of episodic information, whereas the perirhinal cortices and related structures in the dorsolateral circuit support judgments of familiarity. In this case, damage to both circuits would impair more functions than would damage to either circuit alone and, therefore, would explain current clinical findings. Future studies of patients who present with selective lesions will be needed to resolve this debate.
The finding of temporally graded retrograde amnesia in association with damage to the medial temporal lobe reveals that this brain region plays a critical role in the establishment of memory and also suggests a subsequent slow transfer of memory to other brain regions. The finding that old memories, both autobiographical and semantic, are left untouched by damage limited to the hippocampus suggests that memories are not stored there. Long-term storage takes place in neural networks in the neocortex.
6.2. Nondeclarative Memory
Nondeclarative memory systems are supported by widely varying brain regions, depending on which sensory mode is involved in a given task and whether or not performance of the task involves higher associative functions. For example, evidence from neuroimaging studies, together with clinical data from individuals who have suffered focal cortical damage, has established that priming finds its substrate in the neocortex. Specifically, the substrate for perceptual priming is the relevant unimodal cortex (i.e., visual priming in the occipital visual cortex, auditory priming in the auditory cortex), whereas the substrate for conceptual priming is located in multimodal association cortices. The same brain regions that are involved in the initial processing of information are also involved in the more fluent processing that follows repetition, and priming is accompanied by a reduction in neural activity in these regions.
Although priming manifests after a single exposure to a stimulus, procedural memory requires a series of repetitions for its manifestation. Consequently, the involvement of relevant brain regions and their changes over time is more complex for procedural memory. The initial acquisition of motor skills engages the motor/prefrontal cortices, basal ganglia, and the cerebellum. Over time, however, two opposite tendencies are evident. On the one hand, as procedural learning develops and a skill can be performed with less effort, the prefrontal cortex and cerebellum gradually become less activated. This repetition suppression effect mirrors that seen in the neural substrate for priming. On the other hand, repetition leading to increased skill engages the higher order motor cortex more than it had initially been engaged. This latter finding indicates expanded cortical involvement in the retention of procedural memory for motor tasks that mirrors the increased neocortical involvement in the long-term retention of declarative memories.
7. Approaches To Treatment Of Amnesic Disorders
The treatment of memory disorders aims at enhancing day-to-day memory functioning and routine so as to increase an individual’s level of independence. The choice of treatment will depend on both cognitive and noncognitive factors. Noncognitive factors to be considered include psychosocial context (e.g., family situation, educational background, lifestyle habits) and emotional factors (e.g., level of insight, motivation, neuropsychiatric symptoms). Of critical importance among these factors are level of insight and motivation. Research has shown that interventions are unsuccessful in patients who fail to appreciate that their memory is impaired and/or who are unmotivated. In these patients, efforts should initially focus on increasing level of insight and/or motivation. Cognitive factors that must be taken into account include premorbid abilities and skills and postmorbid neuropsychological deficits, including a clear delineation of those areas of memory that are impaired and preserved. Within the context of a holistic individualized approach, a memory remediation program can be developed based on current understanding of the processes that support learning and memory.
Several treatment approaches for densely amnesic patients capitalize on nondeclarative memory processes because this form of memory remains intact in most patients. The ‘‘vanishing cues’’ technique is an example of a treatment method that recruits preserved implicit perceptual memory processes to teach patients domain-specific facts or concepts. The technique takes advantage of patients’ preserved ability to complete studied items in response to word fragment cues. In a typical vanishing cue paradigm, patients are given a definition and are then presented with as many letters as is necessary to produce the target word. With training, the letter cues are gradually reduced until the patients can spontaneously generate the sought after information. Success has been achieved using this technique in teaching patients computer-related vocabulary, business-related terms, and novel concepts. Learning by means of this technique is slow and laborious but can lead to surprisingly good retention, particularly if the information to be learned uses a knowledge base that is already familiar to the individual. However, a caveat arises from the inherent reliance of the vanishing cues method on the perceptual cues given during learning. As a result, generalization has often been limited, and benefits have been found to be best when the information is used in situations similar to those where learning occurred.
Attention to training contexts may be important when using techniques that take advantage of preserved implicit memory processes. Because amnesic patients have no recollection of the learning episodes, they fail to remember their mistakes and consequently fail to benefit from ongoing error correction. Instead, incorrect responses made during learning are often unconsciously repeated, leading to errors becoming primed and more likely being repeated subsequently. To avoid the perpetuation of errors through priming, some investigators have emphasized the importance of ‘‘errorless learning’’ for patients who have explicit memory impairments. In errorless learning, the possibility of making errors is eliminated by using cues and prompts or by providing the correct answer. The approach has met with some success in teaching memory-impaired patients both new skills (e.g., use of a memory book, programming of an electronic organizer) and new knowledge (e.g., learning of new words). Errorless learning is thought to operate by strengthening residual explicit memory, either alone or together with implicit memory. Its applicability as a method to facilitate learning appears to be broad and promising because errorless learning principles can be applied to a variety of remediation methods.
Other treatment approaches capitalize on preserved procedural learning. Through repetition, skills and habits that are important for activities of daily living or occupation can be taught. Such skills can range from simple assembly tasks to more complex multistep tasks such as learning to type. A variety of compensatory aids (e.g., notebooks, scheduling books, diaries, alarms) and augmentative technologies (e.g., computers, personal digital assistants, paging systems) rely on procedural memory. The notebook is an example of a low-tech aid. It is usually created at the early stage of rehabilitation and contains sections aimed at drilling overlearned personal information (e.g., date of birth, age, address), information about immediate family members (including their telephone numbers), daily schedules, and a daily record of activities. The book is tailored to the individual and can be gradually increased in complexity. Electronic organizers, the most favored external memory aid among normal individuals, are now also being used by memory-impaired patients. Training in the use of such technology requires lengthy practice sessions, within and outside the rehabilitation environment, to foster generalization. Because the acquisition of new skills is time-consuming for everyone involved, careful consideration needs to be given as to whether an electronic device is appropriate for an individual before investing the time and effort. Factors that would argue against it include dense amnesia associated with poor insight, lack of initiative, impaired visual attention, poor motor control, and limited problem-solving skills. Patients who are good candidates for this technology are generally younger, have experience in using electronic devices, and have achieved higher educational levels. Devices used premorbidly are preferable because familiarity increases the likelihood that they will be used effectively outside the clinic.
The preceding examples illustrate approaches that focus on preserved memory systems to teach new skills and habits. Another approach focuses on enhancing impaired forms of memory to improve day-to-day episodic memory by means of internal strategies. Internal strategies require awareness of the learning method and recall of the strategy itself; therefore, they are of limited use to patients who are moderately or densely amnesic. However, they are useful for patients who have mild memory deficits secondary to impaired effortful encoding or retrieval, who have good awareness of their deficits, and who have adequate motivation. These patients are more likely to generalize their training to situations that go beyond the clinic setting.
Examples of internal strategies include mental retracing, feature–name association, and verbal elaboration by means of a story or an association—all of which are skills that promote the use of imagery. The choice of technique will depend on the memory process that is targeted for remediation. For example, techniques that focus on strengthening encoding, and therefore storage, are effective at remediating consolidation problems. Story elaboration is effective in linking together a list of unrelated words through the development of a scenario that features the target words. The use of verbal associations is often effective in recalling a surname. In all of these instances, repeated use of the strategy is important and spaced repetitions, at different times and in different contexts, generally increases the likelihood that information will be learned and become conceptually integrated within a matrix of old memories. Strategies that are most effective when the deficit is at the level of strategic processes that enhance encoding are those that increase the organizational structure of incoming information. For example, learning how to ‘‘chunk’’ incoming information is helpful in streamlining and organizing that information. Organizing information according to themes or categories can also structure learning so that a thematic cue can serve to trigger recall when necessary.
These remediation methods are guided by knowledge regarding the cognitive processes that support learning and memory. More than 50 years ago, the early clinical findings with H.M. and other patients informed the theoretical understanding of the functional systems that comprise human memory. Current cognitive neuroscience has evolved from those early findings and now, in turn, can inform clinical approaches to remediation that enable amnesics to function more effectively in their daily lives.
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