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Amnesia (neurological amnesia and functional amnesia) refers to difficulty in learning new information or in remembering the past. Neurological amnesia is characterized by a loss of declarative memory. Declarative memory refers to conscious knowledge of facts and events. In contrast, nondeclarative memory, which refers to a collection of non-conscious knowledge systems, is largely thought to remain intact. The terms explicit implicit memory are sometimes used and have approximately the same meanings as declarative and nondeclarative, respectively. Neurological amnesia occurs following brain injury or disease that damages the medial temporal lobe or medial diencephalon. Neurological amnesia causes severe difficulty in learning new facts and events (anterograde amnesia). Patients with neurological amnesia also typically have some difficulty remembering facts and events that were acquired before the onset of amnesia (retrograde amnesia). Functional amnesia is rarer than neurological amnesia and can occur as the result of an emotional trauma. It presents as a different pattern of anterograde and retrograde memory impairment than neurological amnesia. Functional amnesia is characterized by a profound retrograde amnesia with little or no anterograde amnesia. In some cases, patients fully recover. Functional amnesia is a psychiatric disorder, and there is no particular brain structure or region whose damage is known to underlie this condition.
Types of amnesiaEdit
- In anterograde amnesia, new events are not transferred to long-term memory, so the sufferer will not be able to remember anything that occurs after the onset of this type of amnesia for more than a few moments. The complement of this is retrograde amnesia, where someone will be unable to recall events that occurred before the onset of amnesia. The terms are used to categorise patterns of symptoms, rather than to indicate a particular cause or etiology. Both categories of amnesia can occur together in the same patient, and commonly result from damage to the brain regions most closely associated with episodic/declarative memory: the medial temporal lobes and especially the hippocampus.
- Traumatic amnesia is generally due to a head injury (fall, knock on the head). Traumatic amnesia is often transient; the duration of the amnesia is related to the degree of injury and may give an indication of the prognosis for recovery of other functions. Mild trauma, such as a car accident that could result in no more than mild whiplash, might cause the occupant of a car to have no memory of the moments just before the accident due to a brief interruption in the short/long-term memory transfer mechanism.
- Dissociative amnesia is used to refer to long-term repressed memory that is the result of psychological, or emotional trauma.
- Long-term alcoholism can cause a type of memory loss known as Korsakoff's syndrome. This is caused by brain damage due to a Vitamin B1 deficiency and will be progressive if alcohol intake and nutrition pattern are not modified. It will usually improve little over time even if they are. Other neurological problems are likely to be present.
- Lacunar amnesia is the loss of memory about one specific event.
- Fugue state is also known as dissociative fugue. It is caused by psychological trauma and is usually temporary. The Merck Manual defines it as "one or more episodes of amnesia in which the inability to recall some or all of one's past and either the loss of one's identity or the formation of a new identity occur with sudden, unexpected, purposeful travel away from home" .
- Childhood amnesia (also known as Infantile amnesia) is the common inability to remember events from your own childhood. Whilst Sigmund Freud attributed this to sexual repression, others have theorised that this may be due to language development or immature parts of the brain.
- Global amnesia is total memory loss. This may be a defence mechanism which occurs after a traumatic event. Post-traumatic stress disorder can also involve the spontaneous, vivid retrieval of unwanted traumatic memories.
- Transient Global Amnesia is a well described medical and clinical phenomenon. This form of amnesia is distinct in that abnormalities in the hippocampi can sometimes be visualized using a special form of MRI of the brain known as diffusion-weighted imaging (DWI). Symptoms typically last for less than a day and there is often no clear precipitating factor nor any other neurological deficits. The cause of this syndrome is not clear, hypotheses include transient reduced blood flow, possible seizure or an atypical type of migraine. Patients are typically amnestic of events more than a few minutes in the past, though immediate recall is usually preserved.
- Transient epileptic amnesia (TEA) is a rare but probably underdiagnosed neurological condition which manifests as relatively brief and generally recurring episodes of amnesia caused by underlying temporal lobe epilepsy.
- Posthypnotic amnesia is where events during hypnosis are forgotten, or where past memories are unable to be recalled.
- Psychogenic amnesia is when one loses the ability to remember who oneself is. It is a common type of amnesia in popular culture; it may or may not be a real phenomenon.
- Source amnesia is a memory disorder in which someone can recall certain information, but they do not know where or how they obtained it.
- Memory distrust syndrome is a term invented by the psychologist Gisli Gudjonsson to describe a situation where someone is unable to trust their own memory.
- Excessive short-term alcohol can cause a blackout phenomenon with similar symptoms to amnesia.
Etiology of neurological amnesia Neurological amnesia results from a number of conditions including Alzheimer’s disease or other dementing illnesses, temporal lobe surgery, chronic alcohol abuse, encephalitis, head injury, anoxia, ischemia, infarction, and the rupture and repair of an anterior communicating artery aneurism. In all of these conditions, the common factor is the disruption of normal function in one of two areas of the brain - the medial aspects of the temporal lobe, and the diencephalic midline. Bilateral damage results in amnesia for all types of material, and unilateral damage results in material-specific amnesia. Specifically, left-sided damage especially affects memory for verbal material, while right-sided damage especially affects memory for nonverbal material (e.g., memory for faces and spatial layouts).
Anatomy of neurological amnesiaEdit
Well-studied cases of human amnesia and animal models of amnesia provide information about the neural connections and structures that are damaged. In humans, damage limited to the hippocampus (a structure within the medial temporal lobe) is sufficient to cause moderately severe amnesia. The severity of memory impairment is exacerbated by additional damage to medial temporal lobe structures outside of the hippocampus. (Animal studies later elucidated the critical anatomical components of this memory system. See Below.) One well-studied case (H.M.) had surgery in 1953 to treat severe epilepsy. Most of the hippocampus and much of the surrounding medial temporal lobe cortices were removed bilaterally (the entorhinal cortex and most of the perirhinal cortex). Although the surgery was successful in reducing the frequency of H.M.’s seizures, it resulted in a severe and persistent amnesia. To understand the anatomy of human amnesia, and ultimately the anatomy of normal memory, animal models of human amnesia have been established in the monkey (Mishkin 1982, Squire and Zola-Morgan 1983) (Fig. 1) and in the rodent. Following lesions of the bilateral medial temporal lobe or medial diencephalon, memory impairment is exhibited on the same kinds of tasks of new learning ability that human amnesic patients fail. The same animals succeed at tasks of motor skill learning, and they also do well at learning pattern discriminations, which share with motor skills the factors of incremental learning and repetition over many trials. Systematic and cumulative work in monkeys, using the animal model, succeeded in identifying the system of structures in the medial temporal lobe essential for memory (Squire and Zola-Morgan 1991). The important structures are the hippocampal region (hippocampus proper, dentate gyrus, and subicular complex) and adjacent, anatomically related structures (entorhinal cortex, perirhinal cortex, and parahippocampal cortex). Damage limited to the hippocampal region causes significant memory impairment, and damage to the adjacent cortex increases the severity of memory impairment. It is also important to note that the discovery that larger medial temporal lobe lesions produce more severe amnesia than smaller lesions is compatible with the idea that structures within the medial temporal lobe might make qualitatively different contributions to memory function. The amygdala, although critical for aspects of emotional learning (Davis, 1994; LeDoux, 1996) and for the enhancement of declarative memory by emotion (Adolphs et al., 1997), is not a part of the declarative memory system itself. The consistency between the available neuroanatomical information from humans and the findings from monkeys have considerably illuminated the description of memory impairment and its anatomical basis. These lines of work have also made it possible to pursue parallel studies in simpler animals like rats and mice. As a result, one can now study memory in rodents and have some confidence that what one learns will be relevant to the human condition. Another important brain area for memory is the diencephalon. The structures important for memory include the mediodorsal thalamic nucleus, the anterior thalamic nucleus, the internal medullary lamina, the mamillary nuclei, and the mammillo-thalamic tract. Monkeys with medial thalamic lesions exhibit an amnesic disorder, and monkeys with mammillary nuclei exhibit a modest impairment. Because diencephalic amnesia resembles medial temporal lobe amnesia in the pattern of sparing and loss, these two regions likely form an anatomically linked, functional system.
The nature of neurological amnesiaEdit
Impairment in declarative memoryEdit
It is important to appreciate that amnesic patients are not impaired at all kinds of long-term memory. The major distinction is between declarative and nondeclarative memory. Declarative memory is the kind of memory impaired in amnesia, and it refers to the capacity to remember the facts and events of everyday life. It is the kind of memory that is meant when the term “memory” is used in ordinary language. Declarative memory can be brought to mind as a conscious recollection. Declarative memory provides a way to model the external world and in this sense it is either true or false. The stored representations are flexible in that they are accessible to multiple response systems and can guide successful performance under a wide range of test conditions. Lastly, declarative memory is especially suited for rapid learning and for forming and maintaining associations between arbitrarily different kinds of material (for example, learning to associate two different words).
Since the discovery of hippocampal place cells in the rodent (O’Keefe and Dostrovsky, 1971), an influential idea has been that the hippocampus creates and uses spatial maps and that its predominant function is to support spatial memory (O’Keefe and Nadel, 1978). As a result, discussions of amnesia have focused especially on the status of spatial memory. It is clear that spatial memory is impaired in human amnesia. Amnesic patients are impaired on tests that assess their knowledge of the spatial layout of an environment, and they are also impaired when asked to navigate to a destination in a virtual environment (Maguire et al., 1996; Spiers et al., 2000). Similarly, the noted patient H.M. was impaired at recalling object locations (Smith, 1988). It is also clear, though, that amnesic patients are impaired on memory tests that have no obvious spatial component, such as recall or recognition of items (Squire and Shimamura, 1986). Furthermore, formal experiments that directly compared spatial and nonspatial memory in amnesic patients showed that the patients were similarly impaired on tests of spatial memory and tests of nonspatial memory. There was not a special difficulty with tests of spatial memory (Cave and Squire, 1991).
As is the case with nonspatial memory, remote spatial knowledge is intact. One well-studied patient with large medial temporal lobe lesions and severe amnesia (E.P.) was able to mentally navigate the neighborhood where he grew up, use alternate and novel routes to describe how to travel from one place to another, and point correctly to locations in the neighborhood while imagining himself oriented at some other location (Teng and Squire, 1999). These findings show that the medial temporal lobe is not needed for the long-term storage of spatial knowledge and does not maintain a spatial layout of learned environments that is necessary for successful navigation. Accordingly, the available data support the view that the hippocampus and related medial temporal lobe structures are involved in learning new facts and events, both spatial and nonspatial. Further, these structures are not repositories of long-term memory, either spatial or nonspatial.
Spared learning and memory abilitiesEdit
It is a striking feature of amnesia that many kinds of learning and memory are spared. Memory is not a unitary faculty of the mind but is composed of many parts that depend on different brain systems. Amnesia impairs only declarative memory and spares immediate and working memory as well as nondeclarative memory.
Immediate and working memoryEdit
Amnesic patients have intact immediate memory. Immediate memory refers to what can be held actively in mind beginning the moment that information is received. It is the information that forms the focus of current attention and that occupies the current stream of thought. The capacity of immediate memory is quite limited. This type of memory is reflected, for example, in the ability to repeat back a short string of digits. Intact immediate memory explains why amnesic patients can carry on a conversation and appear quite normal to the casual observer. Indeed, if the amount of material to be remembered is not too large (e.g., a 3-digit number), then patients can remember the material for minutes, or as long as they can hold it in mind by rehearsal. One would say in this case that the patients have carried the contents of immediate memory forward by engaging in explicit rehearsal. This rehearsal-based activity is referred to as working memory, and it is independent of the medial temporal lobe system. The difficulty for amnesic patients arises when an amount of information must be recalled that exceeds immediate memory capacity or when information must be recalled after a distraction-filled interval or after a long delay. In these situations, when the capacity of working memory is exceeded, patients will remember fewer items than their healthy counterparts.
Nondeclarative memory refers to a collective of non-conscious knowledge systems that operate outside of awareness. It is not itself a brain-systems construct. Rather, the term encompasses several different kinds of memory. Nondeclarative forms of memory have in common the feature that memory is non-conscious. Memory is expressed through performance and does not require reflection on the past or even the knowledge that memory is being influenced by past events. The following examples illustrate that nondeclarative memory is distinct from declarative memory. Nondeclarative forms of memory depend variously on the neostriatum, the amygdala, the cerebellum, and on processes intrinsic to neocortex
Motor and perceptual skillsEdit
One can learn how to ride a bicycle but be unable to describe what has been learned, at least not in the same sense that one might recall riding a bicycle on a particular day with a friend. This is because the learning of motor skills is largely nondeclarative, and it has been shown that amnesic patients can learn skills at a normal rate. In one experiment, amnesic patients and control participants performed a serial reaction-time task, where they responded successively to a sequence of four illuminated spatial locations. The task was to press one of four keys as rapidly as possible as soon as the location above each key was illuminated. The amnesic patients learned the sequence, as did the normal participants, as measured by their decreased reaction times to press a key when it was illuminated. When the sequence was changed, the reaction times increased for both groups. Strikingly, the amnesic patients had little or no declarative knowledge of the sequence, though they had learned it normally (Reber and Squire, 1994).
Perceptual skills are also often intact in amnesic patients. These include such skills as reading mirror-reversed print and searching a display quickly to find a hidden letter. In formal experiments, amnesic patients acquired perceptual skills at the same rate as individuals with intact memory, even though the patients did not remember what items were encountered during the task and sometimes did not remember the task itself. For example, amnesic patients learned to read mirror-reversed words at a normal rate and then retained the skill for months. Yet, after they had finished the mirror-reading task, they could not remember the words that they had read and in some cases could not remember that they had ever practiced the mirror-reading skill on a previous occasion (Cohen and Squire, 1980).
Priming refers to an improved ability to identify or produce a word or other stimulus as a result of its prior presentation. The first encounter with an item results in a representation of that item, and that representation then allows it to be processed more efficiently than items that were not encountered recently. For example, suppose that a line drawing of a dog, hammer, and airplane, are presented in succession, with the instruction to name each item as quickly as possible. Typically, about 800 milliseconds are needed to produce each name aloud. If in a later test these same pictures are presented intermixed with new drawings, the new drawings will still require about 800 milliseconds to name, but now the dog, hammer, and airplane are named about 100 milliseconds more quickly. The improved naming time occurs independently of whether one remembers having seen the items earlier. Amnesic patients exhibit this effect at full strength, despite having poor declarative memory of seeing the items earlier.
Adaptation-level effects refer to the finding that experience with one set of stimuli influences how a second set of stimuli is perceived (e.g., their heaviness or size). For example, experience with light-weighted objects subsequently causes other objects to be judged as heavier than they would be if the light-weighted objects had not been presented. Amnesic patients show this effect to the same degree as healthy individuals, even when they experience the first set of objects with one hand and then make judgments with the other hand. However, they have difficulty remembering their prior experience accurately (Benzing and Squire, 1989).
Classical conditioning refers to the development of an association between a previously neutral stimulus (CS) and an unconditioned stimulus (US) and is a quintessential example of nondeclarative memory. One of the best-studied examples of classical conditioning in humans is delay conditioning of the eyeblink response. It is reflexive and automatic and depends solely on structures below the forebrain, including the cerebellum and associated brainstem circuitry (Thompson and Krupa, 1994). In a typical conditioning procedure, a tone repeatedly precedes a mild airpuff directed to the eye. The tone overlaps the airpuff, and they terminate together. After a number of pairings, the tone comes to elicit an eyeblink in anticipation of the airpuff. Amnesic patients acquire and retain the tone-airpuff association at the same rate as healthy individuals. In both groups, awareness of the temporal contingency between the tone and the airpuff is unrelated to successful conditioning.
In trace conditioning, a brief interval of 500-1000 msec is interposed between the CS and the US. This form of conditioning requires the hippocampus (McGlinchey-Berroth et al., 1997). Formal experiments suggest that trace conditioning is hippocampus-dependent because it requires the acquisition and retention of conscious knowledge during the course of the conditioning session (Clark and Squire, 1998). Only those who became aware of the CS-US relationship acquired differential trace conditioning. There was a correlation between measures of awareness taken after the conditioning and trace conditioning performance itself, whereas there was no correlation between awareness and conditioning performance on a delay conditioning task.
Habit learning refers to the gradual acquisition of associations between stimuli and responses, such as learning to make one choice rather than another. Habit learning depends on the neostriatum (basal ganglia). Many tasks can be acquired either declaratively, through memorization, or nondeclaratively as a habit. For example, healthy individuals will solve many trial-and-error learning tasks quickly by simply engaging declarative memory and memorizing which responses are correct. In this circumstance, amnesic patients are disadvantaged. However, tasks can also be constructed that defeat memorization strategies, for example, by making the outcomes on each trial probabilistic. In such a case, amnesic patients and healthy individuals learn at the same gradual rate (Knowlton et al., 1996). It is also true that severely amnesic patients who have no capacity for declarative memory can gradually acquire trial-and-error tasks, even when the task can be learned declaratively by healthy individuals. In this case they succeed by engaging habit memory. This situation is nicely illustrated by the 8-pair concurrent discrimination task, which requires individuals to learn the correct object in each of eight object pairs. Healthy individuals can learn all eight pairs in one or two test sessions. Severely amnesic patients acquire this same task over many weeks, even though at the start of each session they cannot describe the task, the instructions, or the objects. It is known that this task is acquired at a normal (slow) rate by monkeys with medial temporal lobe lesions, and that monkeys with lesions of the neostriatum (basal ganglia) are impaired. Thus, humans appear to have a robust capacity for habit learning that operates outside of awareness and independently of the medial temporal lobe structures that are damaged in amnesia (Bayley et al., 2005a).
Functional amnesia, also known as dissociative amnesia, is a dissociative psychiatric disorder that involves alterations in consciousness and identity. Although no particular brain structure or brain system is implicated in functional amnesia, the cause of the disorder must be due to abnormal brain function of some kind. Its presentation varies considerably from individual to individual, but in most cases functional amnesia is preceded by physical or emotional trauma and occurs in association with some prior psychiatric history (Kritchevsky et al., 2004). Often, the patient is admitted to the hospital in a confused or frightened state. Memory for the past is lost, especially autobiographical memory and even personal identity. Semantic or factual information about the world is often preserved, though factual information about the patient’s life may be unavailable. Despite profound impairment in the ability to recall information about the past, the ability to learn new information is usually intact. The disorder sometimes clears and the lost memories return. Sometimes, the disorder lasts longer, and sizable pieces of the past remain unavailable.
See also Edit
- Dissociative disorders
- False memory
- HM (patient)
- Clive Wearing
- Repressed memory
References & BibliographyEdit
- Tulving, E. 1983. Elements of Episodic Memory. Oxford University Press, New York.
- Whitty,C.W.N. and Zangwill, 0.(eds) Amnesia, London: Butterworth.
- Briere, J. and Conte, J. R. (1993) Self-reported amnesia for abuse in adults molested as children, Journal of Traumatic Stress, 6, 21-31.
- Corkin, S. (2002). What's new with the amnesic patient H.M.? , Nature Reviews Neuroscience 3, 153-6o.
- Graf, P., Squire, L. R. and Mandler, G. (1984). The information that amnesics do not forget . Journal of Experimental Psychology 10, 164-78.
- Hamann, S.B., Cahill, L., McGaugh, J.l., Squire, L.R. (1997). Intact enhancement of declarative memory for emotional material in amnesia , Learning and Memory 4, 301-9.
- Milner, B., (1966), Amnesia following operation on the temporal lobes , in Whitty, C. W. M. and Zangwill, O. L. (eds.), Amnesia, AppletonCentury-Crofts.
- Warrington, E. K., and Weiskrantz, L., The effect of prior learning on subsequent retention in amnesic patients , Neuropsychologia 12 (1974), 419-28.
Adolphs, R., Cahill, L., Schul, R., and Babinsky, R. 1997. Impaired declarative memory for emotional material following bilateral amygdala damage in humans. Learn Mem 4(3), 291-300.
- Bayley, P. J., Hopkins, R. O., and Squire, L. R. 2003. Successful recollection of remote autobiographical memories by amnesic patients with medial temporal lobe lesions. Neuron 38(1), 135-144.
- Bayley, P. J., Frascino, J. C., & Squire, L. R. 2005a. Robust habit learning in the absence of awareness and independent of the medial temporal lobe. Nature 436, 550-553.
- Bayley, P. J., Gold, J. J., Hopkins, R. O., and Squire, L. R. 2005b. The neuroanatomy of remote memory. Neuron 46(5), 799-810.
- Bayley, P. J., Wixted, J. T., Hopkins, R. O., and Squire, L. R. 2008. Yes/no recognition, forced-choice recognition, and the human hippocampus. J Cogn Neurosci 20(3), 505-512.
- Benzing, W. C. and Squire, L. R. 1989. Preserved learning and memory in amnesia: intact adaptation-level effects and learning of stereoscopic depth. Behav Neurosci. 103(3), 538-547.
- Cave, C. B., Squire, L. R. 1991 Equivalent impairment of spatial and nonspatial memory following damage to the human hippocampus. Hippocampus 1, 329-340.
- Clark, R. E. and Squire, L. R. 1998. Classical conditioning and brain systems: the role of awareness. Science 280(5360), 77-81.
- Cohen, N. J. and Squire, L. R. 1980. Preserved learning and retention of pattern-analyzing skill in amnesia: dissociation of knowing how and knowing that. Science. 210(4466), 207-210.
- Conroy, M. A., Hopkins, R. O., and Squire, L. R. 2005. On the contribution of perceptual fluency and priming to recognition memory. Cogn Affect Behav Neurosci 5(1), 14-20.
- Damasio, A. R., Eslinger, P. J., Damasio, H., Van Hoesen, G. W., and Cornell, S. 1985. Multimodal amnesic syndrome following bilateral temporal and basal forebrain damage. Arch Neurol. 2(3), 252-259.
- Davis, M. 1994. The role of the amygdala in emotional learning. Int. Rev. Neurobiol. 36, 225-266.
- Hamann, S. B. and Squire, L. R. 1995. On the acquisition of new declarative knowledge in amnesia. Behav. Neurosci. 109, 1027-1044.
- Hamann, S. B. and Squire, L. R. 1997. Intact perceptual memory in the absence of conscious memory. Behav Neurosci. 111, 850-854.
- Janowsky, J. S., Shimamura, A. P., and Squire, L. R. 1989. Source memory impairment in patients with frontal lobe lesions. Neuropsychologia. 27(8), 1043-1056.
- Kim, J. J., Clark, R. E., and Thompson, R. F. 1995. Hippocampectomy impairs the memory of recently, but not remotely, acquired trace eyeblink conditioned responses. Behav Neurosci. 109(2), 195-203.
- Kirwan, C. B., Bayley, P. J., Galvan, V. V., and Squire, L. R. 2008. Detailed recollection of remote autobiographical memory after damage to the medial temporal lobe. Proc Natl Acad Sci U S A 105(7), 2676-80.
- Knowlton, B. J., Ramus, S. J., and Squire, L. R. 1992. Intact artificial grammar learning in amnesia: Dissociation of classification learning and explicit memory for specific instances. Psychol Sci. 3, 172-179.
- Knowlton, B. J. and Squire, L. R. 1993. The learning of categories: parallel brain systems for item memory and category knowledge. Science. 262(5140), 1747-1749.
- Knowlton, B. J. and Squire, L. R. 1994. The information acquired during artificial grammar learning. J Exp Psychol Learn Mem Cogn. 20(1), 79-91.
- Knowlton, B. J. and Squire, L. R. 1995. Remembering and knowing: two different expressions of declarative memory. J Exp Psychol Learn Mem Cogn. 21(3), 699-710.
- Knowlton, B. J. and Squire, L. R. 1996. Artificial grammar learning depends on implicit acquisition of both abstract and exemplar-specific information. J Exp Psychol Learn Mem Cogn. 22(1), 169-181.
- Kritchevsky, M., Chang, J., and Squire, L. R. 2004. Functional amnesia: clinical description and neuropsychological profile of 10 cases. Learn Mem 11(2): 213-26.
- LeDoux, J.E. 1996. The Emotional Brain. New York, Simon and Schuster.
- Lee, A. C., Buckley, M. J., Pegman, S. J., Spiers, H., Scahill, V. L., Gaffan, D., Bussey, T. J., Davies, R. R., Kapur, N., Hodges, J. R., and Graham, K. S. 2005a. Specialization in the medial temporal lobe for processing of objects and scenes. Hippocampus 15(6): 782-97.
- Lee, A. C., Bussey, T. J., Murray, E. A., Saksida, L. M., Epstein, R. A., Kapur, N., Hodges, J. R., and Graham, K. S. 2005b. Perceptual deficits in amnesia: challenging the medial temporal lobe 'mnemonic' view. Neuropsychologia 43(1): 1-11.
- Levy, D. A., Hopkins, R. O., and Squire, L. R. 2004. Impaired odor recognition memory in patients with hippocampal lesions. Learn Mem. 11(6), 794-796.
- Levy, D. A., Shrager, Y., and Squire, L. R. 2005. Intact visual discrimination of complex and feature-ambiguous stimuli in the absence of perirhinal cortex. Learn Mem. 12(1), 61-66.
- Maguire, E. A., Burke, T., Phillips, J., Staunton, H. 1996. Topographical disorientation following unilateral temporal lobe lesions in humans. Neuropsychologia 34, 993-1001.
- Manns, J. R., Hopkins, R. O., Reed J. M., Kitchener, E. G., and Squire, L. R. 2003. Recognition memory and the human hippocampus. Neuron 37(1), 171-180.
- McGlinchey-Berroth, R., Carrillo, M. C., Gabrieli, J. D., Brawn, C. M., and Disterhoft, J. F. 1997. Impaired trace eyeblink conditioning in bilateral, medial-temporal lobe amnesia. Behav Neurosci 111(5), 873-882.
- Mishkin, M. 1982. A memory system in the monkey. Philos Trans R Soc Lond B Biol Sci 298, 83-95.
- Nosofsky, R. M. and Zaki, S. R. 1998. Dissociation between categorization and recognition in amnesic and normal individuals: An exemplar-based interpretation. Psychol Sci 9, 247-255.
- O’Keefe, J. and Dostrovsky, J. 1971. The hippocampus as a spatial map. Preliminary evidence from unit activity in the freely-moving rat. Brain Res. 34(1), 171-175.
- O'Keefe J, Nadel L (1978) The Hippocampus as a Cognitive Map. Oxford, UK: Oxford Univ. Press.
- Parkin, A. J. and Walter, B. M. 1992. Recollective experience, normal aging, and frontal dysfunction. Psychol. Aging 7, 290-298.
- Reber, P. J. and Squire, L. R. 1994. Parallel brain systems for learning with and without awareness. Learn Mem. 1(4), 217-229.
- Reed, J. M. and Squire, L. R. 1998. Retrograde amnesia for facts and events: findings from four new cases. J Neurosci. 18(10), 3943-3954.
- Rempel-Clower, N. L, Zola, S. M., Squire, L. R., and Amaral, D. G. 1996. Three cases of enduring memory impairment after bilateral damage limited to the hippocampal formation. J Neurosci. 16(16), 5233-5255.
- Ribot, T. 1881. Les Maladies de la Memoire [English translation: Diseases of Memory]. New York: Appleton-Century-Crofts.
- Rutishauser, U., Mamelak, A. N., and Schuman, E. M. 2006. Single-trial learning of novel stimuli by individual neurons of the human hippocampus-amygdala complex. Neuron 49(6), 805-813.
- Schacter, D. L. and Tulving, E. 1994. Memory Systems. Cambridge, MA: MIT Press.
- Shrager, Y., Gold, J. J., Hopkins, R. O., and Squire, L. R. 2006. Intact visual perception in memory-impaired patients with medial temporal lobe lesions. J Neurosci. 26(8), 2235-2240.
- Smith, M. L. 1988. Recall of spatial location by the amnesic patient H.M. Brain Cogn 7, 178-183.
- Spiers, H. J., Burgess, N., Maguire, E. A., Baxendale, S. A., Hartley, T., Thompson, P. J., O'Keefe, J. 2001b. Unilateral temporal lobectomy patients show lateralized topographical and episodic memory deficits in a virtual town. Brain 124, 2476-2489.
- Squire, L. R. 1992. Memory and the hippocampus: a synthesis from findings with rats, monkeys, and humans. Psychol. Rev 99(2), 195-231.
- Squire, L. R. and Shimamura, A. P. 1986. Characterizing amnesic patients for neurobehavioral study. Behav Neurosci. 100(6), 866-77.
- Squire, L. R. and Zola, S. M. 1998. Episodic memory, semantic memory, and amnesia. Hippocampus 8, 205-211.
- Squire, L. R. and Zola-Morgan, S. 1983. The neurology of memory: The case for correspondence between the findings for human and nonhuman primate. In: The Physiological Basis of Memory (ed. J. A. Deutsch). Academic Press, New York.
- Squire, L. R. and Zola-Morgan, S. 1991. The medial temporal lobe memory system. Science 253, 1380-1386.
- Stefanacci, L., Buffalo, E. A., Schmolck, H., and Squire, L. R. 2000. Profound amnesia after damage to the medial temporal lobe: A neuroanatomical and neuropsychological profile of patient E. P. J Neurosci. 20(18), 7024-7036.
- Suzuki, W.A. and Amaral, D.G. 1994a. Perirhinal and parahippocampal cortices of the Macaque monkey: Cortical afferents. J. Comp. Neurol. 350, 497-533.
- Suzuki, W.A. and Amaral, D.G. 1994b. Topographic organization of the reciprocal connections between the monkey entorhinal cortex and the perirhinal and parahippocampal cortices. J. Neurosci. 14, 1856-1877.
- Teng, E. and Squire, L. R. 1999. Memory for places learned long ago is intact after hippocampal damage. Nature 400, 675-677.
- Thompson, R. F. and Krupa, D. J. 1994. Organization of memory traces in the mammalian brain. Annu Rev Neurosci. 17, 519-549.
- Tulving, E. 1985. How many memory systems are there? Am. Psychol. 40, 385-398.
- Wais, P. E., Wixted, J. T., Hopkins, R. O., and Squire, L. R. 2006. The hippocampus supports both the recollection and the familiarity components of recognition memory. Neuron 49, 459-466.
- Zola-Morgan, S., Squire, L. R., and Amaral, D. G. 1986. Human amnesia and the medial temporal region: enduring memory impairment following a bilateral lesion limited to field CA1 of the hippocampus.J Neurosci. 6(10), 2950-2967
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