Anterograde Amnesia and the Human Mind


This paper will examine the medical condition known as anterograde amnesia from the physiological perspective. Anterograde amnesia is the condition wherein an individual becomes physically incapable of forming new memories, normally immediately after an injury occurs. Beginning with the psychological phenomenon, covering the general emotional response to the condition and the role which personality plays in establishing variance and emotional compensation. This paper will then discuss four neurogical aspects of anterograde amnesia broken including the functions, the origin of the condition, the brain structures involved, and animal models. Anterograde amnesia affects explicit memory and spatial memory. Anterograde amnesia is a physically derived condition, occurring from injury sustained during medical procedures, physical injury, or diseases which damage the hippocampus or the surrounding neural pathways.. The hippocampus is a key component of anterograde amnesia. Animal models allow for testing the surviving structures of the brain. Possible treatments for anterograde memory loss involve utilizing the surviving learning mechanisms to compensate for memory loss.

Anterograde Amnesia and the Human Mind

Anterograde amnesia is an imperfectly understood physical disability of the brain which drastically alters and impairs an individual’s personal narratives and continuity of self. The Western concept of human spirit is closely tied to the human consciousness. This concept explains in part the fascination with mental illnesses as well as the emotional dread felt towards illnesses and injuries which harm our ability to reason, recall, and think. Famous fiction writer Terry Pratchett vehemently declared that he preferred suicide over the mental degradation of Alzheimer’s (Hendry, Pasterfield, Lewis, Carter, Hodgson, Wilkinson, 2013). Few diseases pique Western imaginations more than amnesia, the seemingly impossible condition wherein our memories are taken out of our reach. Few conditions are as frightening as that known as anterograde amnesia.

Anterograde amnesia is the condition in which an individual becomes physically incapable of forming new memories, and anterograde amnesia normally presents itself immediately after an injury occurs. Individuals suffering from this condition live in a perpetual state of confusion and disorientation, unable to recall the context for the situations in which they find themselves. Former symphony composer and orchestrator Clive Wearing, who suffered from anterograde amnesia following a brain viral infection,  kept a journal in which he would repeatedly write sentences like “finally now, I am aware”, only for him to strike out what he had just written when his memory would effectively reset after just ten or fifteen seconds (Wilson, Kopelman, & Kapur, 2008). Although anterograde amnesia is a relatively rare physical condition, the disease has revealed much of the mental structures and functions which underpin human memory and consciousness.

Psychological Impact

The psychological symptoms of anterograde amnesia are relatively simple in concept, typified as an impaired ability to form new declarative memories after the point of injury, yet the severity of condition and the psychological response varies from individual to individual (Cavaco, Anderson, Allen, Castro-Calda, & Damasio, 2004). This differentiation occurs because the anterograde amnesia is tied to actual damage or impairment of the brain and the specifics of the damage generally vary between subjects. Some patients are continually disoriented by their surroundings because their cognitive narratives provide them with no history or with broken heuristics of how they came to be in their current situation (Wilson et al., 2008). As previously mentioned, retrograde amnesiac Clive Wearing would become upset whenever prompted to access sequential information. Even such benign questions as “How are you feeling?” would lead Wearing to consider his emotions, realize that he could not find a memory of how he was feeling and then become emotionally distressed (Wilson et al., 2008). Other retrograde amnesiacs develop compensating memory strategies that allow them to continue to develop as individuals. An example of someone using this coping technique is the influenza-induced amnesiac known as Angie who, despite losing her memory formation abilities, managed to complete her education degree, remarry, and raise three children (Duff, Wszalek, Tranel, & Cohen, 2008).

The most famous and influential case of anterograde amnesia is found in a man who in life was referred to as H.M., or Henry Molaison. H.M. was a normal man who suffered from progressively worsening seizures. When his seizures forced H.M. to quit his job, a doctor offered an opportunity to cure H.M.’s seizures once and for all, by removing a small portion of H.M’s brain known as the hippocampus. Readily agreeing to the procedure, H.M. was soon cured of his seizures but at an unfortunate cost. H.M. could no longer form memories, and was thus condemned to live a life where no memory, no matter how extraordinary or memorable, could be recalled. H.M. described the sensation as “Every day is alone by itself” (Wilson et al., 2008).

Physiological Function

The majority of this paper will cover the physiological causes and functions of anterograde amnesia. The psychological effects of anterograde memory loss are fairly well defined in terms of their effects and yet still not fully understood in terms of their causes. The positions generally accepted are that the condition exhibits distinct functions lost and retained, the condition is physically derived, and that the hippocampus forms a key component in anterograde amnesia.

Functions Lost and Functions Retained

 The anterograde amnesia condition implies the loss or serious impairment of a single memory function known as the declarative memory or spatial memory (Spiers, Maguire, Burgess, 2001). The declarative memory affected diverges into two relatively distinct yet interdependent forms, explicit memory and spatial memory. Explicit memory refers to distinct personal experiences which can be put into words (Spiers et al., 2001). Spatial memory refers to the ability to recall and place a series of events into sequence (Annese, et al 2014).The forms of learning unaffected by anterograde amnesia are referred to as non-declarative learning, including short-term memory, habitual skill learning, priming, classical condition, and simple category learning skills (Spiers et al., 2001). These learning abilities are believed to persist because they do not rely on the hippocampal structure. These functions form the majority of the cognitive abilities seen in retrograde amnesiacs and so most studies focus on the distinguishing between remnants of anterograde memory, memory functions unaffected by anterograde amnesia, and similar symptoms of anterograde amnesia caused by third party conditions (Spiers et al. 2001).

One important note to make is that because the condition is physically derived, other areas of the brain may also be damaged. For instance, the previously mentioned anterograde amnesiac Clive Wearing suffers from both anterograde and retrograde amnesia, and some findings indicate that his extreme disorientation may be exacerbated by a physiological partial loss of self-concept (Wilson et al. 2008). This finding demonstrates that while anterograde is understood in the abstract, there are gaps in the physiological understanding of the condition. This in turn can make exact analysis and distinction of some functions of the anterograde amnesia’s condition difficult to define (Spiers et al. 2001).

Physically Derived

Anterograde amnesia symptoms derive from physical brain damage and not from chemical reactions. Post-mortem findings for H.M.’s brain were that the following brain structures were damaged: the medial temporal polar cortex, most of the amygdaloid complex and entorhinal cortex (EC), about half of the rostro-caudal extent of the intraventricular segment of the hippocampal formation (Annese, et al 2014, p.2). Although portions of the hippocampal remained, they were assumed to have lost their function without the enthorhinal cortex (Annese, et al 2014).

Corroborating the argument that anterograde amnesia is a physically derived condition is that chemically induced diseases such as Korsakoff’s syndrome which exhibit anterograde amnesia symptoms act by creating physical lesions on the mammillary bodies of the hypothalamus (Cipolotti, Bird, Good, Macmanus, Rudge, Shallice, 2006). These findings indicate that anterograde amnesia is a physically derived condition that may be induced through chemical means.

Hippocampus as consolidation hub

The relationship between the hippocampus and memory functions is that the hippocampus acts as a centralized hub for various memory consolidations. This then explains how anterograde amnesiacs are able to process information in the immediate present and still have no declarative memory afterwards. Because they do have moment by moment sequential memories, but are unable to store and later retrieve these memories. Additionally, because anterograde amnesiacs are capable of the other three forms of memory, namely perceptual learning, stimulus-response learning, and motor learning, they are otherwise mentally capable (Corkin, 2002).

The earliest discovered brain structure related to relational memory and anterograde amnesia was the hippocampus (Annese, et al 2014). As previously mentioned, this relationship was discovered when the patient H.M. lost his ability to form new declarative memories after an otherwise successful surgery. Because the hippocampus is connected to multiple sections of the brain, such as the amygdala, orbitofrontal cortex, and nucleus accumbens, the researchers speculate that the structure known as the hippocampus forms a dual structure, the posterior portion which facilitates memory formation and the anterior portion which helps to regulate emotion, stress, and sensorimator integration (Annese, et al 2014, p.6). The posterior region and related structures then form a memory consolidation loop which allow the hippocampus to access and interact with information and while trading off information to then be added to long term memory. Disconnection of one of these peripheral structures then leads to an inability to form new memories because the information processed through the hippocampus has nowhere to go (Annese, et al 2014).

In the case of H.M., H.M.’s entorhinal cortex was removed almost completely from both hemispheres, and the hippocampus therefore had no immediate points to carry out its function of memory consolidation. In essence, H.M’s inability to form memories came more from the lack of the EC surrounding the surviving hippocampus than the intended damage to the hippocampus directly (Annese, et al 2014, p.6). This loop system also explains why certain anterograde amnesiacs exhibit such confusion, as the majority of their cognitive functions remain intact; they are unable to account for why they are in a foreign situation or why they are so confused (Annese, et al 2014).

The exact cause for anterograde amnesia is not yet known. H.M.’s inability to form new explicit memories is assumed to be because of the accidental removal of his enthorhinal cortex (Annese, et al 2014). However, based on other MRIs, CAT scans, and post-mortems of anterograde amnesiac subjects, the enthorhinal cortex is undamaged and yet a different surrounding brain structure connected to the hippocampal structure is damaged (Annese, et all, 2014; Duff et al., 2008; Svoboda & Richards, 2009). So, while the hippocampus is the epicenter of the condition, it is not the only factor that requires consideration. In fact, because the hippocampus operates as a centralized hub, the hippocampus can conceivably remain intact and yet the patient may still suffer from anterograde amnesia (Annese, et all, 2014).

Animal model

Creating an animal model of human amnesia is difficult due to the increased complexity of the human memory. “Memory includes storing, retaining, and later recalling information” (Kesner, & Goodrich-Hunsaker, 2010, p.2290). Because human memory relies heavily on mnemonic and linguistic models, animal modeling is a less effective method for creating models of comparison between animal models and human models of amnesia. That said, researchers Raymond Kesner and Naomi Goodrich-Hunsaker found that rat models of amnesia are similar to human models in terms of spatial memory, spatial pattern separation, and memory of temporal order, and sequential learning (Kesner et al., 2010, p.2290).

Speculatively, it is possible to determine correlations between the rat models and human models by observing changes after lesions on the hippocampal structure. One example of the similarities is with spatial memory. More specifically, the similar strategies displayed by rats in their abilities to create mental maps of environments previously encountered. Similar to human subjects, rats with hippocampal injuries continue to respond to cue-response learned association and yet appear hampered in place learning (Kesner et al., 2010).

Hippocampal damage prevented the mice from learning routes yet could still learn via the stimulus-response learning techniques (Kesner et al., 2010, p.2291). These results are similar to those of human beings suffering from hippocampal related memory loss. In both mice and men, these apparent abilities indicate that the hippocampus is primarily tied to relational memory consolidation and not the other types of learning. This connection implies that experiential memory is tied to relational memory but not the other forms of learning. Accordingly, the concept of memory has broadened to account for this apparent division, as learning stimulus-response learning has in the past been considered a subset of declarative or relational memory (Kesner et al., 2010).


While science is currently unable to cure anterograde amnesia, the specific regions of the brain involved and their interplay being only partially understood, there are studies which imply that there are certain rehabilitative activities which sidestep the condition. For instance, Cavaco et al. (2004) demonstrated that anterograde amnesiacs could learn motor learning skills like weaving, drawing, and pouring liquids into jars in approximately commensurate ability to physically well individuals. Assuming that activities were properly supervised, anterograde amnesiacs could be enabled to engage in limited productive activities. Although the costs of such supervision would likely make their activity a net loss, the physical activity may produce greater feelings of personal satisfaction.

Recent efforts have made use of modern technologies to compensate for impaired explicit memories. Use of reminders and technology offer new avenues of reducing costs for rehabilitation via smart phones. (Duff, et al., 2008). Eva Svoboda and Brian Richards demonstrated that anterograde amnesiacs can use smart phones and increase in their affinity for the technologies over time (2009). This finding is consistent with prior research on anterograde patients like H.M. as because the majority of their learning abilities remain intact, they are able to learn via repetition priming to use technologies nearly as well as a healthy patient because the behaviors become nearly automatic (Svoboda & Richards, 2009).

Rehabilitative treatments operate by engaging the surviving mental features of retrograde amnesiacs. Because retrograde amnesia is derived from damage to the declarative memory formations, the rest of the retrograde amnesiac’s learning continues to function relatively as expected. Svoboda and Richard’s case study involving a woman suffering from severe anterograde amnesia used an errorless learning and vanishing cues technique to gradually teach the necessary actions to operate a smartphone (Svoboda & Richards, 2009). The patient became able to take photos of grandchildren, take notes during meetings as well as be reminded to ask specific questions, and keep engagements as well as arrive at specific destinations.

This technique was successful because it operated on the implicit and motor systems of memory. So long as the individual is allowed access to their memory aids, their condition ought to improve. Some supervision is still required however as the subject is still dependent on their memory aids (Svoboda & Richards, 2009).


Retrograde amnesia can be a psychologically devastating condition which effectively ends people’s emotional and cognitive growth. However, the condition is by no means uniform in its effects and limitations. Brought about by a variety of causes, victims of this condition are neither fully present nor absent, they are in effect caught in a moment without all the relevant context with no immediate cure or remedy in sight. The foreseeable future for those suffering from the condition is one of repeated acceptance or denial, where the victim may either accept their condition and allow their minds to coalesce into an operational system like the patient Angie or they can continually deny their situation only to be confronted with its realities anew as is the case of Clive Wearing.

Repeated case studies, brain scans, and tests reveal the operating deficiency and the general regions involved in anterograde amnesia, yet researchers as of yet have been unable to determine long term cures or even exactly how much will or will not result in anterograde amnesia. The general consensus on anterograde amnesia is that it represents a distinct break in the temporal lobe region, focusing on the hippocampal region, which results in the distinct ability to interact with the world without having the subsequent ability to recall these encounters. As animal models better developed, neuroscience’s understanding of this condition may improve to the point where preventive methods and a true cure is developed.

Until such a working model of anterograde amnesia is developed however, victims of this condition will have to settle for creative workarounds that allow them to live relatively normal lives. As science continues to develop stronger, more descriptive models of the human memory, other medical conditions may also be discovered.


Annese, J., Schenker-Ahmed, N. M., Bartsch, H., Maechler, P., Sheh, C., Thomas, N., … Corkin, S. (2014, January 28). Postmortem examination of patient H.M.’s brain based on histological sectioning and digital 3D reconstruction. Nature Communications, 5. doi:10.1038/ncomms4122

Cavaco, S., Anderson, S. W., Allen, J. S., Castro-Caldas, A., and Damasio, H. The scope of preserved procedural memory in amnesia. Brain, 2004, 127, 1863–1867.

Cipolotti, L., Bird, C., Good, T., Macmanus, D., Rudge, P., & Shallice, T. (2006). Recollection and familiarity in dense hippocampal amnesia: A case study. Neuropsychologia, 44(3), 489-506.

Corkin, S. (2002). What’s new with the amnesic patient H.M.? Nature Reviews. Neuroscience, 3(2), 153-60.

Duff, M. C., Hengst, J., Tranel, D., & Cohen, N. J. (2006). Development of shared information in communication despite hippocampal amnesia. Nature Neuroscience, 9(1), 140+. Retrieved from

Duff, M. C., Wszalek, T., Tranel, D., & Cohen, N. J. (2008). Successful life outcome and management of real-world memory demands despite profound anterograde amnesia. Journal Of Clinical And Experimental Neuropsychology, 30(8), 931-945. doi:10.1080/13803390801894681

Hendry, M., Pasterfield, D., Lewis, R., Carter, B., Hodgson, D., & Wilkinson, C. (2013). Why do we want the right to die? A systematic review of the international literature on the views of patients, carers and the public on assisted dying. Palliative Medicine, 27(1), 13-26. doi:

Kesner, R. P., & Goodrich-Hunsaker, N. J. (2010, July). Developing an animal model of human amnesia: The role of the hippocampus. Neuropsychologia, 48(8), 2290-2302.

Milner, B. Memory and the temporal regions of the brain. In Biology of Memory, edited by K. H. Pribram and D. E. Broadbent. New York: Academic Press, 1970.

Spiers, H. J., Maguire, E. A., and Burgess, N. Hippocampal amnesia. Neurocase, 2001, 7, 357–382.

Svoboda, E., & Richards, B. (2009). Compensating for anterograde amnesia: A new training method that capitalizes on emerging smartphone technologies. Journal of the International Neuropsychological Society, 15.

Wilson, B. A., Kopelman, M., & Kapur, N. (2008, October). Prominent and persistent loss of past awareness in amnesia: Delusion, impaired consciousness or coping strategy? Neuropsychological Rehabilitation, 18(5/6), 527.


Leave a Reply

Your email address will not be published. Required fields are marked *