Retrograde Amnesia: Causes, Diagnosis, and Treatment

Introduction to Amnesia and Memory

Amnesia is the loss of the faculty of memory and one of the most common forms of brain disorders. It is caused by organic factors such as infections, psychological trauma, or physical injuries to the brain. Amnesia can be associated either with loss of recollection of past events or with loss of memory for events that immediately follow an accident. In the former case it is called retrograde amnesia, while the latter condition is referred to as anterograde amnesia. Retrograde amnesia is generally viewed as a problem with recovering remote information, while anterograde amnesia represents problems with registering new information. This paper offers a focused examination of the diagnosis, causes, and treatment of retrograde amnesia.

Types of Amnesia

There are different types of amnesia, including retrograde, anterograde, lacunar, transient global, and hysterical amnesia. Among these, retrograde and anterograde amnesia are the two most prevalent conditions. Amnesia can be caused by brain damage resulting from accidents or infectious diseases, and the condition can be temporary or more lasting depending on the severity of the damage. In general, amnesia due to organic causes is of a more permanent nature. The DSM defines retrograde amnesia as "the loss of memory of events that occurred before the onset of the etiological condition or agent." In retrograde amnesia, the amnesiac loses long-term memory and cannot recollect events that happened prior to the trauma.

Before going into detail about retrograde amnesia, it is necessary to have a brief overview of the mechanisms of brain function. The human brain is a highly complex network divided into distinct regions such as the frontal lobes, temporal lobes, and parietal lobes. The information we process every day is either stored temporarily (and discarded shortly thereafter) or permanently embedded within the brain. For any particular piece of information to be permanently stored, a permanent chemical change must occur in the brain. This happens naturally when we use and reuse the same information repeatedly. The process by which temporary data are converted and stored as permanent data is known as consolidation.

The hippocampus, located in the temporal area of the brain, plays a vital role in permanently encoding information into brain cells. As researcher Fanselow (2000) observes, "with the aid of the hippocampus, this memory becomes permanently stored in other, probably cortical, structures." Any damage caused to the hippocampal region therefore directly affects this conversion process, leading to loss of long-term memory.

Diagnostic Tests

Aside from the normal symptoms of reported memory loss, certain procedures help physicians in diagnosing amnesia. Cerebral angiography is one such procedure, which helps the physician identify the exact location of any abnormality in the arteries of the brain; using a contrast dye, the blood flow in the brain can be traced. CT scans may also be performed to identify any intracranial infarctions and to monitor motor neuron activity within the brain. The electroencephalogram (EEG) is another test used to monitor electrical activity within the brain and to identify any anomalies.

Causes of Amnesia

Amnesia is a symptomatic response to many different kinds of brain diseases. It may result from physical injury to the brain, infections, or other degenerative brain disorders. Alzheimer's disease, dementia, brain tumors, encephalitis, and brain infections are all leading causes of amnesia. Amnesia may also result from epileptic seizures. Electroconvulsive therapy, used to treat patients with chemical imbalances in the brain, is also reported to cause amnesia. Similarly, temporal lobe surgery performed for tumors and other diseases invariably results in some degree of amnesia.

Diagnosis of amnesia basically involves identifying the pattern of cognitive impairment and memory disorder. Brain lesions within particular regions can be attributed to specific symptoms and specific types of amnesia. It was not until 1970, when computerized tomography became available, that studying the exact locations of lesions was possible. In general, particular patterns of lesions are identified with particular types of organic amnesia. For example, amnesia caused by encephalitis and Korsakoff syndrome is largely due to lesions localized within a certain segment of the brain. However, even within a particular aetiological group, the pattern of damage varies considerably (Alan J. Parkin, 8).

Retrograde Amnesia: Key Facts and Brain Regions

Retrograde amnesia is a condition characterized by an inability to retrieve remote or long-term memories. It can result from damage to different regions within the brain. Retrograde amnesia may be temporally graded, in which case only data pertaining to a certain period may be lost, or it may involve the loss of all memory prior to the accident. There are different subtypes of retrograde amnesia, namely autobiographical amnesia, focal retrograde amnesia, and semantic amnesia. These different conditions manifest as a result of damage to different areas of the brain.

As noted above, the exact location of brain damage (lesions) is widely variant even within a particular aetiological group. Studies have confirmed that damage caused by encephalitis may not be confined to the hippocampus but may extend as far as the orbitofrontal cortex and even into the thalamus. However, recent neuroradiological systems have made it easier to link patterns of brain lesions to particular forms of cognitive impairment. Using MRI scans, it is possible to study brain structure in minute detail and clearly identify damaged areas. Positron emission tomography (PET) has further improved our understanding of brain function by enabling the study of glucose metabolism in the brain.

Using PET, the cerebral blood flow can be directly observed using isotopes traced through the brain region. Neuronal activity within the brain is a direct measure of the cerebral blood flow (CBF) and the level of blood oxygenation (Alan Parkin, 10). PET can even identify non-functional areas within the brain that do not show any structural abnormality — a problem observed in brain areas not directly damaged but no longer receiving signal input from damaged regions.

The bilateral temporal lobe region is found to be damaged in most cases where a patient suffers from retrograde amnesia. Although retrograde amnesia is very rarely found in the absence of anterograde amnesia, some rare cases do exist. Studies have identified that human beings possess discrete memory systems within the brain. For example, episodic memory and semantic memory are two different types of memory systems located in different regions of the brain. However, both types depend on specific neocortical zones within the frontal and temporal lobes for information retrieval. PET studies have also indicated that the right hemisphere is predominantly used in the recovery of episodic information while the left hemisphere is used in the retrieval of semantic details. This type of lateralization was first studied by Kapur et al. (1994) using PET. This is precisely why some patients with retrograde amnesia retain autobiographical memory while their semantic memory is severely impaired. In cases where the left temporal lobe is affected, there is a marked decline in the ability to recollect facts (Hans J. Markowitsch).

Conclusion

Amnesia is not a disease in itself but a symptomatic condition — a syndrome — that may result from a variety of causes, including organic, psychological, and accidental factors. Given this inherent complexity, proper diagnosis is essential to understanding the exact nature of the problem. Extensive studies of retrograde amnesia have indicated that there are clear dissociations between various types of memory and their storage locations within the brain, and that the degree of retrograde amnesia varies widely among individuals. In most cases, patients suffering from retrograde amnesia gradually recover their memory over time. It is hoped that, in the near future, the arrival of safe and improved pharmacological treatments will greatly improve the quality of life for those affected by amnesia.

Bibliography

A. Scriabine, "International Congress of Pharmacology, Munich, Germany, July 26–31, 1998, New Drugs Affecting Central Nervous System." Accessed November 28, 2003. http://www.nevapress.com/cnsdr/full/4/3/287.pdf.

Health News Digest. "Memory Enhancing Drugs May Worsen Working Memory." Accessed November 26, 2003. http://www.healthnewsdigest.com/news/hlth_memory-4.html.

Designed by ADAM Inc. "Memory Loss." http://health.allrefer.com/health/memory-loss-home-care.html.

Francois Sellal et al. "Pure Retrograde Amnesia Following a Mild Head Trauma: A Neuropsychological and Metabolic Study." Accessed November 27, 2003. http://www.masson.it/cortex/pdf/vol38/issue4/Sellal.pdf.

Gloor P. "Experiential phenomena of temporal lobe epilepsy. Facts and hypothesis." Brain, 113: 1673–1694, 1990.

Hans J. Markowitsch et al. "Retrograde Amnesia for World Knowledge and Preserved Memory for Autobiographic Events. A Case Report." Accessed November 28, 2003. http://www.masson.it/cortex/pdf/vol35/issue2/243-252.pdf.

Lynn Nadel and Morris Moscovitch. "Memory consolidation, retrograde amnesia and the hippocampal complex." Accessed November 28, 2003.

Reed JM, Squire LR. "Retrograde amnesia for facts and events: findings from four new cases." Accessed November 29, 2003. http://www.jneurosci.org/cgi/content/full/18/10/3943.

Alan J. Parkin. Neuropsychology of Memory. Psychology Press, 1997.

Babinsky et al. (1994). "Atraumatic Temporal Lobe Pathology and Autobiographical Memory." European Neurology, 34, 290–291.

Lynn Nadel, Veronique Bohbot. "Consolidation of Memory." Accessed November 28, 2003.