Saul McLeod published 2011
Anterograde amnesia refers to loss of memory for events after an incident – often such cases are examples of what are known as pure amnesiacs.
Therefore, a person can’t store new information in their short term memory.
Patients with anterograde amnesia quite often show normal memory for events prior to the incident responsible for the memory deficit but have severely impaired ability to recall information about events occurring after the incident.
Whereas with retrograde amnesia there is almost always a gradual restoration of most of the lost information, with anterograde amnesia there is quite often no such recovery and patients are left with a permanent and debilitating condition. The case which led to the discovery of the condition of anterograde amnesia is that of H.M. (Milner et al 1968).
Anterograde amnesia can be caused by a number of potential factors, such as brain surgery, e.g. HM, or alcohol, e.g. Korsakoffs syndrome.
H.M. Case Study of Anterograde Amnesia
H.M. had brain surgery in 1953 when he was 27 yrs. old. The surgery involved removal of part of the brain known as the hippocampus to alleviate the severe symptoms of epilepsy. Although the surgery controlled the epileptic seizures H.M. suffered serious and debilitating memory impairment as a side effect.
His short-term memory was normal but he was completely unable to transfer any new information into his long-term memory. He showed almost no knowledge of current affairs because he forgot any news item as soon as he had read about it; he knew nothing of recent family events including moving house and the death of his father.
Despite being able to remember people he had known long ago he was never able to store information about new people he encountered and they remained forever complete strangers to him.
In many respects H.M. seemed cognitively 'normal' as he was able to learn and remember perceptual and motor skills although he needed reminding of what he was able to do.
This case and others illustrate the highly selective nature of the problems of anterograde amnesia following brain damage. There is no general deterioration of memory function but specific deficits in which some abilities such as learning new information are severely impaired whilst others, including language and memory span are quite normal.
Alcohol Induced Amnesia
In 1889 Sergei Korsakoff, a Russian physician described a severe memory disorder due to brain damage. The most obvious symptom of what became known as Korsakoffs syndrome is a severe anterograde amnesia where the patients appears to be unable to form any new memories but can still remember some old ones (i.e. short term memory is impaired).
Korsakoff s syndrome usually, although not always, results from a thiamine (vitamin Bl) deficiency after years of alcohol abuse. Alcoholics often have a poor diet because they get sufficient calories from their alcohol intake, thus their vitamin intake from food is very low.
In addition to the problem of taking in few vitamins alcohol also interferes with the absorption of thiamine in the intestines. Very occasionally Korsakoffs syndrome can also result from infusions of glucose given to people suffering from severe malnutrition.
Many patients go through an acute phase, known as Wernicke's encephalopathy, during which they suffer from impairments of movement and emotional and cognitive functioning. In the chronic phase that follows the primary symptom is amnesia, primarily anterograde but also retrograde.
The brain damage in Korsakoff syndrome appears to be widespread with loss of nerve cells often occurring in several regions of the brain including the thalamus, cerebellum, cerebral cortex and frontal lobe. Interestingly, patients who have suffered frontal lobe damage due to-injury often encounter the same problem solving difficulties experienced by Korsakoff patients.
Milner, B., Corkin, S., et al. (1968). Further Analysis of Hippocampal Amnesic Syndrome - 14-Year Follow-up Study of HM. Neuropsychologia, 215-230.
How to reference this article:
McLeod, S. A. (2011). Retrieved from www.simplypsychology.org/anterograde-amnesia.html
Henry Molaison, known by thousands of psychology students as "HM," lost his memory on an operating table in a hospital in Hartford, in August 1953. He was 27 years old and had suffered from epileptic seizures for many years.
William Beecher Scoville, a Hartford neurosurgeon, stood above an awake Henry and skilfully suctioned out the seahorse-shaped brain structure called the hippocampus that lay within each temporal lobe. Henry would have been drowsy and probably didn't notice his memory vanishing as the operation proceeded. The operation was successful in that it significantly reduced Henry's seizures, but it left him with a dense memory loss. When Scoville realized his patient had become amnesic, he referred him to the eminent neurosurgeon, Dr. Wilder Penfield and neuropsychologist Dr. Brenda Milner of Montreal Neurological Institute (MNI) who assessed him in detail. Up until then it had not been known that the hippocampus was essential for making memories, and that if we lose both of them we will suffer a global amnesia. Once this was realized, the findings were widely publicized so that this operation to remove both hippocampi would never be done again.
Penfield and Milner had already been conducting memory experiments on other patients and they quickly realized that Henry's dense amnesia, his intact intelligence, and the precise neurosurgical lesions made him the perfect experimental subject. For 55 years Henry participated in numerous experiments, primarily at Massachusetts Institute of Technology (MIT) where Professor Suzanne Corkin and her team of neuropsychologists assessed him. Access to Henry was carefully restricted to less than 100 researchers (I was honored to be one of them), but the MNI and MIT studies on HM taught us much of what we know about memory. Of course many other patients with memory impairments have since been studied, including a small number with amnesias almost as dense as Henry's, but it is to him we owe the greatest debt. His name (or initials!) has been mentioned in almost 12,000 journal articles, making him the most studied case in medical or psychological history. Henry died on December 2nd, 2008, at the age of 82. Until then, he was known to the world only as "HM" but on his death his name was revealed. A man with no memory is vulnerable, and his initials had been used while he lived in order to protect his identity.
Henry's memory loss was far from simple. Not only could he make no new conscious memories after his operation, he also suffered a retrograde memory loss (a loss of memories prior to brain damage) for an eleven year period before his surgery. It is not clear why this is so, although it is thought this is not because of his loss of the hippocampi on both sides of his brain. More likely it is a combination of his being on large doses of antiepileptic drugs and his frequent seizures prior to his surgery. His global amnesia for new material was the result of the loss of both hippocampi, and meant that he could not learn new words, songs or faces after his surgery, forgot who he was talking to as soon as he turned away, didn't know how old he was or if his parents were alive or dead, and never again clearly remembered an event, such as his birthday party, or who the current president of the United States was. In contrast, he did retain the ability to learn some new motor skills such as becoming faster at drawing a path through a picture of a maze, or learning to use a walking frame when he sprained his ankle, but this learning was at a subconscious level. He had no conscious memory that he had ever seen or done the maze test before, or used the walking frame previously.
We measure time by our memories, and thus for Henry, it was as if time stopped when he was 16 years old, eleven years before his surgery. Because his intelligence in other non-memory areas remained normal he was an excellent experimental participant. He was also a very happy and friendly person and always a delight to be with and to assess. He never seemed to get tired of doing what most people would think of as tedious memory tests, because they were always new to him! When he was at MIT, between test sessions he would often sit doing crossword puzzles, and he could do the same ones again and again if the words were erased, as to him it was new each time.
Henry gave science the ultimate gift; his memory. Thousands of people who have suffered brain damage, whether through accident, disease or a genetic quirk, have given similar gifts to science by agreeing to participate in psychological, neuropsychological, psychiatric and medical studies and experiments, and in some cases by gifting their brains to science after their deaths. Our knowledge of brain disease and how the normal mind works would be greatly diminished if it were not for the generosity of these people and their families (who are frequently also involved in interviews, as well as transporting the "patient" back and forth to the psychology laboratory). After Henry's death his brain was dissected into 2000 slices and digitized as a three-dimensional brain map that could be searched by zooming in from the whole brain to individual neurons. Thus his tragically unique brain has been preserved for posterity.
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HM, aged 60: Copyright J, Ogden, "Trouble In Mind" 2012, p.173, OUP, New York