|Other names||Amnesic syndrome|
Amnesia is a deficit in memory caused by brain damage or disease, but it can also be caused temporarily by the use of various sedatives and hypnotic drugs. The memory can be either wholly or partially lost due to the extent of damage that was caused. There are two main types of amnesia: retrograde amnesia and anterograde amnesia. Retrograde amnesia is the inability to retrieve information that was acquired before a particular date, usually the date of an accident or operation. In some cases the memory loss can extend back decades, while in others the person may lose only a few months of memory. Anterograde amnesia is the inability to transfer new information from the short-term store into the long-term store. People with anterograde amnesia cannot remember things for long periods of time. These two types are not mutually exclusive; both can occur simultaneously.
Case studies also show that amnesia is typically associated with damage to the medial temporal lobe. In addition, specific areas of the hippocampus (the CA1 region) are involved with memory. Research has also shown that when areas of the diencephalon are damaged, amnesia can occur. Recent studies have shown a correlation between deficiency of RbAp48 protein and memory loss. Scientists were able to find that mice with damaged memory have a lower level of RbAp48 protein compared to normal, healthy mice. In people with amnesia, the ability to recall immediate information is still retained, and they may still be able to form new memories. However, a severe reduction in the ability to learn new material and retrieve old information can be observed. People can learn new procedural knowledge. In addition, priming (both perceptual and conceptual) can assist amnesiacs in the learning of fresh non-declarative knowledge. Individuals with amnesia also retain substantial intellectual, linguistic, and social skill despite profound impairments in the ability to recall specific information encountered in prior learning episodes.
The term is from Ancient Greek 'forgetfulness'; from ἀ- (a-) 'without', and μνήσις (mnesis) 'memory'.
Individuals with amnesia can learn new information, particularly if the information is non-declarative knowledge. However, in some situations, people with dense anterograde amnesia do not remember the episodes during which they previously learned or observed the information. Some people with amnesia show abnormal amounts of memory loss, confusion, and difficulty recalling other people or places. People who recover often do not remember having amnesia.
Declarative memory can be broken down into semantic memory and episodic memory, semantic memory being that of facts, episodic memory being that of memory related to events.
While a patient with amnesia might have a loss of declarative memory, this loss might vary in severity as well as the declarative information that it affects, depending on many factors. For example, LSJ was a patient that had retrograde declarative memory loss as the result of bilateral medial temporal lobe damage, but she was still able to remember how to perform some declarative skills. She was able to remember how to read music and the techniques used in art. She had preserved skill-related declarative memory for some things even though she had deficits in other declarative memory tasks. She even scored higher on skill-related declarative memory than the control in watercolor techniques, a technique that she used in her professional career before she acquired amnesia.
The loss of semantic information in amnesia is most closely related with damage to the medial temporal lobe or to the neocortex.
Some patients with anterograde amnesia can still acquire some semantic information, even though it might be more difficult and might remain rather unrelated to more general knowledge. H.M. could accurately draw a floor plan of the home in which he lived after surgery, even though he had not lived there in years. There is evidence that the hippocampus and the medial temporal lobe may help to consolidate semantic memories, but then they are more correlated with the neocortex. While lesions of the hippocampus normally lead to the loss of episodic memory, if there is any effect on semantic memory, it is more varied and usually does not last as long.
One reason that patients could not form new episodic memories is likely because the CA1 region of the hippocampus has a lesion, and thus the hippocampus could not make connections to the cortex. After an ischemic episode (an interruption of the blood flow to the brain), an MRI of patient R.B. following surgery showed his hippocampus to be intact except for a specific lesion restricted to the CA1 pyramidal cells. In one instance, transient global amnesia was caused by a hippocampal CA1 lesion. While this was a temporary case of amnesia, it still shows the importance of the CA1 region of the hippocampus in memory. Episodic memory loss is most likely to occur when there has been damage to the hippocampus. There is evidence that damage to the medial temporal lobe correlates to a loss of autobiographical episodic memory.
Some retrograde and anterograde amnesiacs are capable of non-declarative memory, including implicit learning and procedural learning. For example, some patients show improvement on the pseudorandom sequences experiment just as healthy people; therefore, procedural learning can proceed independently of the brain system required for declarative memory. Some patients with amnesia are able to remember skills that they had learned without being able to consciously recall where they had learned that information. For example, they may learn to do a task and then be able to perform the task later without any recollection of learning the task. According to fMRI studies, the acquisition of procedural memories activates the basal ganglia, the premotor cortex and the supplementary motor area, regions which are not normally associated with the formation of declarative memories. This type of dissociation between declarative and procedural memory can also be found in patients with diencephalic amnesia such as Korsakoff's syndrome. Another example demonstrated by some patients, such as K.C. and H.M, who have medial temporal damage and anterograde amnesia, still have perceptual priming. Priming was accomplished in many different experiments of amnesia, and it was found that the patients can be primed; they have no conscious recall of the event, but the response is there. Those patients did well in the word fragment completion task.[better source needed] There is some evidence that non-declarative memory can be held onto in the form of motor skills. This idea was disputed, though, because it is argued that motor skills require both declarative and non-declarative information.
There are three generalized categories in which amnesia could be acquired by a person. The three categories are head trauma (example: head injuries), traumatic events (example: seeing something devastating to the mind), or physical deficiencies (example: atrophy of the hippocampus). The majority of amnesia and related memory issues derive from the first two categories as these are more common and the third could be considered a subcategory of the first.
Among specific causes of amnesia are the following:
Many forms of amnesia fix themselves without being treated.[unreliable medical source?] However, there are a few ways to cope with memory loss if treatment is needed. Since there are a variety of causes that form different amnesia, it is important to note that there are different methods that response better with the certain type of amnesia. Emotional support and love as well as medication and psychological therapy have been proven effective.
One technique for amnesia treatment is cognitive or occupational therapy. In therapy, amnesiacs will develop the memory skills they have and try to regain some they have lost by finding which techniques help retrieve memories or create new retrieval paths. This may also include strategies for organizing information to remember it more easily and for improving understanding of lengthy conversation.
Another coping mechanism is taking advantage of technological assistance, such as a personal digital device to keep track of day-to-day tasks. Reminders can be set up for appointments when to take medications, birthdays and other important events. Many pictures can also be stored to help amnesiacs remember names of friends, family, and co-workers. Notebooks, wall calendars, pill reminders and photographs of people and places are low-tech memory aids that can help as well.
While there are no medications available to treat amnesia, underlying medical conditions can be treated to improve memory. Such conditions include but are not limited to low thyroid function, liver or kidney disease, stroke, depression, bipolar disorder and blood clots in the brain.[unreliable medical source?] Wernicke–Korsakoff syndrome involves a lack of thiamin and replacing this vitamin by consuming thiamin-rich foods such as whole-grain cereals, legumes (beans and lentils), nuts, lean pork, and yeast.[better source needed] Treating alcoholism and preventing alcohol and illicit drug use can prevent further damage, but in most cases will not recover lost memory.
Although improvements occur when patients receive certain treatments, there is still no actual cure remedy for amnesia so far. To what extent the patient recovers and how long the amnesia will continue depends on the type and severity of the lesion.
French psychologist Theodule-Armand Ribot was among the first scientists to study amnesia. He proposed Ribot's Law which states that there is a time gradient in retrograde amnesia. The law follows a logical progression of memory loss due to disease. First, a patient loses the recent memories, then personal memories, and finally intellectual memories. He implied that the most recent memories were lost first.
Case studies have played a large role in the discovery of amnesia and the parts of the brain that were affected. The studies gave important insight into how amnesia affects the brain. The studies also gave scientists the resources into improving their knowledge about amnesia and insight into a cure or prevention. There are several extremely important case studies: Henry Molaison, R.B, and G.D.
Henry Molaison, formerly known as H.M., changed the way people thought of memory. The case was first reported in a paper by William Beecher Scoville and Brenda Milner in 1957. He was a patient who had severe epilepsy attributed to a bicycle accident at the age of nine. Physicians were unable to control his seizures with drugs, so the neurosurgeon Scoville tried a new approach involving brain surgery. He removed his medial temporal lobe bilaterally by doing a temporal lobectomy. His epilepsy did improve, but Molaison lost the ability to form new long-term memories (anterograde amnesia). He exhibited normal short-term memory ability. If he was given a list of words, he would forget them in about a minute's time. In fact, he would forget that he had even been given a list in the first place. However, H.M.'s working and short-term memory seemed to be intact. He had a normal digit span and could hold a conversation that did not require him to recall past parts of the conversation. Once Molaison stopped thinking about the lists he was unable to recall them again from long-term memory. This gave researchers evidence that short-term and long-term memory are in fact two different processes. Even though he forgot about the lists, he was still able to learn things through his implicit memory. The psychologists would ask him to draw something on a piece of paper, but to look at the paper using a mirror. Though he could never remember ever doing that task, he would improve after doing it over and over again. This showed the psychologists that he was learning and remembering things unconsciously. In some studies it was found that H.M.'s perceptual learning was intact and that his other cognitive skills were working appropriately. It was also found that some people with declarative information amnesia are able to be primed.
Studies were completed consistently throughout Molaison's lifetime to discover more about amnesia. Researchers did a 14-year follow-up study on Molaison. They studied him for a period of two weeks to learn more about his amnesia. After 14 years, Molaison still could not recall things that had happened since his surgery. However, he could still remember things that had happened prior to the operation. Researchers also found that, when asked, Molaison could answer questions about national or international events, but he could not remember his own personal memories. After his death Molaison donated his brain to science, where they were able to discover the areas of the brain that had the lesions which caused his amnesia, particularly the medial temporal lobe. This case study provided important insight to the areas of the brain that are affected in anterograde amnesia, as well as how amnesia works. H.M.'s case showed us that memory processes are consolidated into different parts of the brain and that short-term and working memory are not usually impaired in cases of amnesia.
Another famous historical case of amnesia was that of Clive Wearing. Clive Wearing was a conductor and musician who contracted herpes simplex virus. This virus affected the hippocampal regions of the brain. Because of this damage, Wearing was unable to remember information for more than a few moments. Wearing's non-declarative memory was still functioning but his declarative memory was impaired. To him, he felt that he had just come to consciousness for the first time every time he was unable to hold on to information. This case also can be used as evidence that there are different memory systems for declarative and non-declarative memory. This case was more evidence that the hippocampus is an important part of the brain in remembering past events and that declarative and non-declarative memories have different processes in different parts of the brain.
Patient R.B. was a normally functioning man until the age of 52. At age 50, he had been diagnosed with angina and had surgery for heart problems on two occasions. After an ischemic episode (reduction of blood to the brain) that was caused from a heart bypass surgery, R.B. demonstrated a loss of anterograde memory, but almost no loss of retrograde memory, with the exception of a couple of years before his surgery, and presented no sign of any other cognitive impairment. It wasn't until after his death that researchers had the chance to examine his brain, when they found his lesions were restricted to the CA1 portion of the hippocampus. This case study led to important research involving the role of the hippocampus and the function of memory.
Patient G.D. was a white male born in 1940 who served in the Navy. He was diagnosed with chronic kidney failure and received hemodialysis treatment for the rest of his life. In 1983, he went to the hospital for elective parathyroidectomy. He also had a left thyroid lobectomy because of the severe loss of blood in his left lobe. He began having cardiac problems as a result of the surgery and became very agitated. Even five days after being released from the hospital he was unable to remember what had happened to him. Aside from memory impairment, none of his other cognitive processes seemed to be affected. He did not want to be involved in much research, but through memory tests he took with doctors, they were able to ascertain that his memory problems were present for the next 9.5 years until his death. After he died, his brain was donated to science, photographed, and preserved for future study.
Global amnesia is a common motif in fiction despite being extraordinarily rare in reality. In the introduction to his anthology The Vintage Book of Amnesia, Jonathan Lethem writes:
Real, diagnosable amnesia – people getting knocked on the head and forgetting their names – is mostly just a rumor in the world. It's a rare condition, and usually a brief one. In books and movies, though, versions of amnesia lurk everywhere, from episodes of Mission Impossible to metafictional and absurdist masterpieces, with dozens of stops in between. Amnesiacs might not much exist, but amnesiac characters stumble everywhere through comic books, movies, and our dreams. We've all met them and been them.
Lethem traces the roots of literary amnesia to Franz Kafka and Samuel Beckett, among others, fueled in large part by the seeping into popular culture of the work of Sigmund Freud, which also strongly influenced genre films such as film noir. Amnesia is so often used as a plot device in films, that a widely recognized stereotypical dialogue has even developed around it, with the victim melodramatically asking "Where am I? Who am I? What am I?", or sometimes inquiring of their own name, "Bill? Who's Bill?"
In movies and television, particularly sitcoms and soap operas, it is often depicted that a second blow to the head, similar to the first one which caused the amnesia, will then cure it. In reality, however, repeat concussions may cause cumulative deficits including cognitive problems, and in extremely rare cases may even cause deadly swelling of the brain associated with second-impact syndrome.
In science fiction involving a masquerade that hides magical or alien societies from humanity, such as Men in Black or the SCP Foundation, fictional organizations can induce deliberate amnesia via drugs or advanced technology to wipe the minds of those that view supernatural phenomena.