Amnesia refers to the loss of memories, including facts, information and experiences. Movies and television tend to depict amnesia as forgetting your identity, but that's not generally the case in real life.
Most people with amnesia have problems with short-term memory, so they can't retain new information. Recent memories are most likely to be lost. More-remote or deeply ingrained memories may be spared.
Isolated memory loss doesn't affect a person's intelligence, general knowledge, awareness or attention span. It also doesn't affect judgment, personality or identity. People with amnesia usually can understand written and spoken words and can learn skills such as bike riding or piano playing. They may understand they have a memory disorder.
Head injuries that cause a concussion, whether from a car accident or sports, can lead to confusion and problems remembering new information. This is especially common in the early stages of recovery. Mild head injuries typically don't cause lasting amnesia, but more-severe head injuries may cause permanent amnesia.
Another rare type of amnesia, called dissociative amnesia, stems from emotional shock or trauma. It can result from being the victim of a violent crime or experiencing other trauma. In this disorder, people may lose personal memories and information about their lives. The memory loss is usually brief.
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.
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.
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.
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.
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.
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. 041b061a72