Amnesia is a deficit in memory caused by brain damage or brain diseases,Gazzaniga, M., Ivry, R., & Mangun, G. (2009) Cognitive Neuroscience: The biology of the mind. New York: W.W. Norton & Company. but it can also be temporarily caused by the use of various sedative and hypnotic drugs. The memory can be either wholly or partially lost due to the extent of damage that is caused."Amnesia." The Gale Encyclopedia of Science. Ed. K. Lee Lerner and Brenda Wilmoth Lerner. 4th ed. Vol. 1. Detroit: Gale, 2008. 182–184. Gale Virtual Reference Library.
There are two main types of amnesia: Retrograde amnesia is the inability to remember information that was acquired before a particular date, usually the date of an accident or operation.Schacter, Daniel. L "Psychology" In some cases, the memory loss can extend back decades, while in other cases, people 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 also occur simultaneously.
In addition to retrograde and anterograde amnesia, other recognized forms include transient global amnesia, a temporary loss of memory that comes on suddenly; dissociative amnesia, which is linked to emotional stress and involves inability to recall personal experiences; childhood amnesia, referring to early life memory loss that is common across individuals; and post-traumatic amnesia, which can follow a head injury and involves confusion and memory impairment for events around the time of the trauma.
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 skills despite profound impairments in the ability to recall specific information encountered in prior learning episodes.
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Signs and symptoms 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 amount of memory loss, confusion, and difficulty recalling other people or places. People who recover often do not remember having amnesia.
Declarative information 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 who 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.
Semantic information 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.
Episodic information 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.
Non-declarative information 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. 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.
Causes 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. Head trauma is a very broad range as it deals with any kind of injury or active action toward the brain which might cause amnesia. Retrograde and anterograde amnesia is more often seen from events like this, an exact example of a cause of the two would be electroconvulsive therapy, which would cause both briefly for the receiving patient. Traumatic events are more subjective. What is traumatic is dependent on what the person finds to be traumatic. Regardless, a traumatic event is an event where something so distressing occurs that the mind chooses to forget rather than deal with the stress. A common example of amnesia that is caused by traumatic events is dissociative amnesia, which occurs when the person forgets an event that has deeply disturbed them.Myers, David G. Psychology. fifth ed. New York: Worth Publishers, 1998. N. pag. Print An example would be a person forgetting a fatal and graphic car accident involving their loved ones. Physical deficiencies are different from head trauma because physical deficiencies lean more toward passive physical issues. Examples of physical deficiencies include Alzheimer's disease, neurological paraneoplastic syndromes such as anti-NMDA receptor encephalitis, and vitamin B12 deficiency.
Among specific causes of amnesia are the following: Electroconvulsive therapy in which seizures are electrically induced in patients for therapeutic effect can have acute effects including both retrograde and anterograde amnesia.Benbow, SM (2004) "Adverse effects of ECT". In AIF Scott (ed.) The ECT Handbook, second edition. London: The Royal College of Psychiatrists, pp. 170–174. Alcohol can both cause blackouts and have deleterious effects on memory formation.
Diagnosis Types Anterograde amnesia is the inability to create new memories due to brain damage, while long-term memories from before the event remain intact. The brain damage can be caused by the effects of long-term alcoholism, certain drugs (e.g., midazolam, scopolamine), severe malnutrition, stroke, head trauma, encephalitis, surgery, Wernicke–Korsakoff syndrome, cerebrovascular events, anoxia or other trauma.Carlson, N. R. (19992000). Memory. Psychology: the science of behaviour (Canadian ed., p. 250). Scarborough, Ontario: Allyn and Bacon Canada. The two brain regions related with this condition are medial temporal lobe and medial diencephalon. Anterograde amnesia cannot be treated with pharmacological methods due to neuronal loss. However, educating patients on defining their daily routines can benefit their procedural memory. Procedural memory can be intact even when other forms of memory is not, although not always the case. Likewise, social and emotional support is critical to improving quality of life for those with anterograde amnesia. Fentanyl use by opioid users has been identified as a potential cause in a cluster of cases that occurred in Boston, Massachusetts.