Instruct: Given a question, retrieve documents that can help answer the question.
Query: How long can amnesia last?
Amnesia is a deficit in memory caused by brain damage, disease, or psychological trauma.[1] Amnesia 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.[2] 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.[3] 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 this type of amnesia cannot remember things for long periods of time. These two types are not mutually exclusive; both can occur simultaneously.
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.
Priming studies on Cochrane revealed that individuals with severe amnesia can display intact priming capabilities regardless of episodic memory damage. Priming involves initially exposing a subject to a word or image so that a memory of that word or image can be formed. This is meant to improve a subject's recall of that word or image when that word or image is shown at a later time. Cochrane additionally showed that priming effects can last for long periods of time; in one study, researchers presented Cochrane with a list of words, and after 12 months showed him the same words with letters missing. Cochrane was able to complete these fragmented words as successfully as a person with normal brain function who was shown the same list initially. This challenged the previous opinion that patients with anterograde amnesia are incapable of adding information to their declarative memory.
Another way in which older adults can avoid source amnesia is to think about the relationship between the content and context of an experience or memory. This preventative measure must be taken when information is being encoded in order to direct attention to the source and to be aware of how it relates to the content. Participants experiencing source amnesia performed at the same level of groups not at risk of source amnesia when these strategies were implicated suggesting that those who do not experience this memory deficit may integrate content and context implicitly.
RA can also be an inherent aspect of other forms of amnesia, namely transient global amnesia (TGA). TGA is the sudden onset of AA and RA caused by a traumatic event, however it is short lived, typically lasting only 4 to 8 hours. TGA is very difficult to study because of the patients' quick recovery. This form of amnesia, like AA, remains distinct from RA.
The most frequent side effects of ECT include memory impairment, headaches, and muscle aches. In some instances, ECT can produce significant and long-lasting cognitive impairment, including anterograde amnesia, and retrograde amnesia.
One’s familiarity with a task influences how selective amnesia affects the subject’s memories. To study this phenomenon, Lewis and colleagues (1969) taught rats a simple passive avoidance task, a fear-aggravated test used to evaluate learning and memory in rodent models. Some rats were allowed to familiarize themselves with the task while others were only allowed to experience the task once. After the rats had completed their task a pre-determined number of times, the experimenters administered an electroconvulsive shock to the rats meant to induce selective amnesia. These shocks varied in duration, lasting from zero to five seconds. The results of this study showed that only the rats unfamiliar with the task demonstrated selective amnesia 24 hours later. The rats that were familiar with the task seemed to display normal memory for the task. Thus, there might be a particular stage in the memory process that is vulnerable to selective amnesia. The current hypothesis is that this vulnerable stage is located during the transition from active memory to short term memory.
"Datura" intoxication typically produces delirium, hallucination, hyperthermia, tachycardia, bizarre behavior, and severe mydriasis with resultant painful photophobia that can last several days. Pronounced amnesia is another commonly reported effect. The onset of symptoms generally occurs around 30 to 60 minutes after ingesting the herb. These symptoms generally last from 24 to 48 hours, but have been reported in some cases to last as long as two weeks.
These forms of memory deficit raise issues about the nature of memories in the neuroanatomy and how conflicting observations can be reconciled with either the standard or the multiple trace models. It has been noted that "People with temporal lobe epilepsy provide a natural laboratory for the study of human memory." TEA, as a form of temporal lobe epilepsy, is of particular interest as one must consider both the loss of long-encoded memories (as long as 40 years or one's whole life) and the simultaneous failure of recently encoded but not immediately short-term memories. The issue of topographical amnesia, which would seem to involve parts of the brain not usually associated with other TEA symptoms, was referred to earlier. These are often considered different kinds of memories with distinct neuroanatomical loci, so that a model to explain both conditions with one etiology is elusive.
Sedatives can sometimes leave the patient with long-term or short-term amnesia.
Lorazepam is one such pharmacological agent that can cause anterograde amnesia. Intensive care unit patients who receive higher doses over longer periods, typically via IV drip, are more likely to experience such side effects.
As previously mentioned, RA commonly results from damage to the brain regions most closely associated with episodic and declarative memory, including autobiographical information. In extreme cases, individuals may completely forget who they are. Generally, this is a more severe type of amnesia known as global or generalized amnesia. However, memory loss can also be selective or categorical, manifested by a person's inability to remember events related to a specific incident or topic. Patients also differ in durations of RA (how long they can't recall information) and durations of what is forgotten (past time frame for which information is unavailable).
Studies on specific cases demonstrate how particular impaired areas of the hippocampus are associated with the severity of RA. Damage can be limited to the CA1 field of the hippocampus, causing very limited RA for about 1 to 2 years. More extensive damage limited to the hippocampus causes temporally graded amnesia for 15 to 25 years. Another study also suggests that large medial temporal lobe lesions, that extend laterally to include other regions, produce more extensive RA, covering 40 to 50 years. These findings suggest that density of RA becomes more severe and long-term as the damage extends beyond the hippocampus to surrounding structures.
Retrograde amnesia is typically the result of physical or psychological trauma which manifests itself as the inability to remember information preceding the traumatic event. It is usually accompanied by some type of anterograde amnesia, or inability to acquire new knowledge. Focal retrograde amnesia (FRA), sometimes known as functional amnesia, refers to the presence of retrograde amnesia while knowledge acquisition remains intact (no anterograde amnesia). Memory for how to use objects and perform skills (implicit memory) may remain intact while specific knowledge of personal events or previously learned facts (explicit memory) become inaccessible or lost. Amnesia can result from a number of different causes, including encephalitis, severe traumatic brain injury, vitamin B deficiency as seen in Korsakoff's Syndrome, and psychotic episodes, or by witnessing an emotionally traumatic event (Dissociative amnesia). Dysfunction of the temporal and frontal lobes have been observed in many cases of focal retrograde amnesia, whether metabolic or the result of lesions. However, this evidence only appears to correlate with the symptoms of retrograde amnesia as cases have been observed where patients suffering from minor concussions, showing no visible brain damage, develop FRA. It has been suggested that FRA could represent a variety of different disorders, cognitive deficits, or conditions that result in disproportionate loss of explicit memory, hence Disproportionate Retrograde Amnesia.
Amnesia can result from a side-effect of prescription or non-prescription drugs. Both substance use and alcohol can cause both long-term and short-term memory loss, resulting in blackouts.
ALF and focal retrograde amnesia after TEA offer clues as to the nature of memory consolidation.
This view of consolidation has been disputed, as it seems to suggest consolidation occurs over long spans of time, not just minutes or days, and "requires physiological changes lasting years or decades." Such long-term consolidation processes would seem to require multiple stages of consolidation, which remain hypothetical.
"A Single Thing in Common" is set in an apartment known as "the playpen" by swinging seventies types Richard Sloan, Linda Schneider, and Mike Jarvis. When Mike, a pilot, gets hired to work in Abu Dhabi, the others look for a roommate who will find their lifestyle acceptable. Soon, Richard's old friend George Caulfield shows up at the door. His wife, Joyce, has had an affair and granted him a divorce. He asks to stay until he can find somewhere else. Richard leaves with George still there, and when Linda finds him, she attacks him with a judo move, causing him to have amnesia. Although his amnesia doesn't last long once he looks through his wallet, he feigns amnesia and allows Linda, who has agreed to allow him to room there when she finds out how much money he will make in the divorce, to make him into a new person. Eventually Joyce comes back and causes him to unravel the entire plot, but for this romantic comedy, he and Linda have fallen in love and he decides he doesn't want Joyce back, even though she wants him. The published play makes no indication that it was ever performed professionally.
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.[30]
Anterograde amnesia can also be caused by alcohol intoxication, a phenomenon commonly known as a blackout. Studies show rapid rises in blood alcohol concentration over a short period of time severely impair or in some cases completely block the brain's ability to transfer short-term memories created during the period of intoxication to long-term memory for storage and later retrieval. Such rapid rises are caused by drinking large amounts of alcohol in short periods of time, especially on an empty stomach, as the dilution of alcohol by food slows the absorption of alcohol. Alcohol-related anterograde amnesia is directly related to the rate of consumption of alcohol (and is often associated with binge drinking), and not just the total amount of alcohol consumed in a drinking episode. Test subjects have been found not to experience amnesia when drinking slowly, despite being heavily intoxicated by the end of the experiment. When alcohol is consumed at a rapid rate, the point at which most healthy people's long-term memory creation starts to fail usually occurs at approximately 0.20% BAC, but can be reached as low as 0.14% BAC for inexperienced drinkers. The exact duration of these blackout periods is hard to determine, because most people fall asleep before they end. Upon reaching sobriety, usually after waking, long-term memory creation is completely restored.
During the film, medical experts opine that Bruce is suffering from a syndrome called retrograde amnesia, a form of amnesia where the sufferer cannot recall events from before the onset of the amnesia, although it remains unclear how or whether Bruce suffered a trauma which caused the amnesia.
Loss of memory (amnesia) is created by action of drugs on multiple (but specific) regions of the brain. Memories are created as either declarative or non-declarative memories in several stages (short-term, long-term, long-lasting) the strength of which is determined by the strength of connections between neurons termed synaptic plasticity. Each anesthetic produces amnesia through unique effects on memory formation at variable doses. Inhalational anesthetics will reliably produce amnesia through general suppression of the nuclei at doses below those required for loss of consciousness. Drugs like midazolam produce amnesia through different pathways by blocking the formation of long-term memories.
Anterograde amnesia is a loss of the ability to create new memories after the event that caused amnesia, leading to a partial or complete inability to recall the recent past, while long-term memories from before the event remain intact. This is in contrast to retrograde amnesia, where memories created prior to the event are lost while new memories can still be created. Both can occur together in the same patient. To a large degree, anterograde amnesia remains a mysterious ailment because the precise mechanism of storing memories is not yet well understood, although it is known that the regions involved are certain sites in the temporal cortex, especially in the hippocampus and nearby subcortical regions.
Post-hypnotic amnesia has been induced as a protective measure to help some individuals limit their recall of traumatic experiences. It can be used to limit the magnitude of post-traumatic stress disorder symptoms (vivid memories and dreams), feelings of criminal victimization, the after-math of natural disasters or the theory of UFO abductions. Suggested post-hypnotic amnesia can be induced and left for long periods of time, depending on if the amnesia is significant in reducing specific symptoms or memories, the content of the repressed material or the individual`s motivation to recall events. 
The amnesia that is associated with this syndrome is a result of the atrophy in the structures of the diencephalon (the thalamus, hypothalamus and mammillary bodies), and is similar to amnesia that is presented as a result of other cases of damage to the medial temporal lobe. It has been argued that the memory impairments can occur as a result of damage along any part of the mammillo-thalamic tract, which explains how WKS can develop in patients with damage exclusively to either the thalamus or the mammillary bodies.
Hypnotic amnesia, or forgetting under hypnosis, appears to be similar to naturally occurring clinical amnesia. However, hypnotic amnesia is distinct from naturally occurring amnesia because forgotten memories can be restored through a hypnotist’s prearranged signal. Also, hypnotic amnesia is usually incomplete, meaning that the participants do not forget everything they were instructed to forget. Due to this trait, hypnosis can be used to research selective amnesia through studies that direct attention to the targets, or erased memories, of hypnotic amnesia.
Other forms of amnesia exist and may be confused with RA. For instance, anterograde amnesia (AA) is the inability to learn new information. This describes a problem encoding, storing, or retrieving information that can be used in the future. It is important to note that these two conditions can, and often do both occur in the same patient simultaneously, but are otherwise separate forms of amnesia.