Where is Schellenberg?

Schellenberg is a municipality in the lowland area of Liechtenstein, on the banks of the Rhine., it has a population of 1,090 and covers an area of.

Schellenberg

The area was first settled by Celts, then by Rhaetians. Rome conquered the area in 15 BC, and made it part of the province of Rhaetia. The Province later became a county (countship) under Charlemagne. The county was repeatedly divided among heirs.

The Lordship of Schellenberg was purchased by the Counts of Vaduz in 1437 and the two states have been united in fact ever since. After the Swabian War in 1499, both came under Austrian suzerainty. Different dynasties of counts bought and sold them, until their purchase in the early 18th century by the Liechtenstein dynasty, which had been granted princely status in 1706, but which needed to acquire a territory with imperial immediacy in order to vote in the Diet of the Princes of the Empire. The emperor formally united Vaduz and Schellenberg in 1719 as the Principality of Liechtenstein.

The Russian Monument in the municipality commemorates the asylum given to Russian soldiers during the Second World War. Near the end of World War II, Liechtenstein granted asylum to approximately five hundred soldiers of the First Russian National Army, a collaborationist Russian force within the German Wehrmacht. This act was no small matter, as the country was poor and had difficulty feeding and caring for such a large group of refugees. Eventually, Argentina agreed to resettle the asylum seekers permanently. In contrast, the British repatriated the Russians who fought on the German side to the USSR.

Schellenberg territory borders with the Liechtensteiner municipalities of Eschen, Gamprin, Mauren and Ruggell. It borders also with the Austrian municipality of Feldkirch, in the federal state of Vorarlberg.

In Schellenberg there is a small road crossing to Austria, manned by Austrian and Swiss border guards.

Schellenberg


How long can amnesia last?

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

Retrograde amnesia (RA) is a loss of memory-access to events that occurred, or information that was learned, before an injury or the onset of a disease. It tends to negatively affect episodic, autobiographical, and declarative memory while usually keeping procedural memory intact with no difficulty for learning new knowledge. RA can be temporally graded or more permanent based on the severity of its cause and is usually consistent with Ribot's law: where subjects are more likely to lose memories closer to the traumatic incident than more remote memories. The type of information that is forgotten can be very specific, like a single event, or more general, resembling generic amnesia. It is not to be confused with anterograde amnesia, which deals with the inability to form new memories following the onset of an injury or disease.
The most commonly affected areas are associated with episodic and declarative memory such as the hippocampus, the diencephalon, and the temporal lobes.

Brain plasticity has helped explain the recovery process of brain damage induced retrograde amnesia, where neuro-structures use different neural pathways to avoid the damaged areas while still performing their tasks. Thus, the brain can learn to be independent of the impaired hippocampus, but only to a certain extent.
For example, older memories are consolidated over time and in various structures of the brain, including Wernicke's area and the neocortex, making retrieval through alternate pathways possible.

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).

In temporally graded retrograde amnesia, victims eventually recover most memories following the onset of RA. This suggests that the hippocampal formation is only used in systematic consolidation for temporary, and short periods of time, until long-term consolidation takes place in other brain structures. Here, the fact that damage to the hippocampal formation can eventually overcome RA suggests that other brain structures are able to take over the jobs of the malfunctioning regions. RA can also progress and further deteriorate memory recollection, as in the case of Korsakoff syndrome and Alzheimer's disease, due to the ongoing nature of the damage caused by the illnesses. The degree to which different patients recover from RA differs in time (some take a few days while others a few decades) and content (some will only remember certain specific instances while others more).

These terms are used to describe a pure form of RA, with an absence of anterograde amnesia (AA). In addition, Focal RA in particular, has also been used to describe a RA situation in which there is a lack of observable physical deficit as well. This could be described as a psychogenic form of amnesia with mild anterograde and retrograde loss. A case study of DH revealed that the patient was unable to provide personal or public information, however there was no parahippocampal or entorhinal damage found. Individuals with focal brain damage have minimal RA.

Isolated RA is associated with a visible thalamic lesion. Consistent with other forms of RA, the isolated form is marked by a profound inability to recall past information.

Pure retrograde amnesia (PRA) refers to the behavioral syndrome that is characterized by the inability to retrieve remote information in the face of a normal ability to learn new information, with no other ecological or psychometric evidence of cognitive impairment. It should not be confused with the brief periods of peritraumatic amnesia that are common in mild concussive head traumas. The findings of pure retrograde amnesia have helped form the dissociation between mechanisms for RA and AA. Several studies have found numerous causes for PRA like vascular diseases, head traumas ranging from mild to severe, encephalitis, as well as purely psychological conditions and totally unidentifiable aetiologies. Most people who suffer from PRA can function normally and learn new information and therefore are not severely set back in life. [57] (Lucchelli, Muggia, & Spinnler, 1998).

A pure form of RA is rare as most cases of RA co-occur with AA. A famous example is that of patient ML. The patient's MRI revealed damage to the right ventral frontal cortex and underlying white matter, including the uncinate fasciculus, a band of fibres previously thought to mediate retrieval of specific events from one's personal past.

The causal explanation of retrograde amnesia is still under investigation.

The three main models used to explain RA assume that the hippocampus is one of the main areas of the brain used in memory consolidation. During consolidation, the hippocampus acts as an intermediate tool that quickly stores new information until it is transferred to the neocortex for the long-term. The temporal lobe, which holds the hippocampus, entorhinal, perirhinal and parahippocampal cortices, has a reciprocal connection with the neocortex. The temporal lobe is temporarily needed when consolidating new information; as the learning becomes stronger, the neocortex becomes more independent of the temporal lobe.

The common studied causes of RA do not always lead to the onset of RA. It may even be that in some cases both conscious feigning and unconscious processes are at play.

Traumatic brain injury (TBI), also known as post-traumatic amnesia, occurs from an external force that causes structural damage to the brain, such as a sharp blow to the head, a diffuse axonal injury, or childhood brain damage (e.g., shaken baby syndrome). In cases of sudden rapid acceleration, the brain continues moving around in the skull, harming brain tissue as it hits internal protrusions.

TBI varies according to impact of external forces, location of structural damage, and severity of damage ranging from mild to severe. Retrograde amnesia can be one of the many consequences of brain injury but it is important to note that it is not always the outcome of TBI. An example of a subgroup of people who are often exposed to TBI are individuals who are involved in high-contact sports. Research on football players takes a closer look at some of the implications to their high-contact activities. Enduring consistent head injuries can have an effect on the neural consolidation of memory.

Specific cases, such as that of patient ML, support the evidence that severe blows to the head can cause the onset of RA. In this specific case there was an onset of isolated RA following a severe head injury. The brain damage did not affect the person's ability to form new memories. Therefore, the idea that specific sections of retrograde memory are independent of anterograde is supported. Normally, there is a very gradual recovery, however, a dense period of amnesia immediately preceding the trauma usually persists.

RA can occur without any anatomical damage to the brain, lacking an observable neurobiological basis. Primarily referred to as psychogenic amnesia or psychogenic fugue, it often occurs due to a traumatic situation that individuals wish to consciously or unconsciously avoid through intrapsychic conflicts or unconscious repressions. The onset of psychogenic amnesia can be either global (i.e., individual forgets all history) or situation specific (i.e., individual is unable to retrieve memories of specific situations).

People experiencing psychogenic amnesia have impaired episodic memory, instances of wandering and traveling, and acceptance of a new identity as a result of inaccessible memories pertaining to their previous identity.

Recent research has begun to investigate the effects of stress and fear-inducing situations with the onset of RA. Long-term potentiation (LTP) is the process by which there is a signal transmission between neurons after the activation of a neuron, which has been known to play a strong role in the hippocampus in learning and memory. Common changes in the hippocampus have been found to be related to stress and induced LTP. The commonalities support the idea that variations of stress can play a role in producing new memories as well as the onset of RA for other memories. Also, the amygdala plays a crucial role in memory and can be affected by emotional stimuli, evoking RA.

Studies of specific cases, such as 'AMN', support evidence of traumatic experiences as a plausible cause of RA. AMN escaped a small fire in his house, did not inhale any smoke, and had no brain damage. Surprisingly, the next day, he was unable to recall autobiographical based knowledge. This case shows that RA can occur in the absence of structural brain damage.

After a traumatic head injury, emotional disturbances can occur at three different levels: neurological, reactionary, and long-term disturbances. Neurological disturbances can change emotional and motivational responses. Reactionary disturbances effect emotional and motivational responses as well, but they reflect failure to cope with environmental demands. Someone with this might withdraw from the environment that they are placed in because they no longer know how to handle the cognitive resources.

RA has been found among alcohol-dependent patients who suffer from Korsakoff's syndrome. Korsakoff's syndrome patients suffer from retrograde amnesia due to a thiamine deficiency (lack of vitamin B1). Also, chronic alcohol use disorders are associated with a decrease in volume of the left and right hippocampus.

These patients' regular diet consists mostly of hard alcohol intake, which lacks the necessary nutrients for healthy development and maintenance. Therefore, after a prolonged time consuming primarily alcohol, these people undergo memory difficulties and ultimately suffer from RA. However, some of the drawback of using Korsakoff patients to study RA is the progressive nature of the illness and the unknown time of onset.

Infections that pass the blood–brain barrier can cause brain damage (encephalitis), sometimes resulting in the onset of RA. In the case of patient 'SS', the infection led to focal or isolated retrograde amnesia where there was an absence of or limited AA. Brain scans show abnormalities in the bilateral medial temporal lobes, including two thirds of the hippocampal formation and the posterior part of the amygdala.

Henry Molaison suffered from epilepsy that progressed and worsened by his late twenties. The severity of his condition caused him to undergo surgery in an effort to prevent his seizures. Unfortunately, due to a lack of overall known neurological knowledge, Molaison's surgeons removed his bilateral medial temporal lobe, causing profound AA and RA. The removed brain structures included the hippocampus, the amygdala, and the parahippocampal gyrus, now called the medial temporal lobe memory system. HM was one of the most studied memory cases to date and started the examination of neurological structures in relation to memory.

Other patients who suffered RA due to surgery are 'P.B.' and 'F.C.' who had unilateral removal of the medial areas in the left temporal lobe.

Clinically induced RA has been achieved using different forms of electrical induction.

As previously mentioned, RA can affect people's memories in different degrees, but testing is required to help determine if someone is experiencing RA. Several tests exist, for example, testing for factual knowledge such as known public events. A problem with this form of testing is that people generally differ in their knowledge of such subjects. Other ways to test someone is via autobiographical knowledge using the Autobiographical Memory Interview (AMI), comprising names of relatives, personal information, and job history. This information could help determine if someone is experiencing RA and the degree of memory affected. However, due to the nature of the information being tested, it is often difficult to verify the accuracy of the memories being recalled, especially if they are from a distant past. Some researchers have found that the time interval after the head injury occurred did not seem to matter. The effect of the memory loss was the same no matter how long it had been after from the injury.

Brain abnormalities can be measured using magnetic resonance imaging (MRI), computed tomography scan (CT) and electroencephalography (EEG), which can provide detailed information about specific brain structures. In many cases, an autopsy helps identify the exact brain region affected and the extent of the damage that caused RA once the patient has died.

There are some aspects essential to the patient that remain unaffected by RA. In many patients, their personality remains the same. Also, semantic memory, that is general knowledge about the world, is usually unaffected. However, episodic memory, which refers to one's life experiences, is impaired.

Another real life problem with RA is malingering, which is conceived as the rational output of a neurologically normal brain aiming at the surreptitious achievement of a well identified gain. Since it is common for people who have committed a crime to report having RA for that specific event in order to avoid their punishment, the legal system has pushed for the creation of a standardized test of amnesia. However, since most cases differ in onset, duration, and content forgotten, this task has shown to be a rather complex one.

When someone is suffering from RA, their memory cannot be recovered from simply being told personal experiences and their identity. This is called reminder effect or reminder treatment. The reminder effect consists of re-exposing the patient to past personal information, which cannot reverse RA. Thus, reminding the patient details of their life has no scientific bearings on recovering memory. Fortunately, memory can be and usually is recovered due to spontaneous recovery and plasticity.

Since researchers are interested in examining the effects of disrupted brain areas and conducting experiments for further understanding of an unaffected, normal brain, many individuals with brain damage have volunteered to undergo countless tests to advance our scientific knowledge of the human brain. For example, Henry Molaison (HM) was someone with significant brain damage and participated in a lot of neurological research. Furthermore, he was also the most tested person in neuropsychology. All living people who participate are referred to in literature using only their initials to protect privacy.

Each case of RA has led to different symptoms and durations, where some patients have exhibited an inability to describe future plans, whether in the near future (e.g., this afternoon) or in the distant future (e.g., next summer) because of their inability to consolidate memories. Furthermore, researchers have also found that some patients can identify themselves and loved ones in photographs, but cannot determine the time or place the photo was taken. It has also been found that patients with RA greatly differ from the general population in remembering past events.

A few case examples are:

Although it may seem that people living with brain damage have great difficulty continuing the usual day-to-day aspects, they still can accomplish many feats. People with RA are able to lead a normal life. For instance, KC is a man who has many functional aspects intact; normal intelligence, unaffected perceptual and linguistic skills, short-term memory, social skills, and reasoning abilities. All of these things are necessary in everyday life and contribute to normal living. KC also is fully capable of scripted activities (e.g., making reservations or changing a flat tire).
In addition, patient HC successfully graduated high school and continued into post-secondary studies, an obvious accomplishment despite her condition. DH relearned his childhood memories from his parents and can retell the stories, but cannot recall specifics other than what has been told to him.

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.

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.

Post-traumatic amnesia (PTA) is a state of confusion that occurs immediately following a traumatic brain injury in which the injured person is disoriented and unable to remember events that occur after the injury.

Psychogenic amnesia, or dissociative amnesia, is a memory disorder characterized by sudden retrograde autobiographical memory loss, said to occur for a period of time ranging from hours to years.

Researchers have investigated the relationship between posttraumatic amnesia (PTA) resulting from traumatic brain injury (TBI) and the development of symptoms of posttraumatic stress disorder (PTSD) and acute stress disorder (ASD). 282 outpatients, who were an average of 53 days post-TBI in their recovery, were divided into four groups: PTA episode lasting less than one hour; PTA episode lasting between one hour and 24 hours; PTA episode lasting between 24 hours and one week; and PTA episode lasting for longer than one week. The patients' personal details were used as variables classified for age, gender, marital status, time elapsed between injury and assessment, and type of injury (motor vehicle accident, pedestrian, assault and other). Patients were given two self-report inventories: the Impact of Event Scale (IES) and the General Health Questionnaire (GHQ). The IES measures symptoms of PTSD and contains questions regarding the intrusiveness of the traumatic event (ex. nightmares) and avoidant behaviours related to the traumatic event (ex. avoiding a certain location). The GHQ was used as an indicator of overall psychological health. The majority of subjects were in Group 1 (PTA episode lasting less than one hour), injured in motor vehicle accidents, and male.

Post-traumatic amnesia

Post-traumatic amnesia (PTA) is a state of confusion that occurs immediately following a traumatic brain injury (TBI) in which the injured person is disoriented and unable to remember events that occur after the injury. The person may be unable to state their name, where they are, and what time it is. When continuous memory returns, PTA is considered to have resolved. While PTA lasts, new events cannot be stored in the memory. About a third of patients with mild head injury are reported to have "islands of memory", in which the patient can recall only some events. During PTA, the patient's consciousness is "clouded". Because PTA involves confusion in addition to the memory loss typical of amnesia, the term ""post-traumatic confusional state"" has been proposed as an alternative.

There are two types of amnesia: retrograde amnesia (loss of memories that were formed shortly before the injury) and anterograde amnesia (problems with creating new memories after the injury has taken place). Both retrograde and anterograde forms may be referred to as PTA, or the term may be used to refer only to anterograde amnesia.

A common example in sports concussion is the quarterback who was able to conduct the complicated mental tasks of leading a football team after a concussion, but has no recollection the next day of the part of the game that took place after the injury. Retrograde amnesia sufferers may partially regain memory later, but memories are not regained with anterograde amnesia because they were not encoded properly.

The term "post-traumatic amnesia" was first used in 1940 in a paper by Symonds to refer to the period between the injury and the return of full, continuous memory, including any time during which the patient was unconscious.

The most prominent symptom of post-traumatic amnesia (PTA) is a loss of memory of the present time. As a result, patients are often unaware of their condition and may behave as if they are going about their regular lives. This can cause complications if patients are confined to a hospital and may lead to agitation, distress and anxiety. Many patients report feeling as though they were being "held prisoner" and being prevented from carrying on with their daily lives. Other symptoms include agitation, confusion, disorientation, and restlessness.

Patients also often display behavioral disturbances. Patients may shout, swear and behave in a disinhibited fashion. There have been cases in which patients who do not recognize anyone will ask for family members or acquaintances that they have not seen in years. Some patients exhibit childlike behavior. Other patients show uncharacteristically quiet, friendly and loving behavior. Although this behavior may seem less threatening because of its lack of aggressiveness, it may be equally worrisome.

PTA patients are often unaware of their surroundings and will ask questions repeatedly. Patients may also have a tendency to wander off, which can be a major concern in those who have suffered additional injuries at the time of trauma, such as injured limbs, as it may lead to the worsening of these secondary injuries.

Attention is a cognitive resource that contributes to many mental functions. The ability to engage attention requires a certain level of conscious awareness, arousal and concentration, all mechanisms that are generally impaired by traumatic brain injury. The involvement of attention in such a vast array of cognitive processes has led to the suggestion that attentional deficit may act as an underlying factor in the range of cognitive deficits observed in patients experiencing post-traumatic amnesia (PTA).

Attention has been regarded as an important factor in the healthy functioning of encoding, verbal comprehension and new learning. Automatic attention processes (such as counting forwards) are recovered before simple memory skills (such as a recognition test of verbal material) in individuals with mild to moderate brain injury. This implies that the recovery of attentional ability precedes the progression of memory recovery after injury, helping to pave the way to regain ability for new learning. In terms of more severe brain injuries, this automatic attention task performance recovers before disorientation completely resolves.

One of the weaknesses of the method most often used in assessing PTA, the Galveston Orientation and Amnesia Test (GOAT), is that it does not include any assessment of attention, which could help give a better indication of potential for recovery. By omitting attention, the test is omitting some crucial aspects of a person's cognitive capabilities.

In addition, assessing attention during the period of PTA may help determine whether the patient is still in a state of PTA or if they are suffering from a more permanent form of memory deficit. In patients with mild TBI, the damage consists primarily of diffuse axonal injury (widespread damage to white matter) without any focal damage (damage to specific areas). Sometimes, injury of the brainstem was also observed. In these cases, there is likely the presence of an attentional deficit without a true amnesiac state. In more severely brain-damaged individuals, the damage to the temporal lobes and the frontal lobes serves as good indication that amnesia will result. Patients suffering from more chronic forms of memory impairment showed poor performance when tested with PTA scales, making differentiation between the two types of memory impairment very difficult. PTA patients exhibit poor simple reaction time, reduced information processing speed and reduced verbal fluency, which are all attentional deficits that could be used to distinguish these patients from those suffering from more severe and permanent memory problems.

The effects of PTA on communication skills were studied using the Revised Edinburgh Functional Communication Profile (REFCP), which measures both linguistic elements (related to speech) and pragmatic elements (related to body language and other non-verbal communication skills). PTA has effects on memory, perception and attention, which are all important for communication. Patients showed mild deficits in verbal communication skills, and moderate to severe deficits in nonverbal communication skills such as maintaining eye contact, initiating greetings, and responding appropriately. Also, a negative correlation was found between the duration of a patient's episode of PTA and his REFCP score; the longer the PTA episode, the more severe the deficit in non-linguistic pragmatic skills. However, the small sample size of this study (only 10 males) means that the results must be interpreted with caution, as they may not generalize to larger samples or to the population at large.
Pathophysiology is the study of the changes to an individual's normal physical, biological, and mental functions as a result of disease, injury, or other damage. Currently, the pathophysiological mechanisms which produce post-traumatic amnesia are not completely known. The most common research strategy to clarify these mechanisms is the examination of the impaired functional capabilities of people with post-traumatic amnesia (PTA) after a traumatic brain injury.

Research on the effect of emotional trauma on memory retention and amnesic symptoms has shown that exposure to prolonged levels of extreme stress has a direct effect on the hippocampus. Elevated stress levels can lead to an increase in the production of enkephalins and corticosteroids, which can produce abnormal neural activity and disrupt long-term potentiation (a neural mechanism associated with learning) in the hippocampus. Individuals who have been subjected to repeated sexual abuse during childhood or who have experienced combat show significant impairment and atrophy of the hippocampal region of the brain. The amygdala, an area of the brain involved in emotional regulation, may be involved in producing remembrance for some aspects of the trauma. Even though the trace of a memory for trauma may be lost from the hippocampus, it may remain partially encoded in the form of an emotional memory in the amygdala where it can be subsequently recalled in the form of a flashback or partially recovered memory.

Diaschisis refers to the sudden dysfunction of portions of the brain due to lesions in distant but connected neurons. Diaschisis is implicated as playing an important role in PTA, more particularly in the declarative memory impairments observed in patients experiencing an episode of PTA. The loss of function observed after traumatic brain injuries, as well as the resulting loss of consciousness, was thought to be mediated by the 'neural shock' associated with diaschisis.

Diaschisis was originally believed to be a result of disruption to neural tissue, but more recent evidence implicates increased activity levels of choline acetyltransferase, the enzyme responsible for the production of acetylcholine, as a major cause. Based on these findings, diaschisis could be helped through the use of drugs that would reduce cholinergic (acetylcholine) activity, and reduce the levels of acetylcholine in the brain. This idea is supported by the fact that there is an increase in acetylcholine concentrations in the brain after head injury. Animal studies have shown that concussive injuries in rats lead to changes in the central nervous system's cholinergic system. This increase in acetylcholine levels has also been tied to behavioral suppression and unconsciousness, both symptoms of PTA. In long-term recovery, acetylcholine levels associated with diaschisis may continue to play a role in maintaining memory deficits.

Brain imaging techniques are useful for examining the changes in the brain that occur as a result of damage. Metting et al. (2001) used CT scans to examine the pathophyiological damage in patients currently experiencing an episode of PTA, patients with resolved PTA, and a control group that had not experienced PTA. Bloodflow to the occipital lobe, the caudate nucleus, and the grey matter of the frontal lobe was significantly reduced in patients who were scanned during the episode of PTA. No differences were seen between patients with resolved PTA and the control group. This encouraging finding points to the positive long term prognosis of PTA; most patients return to normal levels of functioning. The frontal lobes are associated with explicit memory retrieval, and deficits on explicit memory tasks are often found with patients experiencing PTA.

Working memory deficits are a common symptom in patients with PTA. The duration of an episode of PTA was correlated with reduced bloodflow to the right hemisphere, a finding which was consistent with functional MRI studies that link working memory with right frontal activity. The prefrontal cortex, which plays an important role in explicit memory retrieval, was also found to have decreased neural activation in patients scanned during the episode of PTA. Researchers noted that the damage was related to vascularization and neural functionality, but not to structural injury, suggesting that the resolution of PTA is dependent on functional changes.

Memory and new learning involve the cerebral cortex, the subcortical projections, the hippocampus, the diencephalon and the thalamus, areas that often suffer damage as a result of TBI. Frontal lobe lesions may also play a role in PTA, as damage to these areas is associated with changes in behavior, including irritability, aggressiveness, disinhibition, and a loss of judgment. Damage to this area may account for the uncharacteristic behavior often exhibited in PTA patients.

Researchers have also found that individuals experiencing PTA show accelerated forgetting. This contrasts with the normal forgetting observed by patients with normal amnesia related to brain damage. The temporal lobes are often the most vulnerable to the diffuse (widely distributed) and focal (more specifically localized) effects of TBI and it is possible that temporal lobe lesions may account for the accelerated forgetting observed in patients with PTA. These predictions were supported by the finding that most of the patients who showed rapid forgetting also had lesions to the temporal lobe. Bilateral damage to the temporal lobes also causes severe anterograde amnesia, making it likely that lesions to this area would be involved in PTA. Patients exhibit a temporal gradient with memory loss, meaning that older memories are preserved at the expense of newer memories. Temporal lobe damage has been linked to a temporal gradient of this sort, because older memories are less dependent on the hippocampus and thus are less influenced by its damage.

There is a significant link between individuals currently suffering from PTA and their performance on the Wechsler Adult Intelligence Scale (WAIS). The scores of those currently experiencing an episode of PTA were compared to individuals who had previously suffered a traumatic brain injury resulting in PTA. Those still suffering from PTA performed significantly worse on both the performance and the verbal subscales of the WAIS. Also, people in early stages of PTA have substantial impairment to anterograde memory function. For example, in the case report of a patient referred to as "JL", Demery et al. noted that his memory impairments were so severe following his injury that he had forgotten that he had attended a Major League Baseball game less than 30 minutes after returning to the center where he was being treated.

The majority of neuropsychological studies available have suggested that the medial temporal lobes are the most important system in the pathophysiology of PTA. However, there is little research done on this topic, and as new research is done, more information should come forth concerning functionality in these areas in PTA patients. One MRI study showed that a long duration of PTA was correlated with damage in the hemispheric and central areas, regardless of whether the duration of the coma was relatively short. In patients who had a longer coma duration, deeper lesions in the central area were observed without extensive damage to the hemispheric area.

PTA has been proposed to be the best measure of head trauma severity, but it may not be a reliable indicator of outcome.
However, PTA duration may be linked to the likelihood that psychiatric and behavioral problems will occur as consequences of TBI.

Classification systems for determining the severity of TBI may use duration of PTA alone or with other factors such as Glasgow Coma Scale (GCS) score and duration of loss of consciousness (LOC) to divide TBI into categories of mild, moderate, and severe. One common system using all three factors and one using PTA alone are shown in the tables at right. Duration of PTA usually correlates well with GCS and usually lasts about four times longer than unconsciousness.

PTA is considered a hallmark of concussion, and is used as a measure of predicting its severity, for example in concussion grading scales. It may be more reliable for determining severity of concussion than GCS because the latter may not be sensitive enough; concussion sufferers often quickly regain a GCS score of 15.

Longer periods of amnesia or loss of consciousness immediately after the injury may indicate longer recovery times from residual symptoms from concussion.
Increased duration of PTA is associated with a heightened risk for TBI complications such as post-traumatic epilepsy.

Duration of PTA may be difficult to gauge accurately; it may be overestimated (for example, if the patient is asleep or under the influence of drugs or alcohol for part of the time) or underestimated (for example, if some memories come back before continuous memory is regained). The Galveston Orientation and Amnesia Test (GOAT) exists to determine how oriented a patient is and how much material they are able to recall.
The GOAT is the most widely used standardized scale for the prospective assessment of PTA in the United States and Canada. The test is made up of 10 items that assess orientation and recollection of the events before and after the injury. It can be used to assess the duration of PTA; this particular GOAT assessment has been found to strongly predict functional outcome as measured by the Glasgow Outcome Scale, return to productivity, psychosocial function and distress.

An alternative to the GOAT is the Westmead Post-Traumatic Amnesia Scale (WPTAS) which examines not only orientation to person, place and time, but also crucially the ability to consistently remember new information from one day to the next. It consists of twelve questions (seven orientation questions, and five memory items) and is administered once daily, each and every day, until the patient scores a perfect score of 12/12 on three "consecutive" days. It is suitable for patients with moderate to severe traumatic brain injury. The WPTAS is the most common post-traumatic amnesia scale used in Australia and New Zealand. An abbreviated version has been developed to assess patients with mild traumatic brain injury, the Abbreviated Westmead PTA Scale (AWPTAS).

Before the development of the current tests for the assessment of post-traumatic amnesia (PTA), a retrospective method was used to determine the patient's condition, consisting of one or more interviews with the patient after the episode of PTA was judged to be over. The retrospective method, however, fails to account for the apparent lucidity of patients who are still experiencing substantial disorientation, or the finding that the recovery from post-traumatic amnesia is often characterized by the presence of "islands of memory" (short periods of clarity). A failure to take these facts into consideration may have biased retrospective methods towards underestimating the length and severity of an episode of PTA. Also, the retrospective method relies on retrospective memory, one's memory for past events, which is not very reliable in healthy individuals, and even less so in patients who have recently experienced a traumatic brain injury (TBI). Patients may also unconsciously or consciously bias their answers because they want to appear more healthy or more ill than they truly were, or because of poor insight. The retrospective method is also flawed because there is no standard measurement procedure. Although the retrospective method may provide useful subjective data, it is not a useful tool for measurement or categorization.

The Galveston Orientation and Amnesia Test (GOAT) is the most frequently used test for assessing PTA in the United States and Canada. The test consists of 10 items that involve the recall of events that occurred right before and after the injury, as well as questions about disorientation. Scores of 75 or more on this scale (out of a total possible score of 100) correspond to the termination of the PTA episode. The GOAT typically classifies orientation into three categories: orientation to the person, orientation to the place, and orientation to the time. The idea behind these questions is that each of these classifications places a large demand on the patient's memory and learning abilities.

The Westmead Post-Traumatic Amnesia Scale (WPTAS) is commonly used in Australia and New Zealand. It questions twelve questions that examine orientation to person, place and time, in addition to the ability to consistently remember new information from one day to the next. The scale is administered once each day, until the patient scores 12/12 on three consecutive days. The WPTAS is suitable for patients with moderate-to-severe traumatic brain injury. An abbreviated version of the WPTAS, the Abbreviated Westmead PTA Scale (AWPTAS) assesses patients with mild traumatic brain injury.

Although the GOAT has proved useful in acute care, recent research has called attention to some of its drawbacks. The GOAT's assessment of orientation may put too much of a focus on memory as the main mechanism behind orientation. The range of cognitive and behavioral symptoms associated with PTA seems to indicate that the patient's disorientation is more than just a memory deficit. Consequently, it may be beneficial to incorporate tests of other cognitive functions, such as attention, which relate to both memory and orientation.

Another recent study compared the success of the GOAT and the Orientation Log (O-Log) in predicting rehabilitation outcomes, and found that, while the O-Log and the GOAT perform similarly as measures of PTA severity and duration, the O-Log provides a more accurate picture of rehabilitation.

While the GOAT is a useful tool, these results suggest that using alternative methods of assessing PTA may increase the amount of information available to physicians and may help in predicting rehabilitative success. The international cognitive (INCOG) expert panel has recommended the use of a validated PTA scale such as the GOAT or WPTAS for assessing PTA duration in patients with moderate-to-severe traumatic brain injury on a daily basis.

The severity of post-traumatic amnesia (PTA) is directly related to its duration, although a longer duration does not necessarily indicate more severe symptoms. The duration of PTA in brain-injured patients is a useful predictor of the expected long-term effects of the injury, along with the duration of loss of consciousness(LOC), and scores on the Glasgow Coma Scale (GCS), which measures degrees of consciousness, with higher scores indicating higher levels of functioning. A score of three indicates complete unconsciousness, and a score of 15 indicates normal functioning.
In patients experiencing PTA for the duration of:

Up to one hour – the injury is very mild in severity and full recovery is expected. The patient may experience a few minor post-concussive symptoms (e.g. headaches, dizziness).

1–24 hours – the injury is moderate in severity and full recovery is expected. The patient may experience some minor post-concussive symptoms (e.g. headaches, dizziness).

1–7 days – the injury is severe, and recovery may take weeks to months. The patient may be able to return to work, but may be less capable than before the injury.

1–2 weeks – the injury is very severe, and recovery is likely to take many months. The patient is likely to experience long-lasting cognitive effects such as decreased verbal and nonverbal intelligence as well as decreased performance on visual tests. Patients should, however, still be able to return to work.

2–12 weeks – the injury is very severe, and recovery is likely to take a year or more. The patient is likely to exhibit permanent deficits in memory and cognitive function, and the patient is unlikely to be able to return to work.

12+ weeks – injury is very severe and accompanied by significant disabilities that will require long-term rehabilitation and management. The patient is unlikely to be able to return to work.

Note: return to work is meant to indicate a return to a reasonable level of functionality, both in professional and personal arenas.

The long-term prognosis of PTA is generally positive. Many patients do recover a great deal of cognitive function, although they may not return to their pre-injury state.

Early research pointed to vasopressin as a potential treatment for improving the memory of patients living with post-traumatic amnesia (PTA). Lysine vasopressin, a modified form of the vasopressin molecule, had positive effects on memory when administered by injection to patients with amnesia resulting from traumatic brain injury and Korsakoff's syndrome. Subsequent animal studies with rats found similar results, particularly in aversion and avoidance learning tasks. Rats lacking adequate vasopressin, either due to genetic defect or hypophysectomy (surgical removal of the pituitary gland), exhibited significant improvements in memory and learning functions when exogenous vasopressin was administered. Particularly encouraging was the finding that a short treatment period produced long-lasting improvements, in both humans and rats. However, the animal models of PTA are highly limited, as the dimension of self-awareness and orientation is almost impossible to model adequately. PTA in animals, especially rats, is often observed post-trauma (commonly post-surgery), but it is often only measured in terms of impaired learning or unusual behavior.

One subsequent human study found no effects of vasopressin on memory. The nonsignificant results were attributed to the study's many potential flaws, particularly its small sample size, the inability of vasopressin to penetrate the blood brain barrier when administered as a nasal spray, inadequate dosing and differences in severity of head injury between the samples. However, Eames et al. (1999) found statistically significant improvements on several tests of memory with the use of a vasopressin nasal spray, with no reported ill effects. Although the degree of improvement was mild, and it could be attributed to numerous other factors of the rehabilitative program, the lack of any ill effects suggests that vasopressin is, at the least, a possible enhancement for a treatment regimen.

Diaschisis, as mentioned earlier, has been linked to the mechanism of PTA. The noradrenergic systems may play a role in diaschisis. Norepinephrine, also known as noradrenalin, is a catecholamine neurotransmitter. Administering a norepinephrine receptor agonist (a substance that initiates a cell response when it binds with a receptor) to patients promoted the recovery of memory and many other cognitive functions after a traumatic brain injury. Conversely, the administration of norpinephrine antagonists slowed recovery, and could lead to the reinstatement of deficits when administered after recovery. Noradrenergic antagonists were not prescribed for the purposes of slowing the recovery of memory. Rather, these findings are based on the effects of other commonly prescribed drugs that happen to block noradrenergic receptors. The alpha-1 adrenergic receptor is specifically implicated. Although it has not yet been thoroughly investigated, there is potential for stimulants, which promote catecholamine release, to be an effective treatment in the early stages of recovery from brain trauma, and these positive effects could reduce the symptoms of PTA.

The North Star Project was developed by researchers at McGill University. Researchers developed a "reality orientation", which involved discussing general facts (e.g. date, time, names of family members, etc.) with amnesic patients twice a day in an attempt to lessen their confusion during the early stages of their recovery. Younger patients often had shorter amnesic episodes than older patients, especially those in the North Star group. Although more improvements were noted in the North Star group than in the control group, researchers did not find a statistically significant effect of their intervention.

A comprehensive analysis of literature based on the effects of early rehabilitation of traumatic brain injury concluded that there is no strong evidence linking any one particular practice of post-injury care to a reduced severity in symptoms. However, even in the absence of a concrete correlation between a specific rehabilitation program and improved outcomes, the evidence and research available can provide many good suggestions for how to proceed with treatment. All rehabilitation strategies reviewed had positive effects on recovery, but none more so than the others.

The most accurate measure of determining the length of amnesia is still the a behavioural measure, the duration of the episode of post-traumatic amnesia, rather than a neuroimaging technique or an electrophysiological or biochemical technique. The length of amnesia is also one of the most accurate predictors for determining later cognitive problems, even more so than the duration of either the coma or the period of loss of consciousness. The duration of amnesia after TBI, therefore, can be very useful in the planning the length and intensity of rehabilitation programs for persons afflicted with PTA.

Although Franklin described PTA, it was the British physician C. P. Symonds who first discussed the specific amnesiac symptoms that often follow a cerebral contusion, which is a specific kind of traumatic brain injury. Symonds observed that the patient remains "stuperose, restless and irritable" after recovering consciousness. He also identified a recovery period of days to weeks for this post-concussive state. Presumably, shorter durations of PTA, which are now included in the definition, were not thought to be serious enough for documentation. Most importantly, he identified the amnesia that the patient experiences during this period of recovery, and recommended the use of "formal tests for memory and retention" to assess recovery.

Although there was a general lack of knowledge about its mechanisms, a review of patients seen during WWI combat reveals the symptoms of post-traumatic amnesia (PTA) in many soldiers. The term shell shock was used to refer to the acute psychological state that accompanied exposure to exploding shells, and more generally, exposure to combat conditions. There are a number of documented cases of shell shock victims. These soldiers commonly displayed dizziness, varying degrees of consciousness, a loss of non-traumatic personal information, and a lack of normal self-awareness lasting anywhere from hours to days. Many of the symptoms of shell shock are highly similar to those of PTA. The following excerpt from a case report illustrates the loss of personal information observed in one patient:
Researchers found that physicians had documented reports of combatants where "[b]oth central and peripheral details of the traumatic experience were lost." Patients displayed gaps in memory recollection for the period following the trauma, sometimes up to the time of hospitalization, which could be weeks later.

An initial assessment supported the role of concussions in causing these symptoms. Concussions could account for the anterograde amnesia and retrograde amnesia observed in patients, as well as the periods of fluctuating consciousness or delirium that sometimes followed. However, many soldiers who showed these amnesiac effects did not suffer injuries that would have led to concussions. As a result, there was controversy over the possible causes of PTA in these non-concussed soldiers, with a separation between proponents of Freudian repression and those supporting a dissociative view of the condition. This dissociative view was ultimately supported, and accounted for the fugue state seen in soldiers who were thought to have dissociated from normal consciousness.

There were no statistical differences found with regards to age, gender, marital status and type of injury. There was an increase in the severity of all indicators of brain damage for the longest durations of PTA; specifically, the GCS scores for this group decreased and the number of patients with an abnormal CT scan increased. There were significant differences in IES scores when comparing the group with the least serious episode of PTA, lasting less than an hour, to all other groups, with the duration of the episode of PTA lasting longer than an hour. The group with an episode of PTA lasting less than an hour had higher IES scores and more intrusive and avoidant symptoms. The fact that GHQ scores were constant throughout all groups, although there were differences in IES scores, suggests that the two scores measure different phenomena.

Grey and white matter are both found in the many areas of the brain, as well as throughout the central nervous system. Grey matter is more involved in nerve function, and white matter is more involved in nerve maintenance, as well as the regulation of unconscious functions. However, both are important for memory and learning. The volume of grey and white matter in the brains of aging individuals has been correlated with working memory and retention of cognitive function. Researchers hypothesized that the lesions of both grey and white matter would be larger in older individuals and in those with more severe traumatic brain injuries, and longer episodes of PTA, and the volume of grey and white matter would be smaller in those injured at an older age. A group of 98 participants, predominantly male, were examined using fMRI. The results supported these hypotheses, leading researchers to suggest that the impact of traumatic brain injury gets more severe as age progresses.

Although grey and white matter volume was reduced throughout the brain, researchers noted that the grey matter of the neocortical brain regions was particularly affected. This is consistent with the fact that older individuals who had experienced PTA showed greater cognitive impairments than a control group of individuals of the same age who had not experienced PTA. The duration of the episode of PTA was related to the size of the grey matter lesion; longer episodes of PTA correlated with larger grey matter lesions. Advanced age also correlated with reduced glial activity. With less grey matter, the patient is less able to retrieve memories effectively, as neuron function is impaired.

On the topic of trauma and memory, Richard McNally (2005) wrote that memories are not videotapes of our experiences, meaning that they are not unchangeable records. The mechanism that retrieves a memory involves activation of several areas of the brain. Similarly, the mechanism that encodes a memory requires the use of different parts of the brain. Any fault in the encoding-retrieval system will degrade memory, and there are many potential faults, such as distortion by emotion, or focusing on the peripheral details at the expense of central details. An example of the latter is the well-known phenomenon where a person being robbed at gunpoint is so distracted by the gun that they don't have time to encode the robber's face.

Misconstruing retrieval failure as traumatic amnesia is not the same phenomenon as post-traumatic amnesia, which describes amnesia for the current elapsing time post-trauma, not amnesia for trauma from the past. Typically, "repressed memory" is the term used to explain this sort of traumatic amnesia; the experience was so horrific that the adult cannot process what occurred years before. The topic of repressed memory is controversial within psychology; many clinicians argue for its importance, while researchers remain skeptical of its existence. A more viable explanation for this forgetting is childhood amnesia, a phenomenon describing the fact that most children do not have recall of events in their lives before the age of three, partially due to the lack of development of cognitive elements such as language.

Amnesia is a deficit in memory caused by brain damage, disease, or psychological trauma. 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. 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 this type of amnesia cannot remember things for long periods of time. These two types are not mutually exclusive; both can occur simultaneously.

Amnesia

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 suffering 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. Patients can learn new procedural knowledge. In addition, priming (both perceptual and conceptual) can assist amnesiacs in the learning of fresh non-declarative knowledge. Amnesic patients 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 ;.

People with amnesia can learn new information, particularly non-declarative knowledge. However, some people with dense anterograde amnesia do not remember the episodes during which they learned or observed the information previously.

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. The reason patients could not form new episodic memories is likely because the CA1 region of the hippocampus was a lesion, and thus the hippocampus could not make connections to the cortex. After an ischemic episode following surgery, an MRI of patient R.B. showed his hippocampus to be intact except for a specific lesion restricted to the CA1 pyramidal cells.

Some retrograde and anterograde amnesics are capable of non-declarative memory, including implicit learning and procedural learning. For example, some patients show improvement on the pseudorandom sequences experiment as healthy people do. Therefore, procedural learning can proceed independently of the brain system required for declarative memory. 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. Those patients did well in the word fragment completion test.

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. However, there are a few ways to cope with memory loss if that is not the case. One of these ways 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. 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. 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 suffered from 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 was even given a list in the first place. 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.

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. This case study provided important insight to the areas of the brain that are affected in anterograde amnesia, as well as how amnesia works.

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 renal 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:

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 his 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.