What is amnesia

Amnesia is loss of memory, such as facts, information and experiences. People with amnesia can struggle to form new memories or remember recent events or experiences. People who have amnesia might also be confused and have trouble learning anything new. But most people with amnesia still remember who they are and can often remember events from their childhood.

Strictly speaking amnesia really means loss of certain memories, rather than a general loss of the ability to remember anything — something that is much rarer. The process of memory is complex and not fully understood. It seems that different areas of the brain are involved in different types of memory — which is really an information storage system rather like a filing cabinet or computer.

Amnesia is not a medical condition on its own, but a description of an experience. It is often a symptom of another condition. It is usually temporary, but can be permanent in some situations.

Amnesia can be caused by damage to areas of the brain that are vital for memory processing. Unlike a temporary episode of memory loss (transient global amnesia), amnesia can be permanent.

There’s no specific treatment for amnesia, but techniques for enhancing memory and psychological support can help people with amnesia and their families cope.

If you’re becoming increasingly forgetful, particularly if you’re over the age of 65, it may be a good idea to talk to your doctor about the early signs of dementia.

As you get older, you may find that memory loss becomes a problem. It’s normal for your memory to be affected by stress, tiredness, or certain illnesses and medications.

This can be annoying if it happens occasionally, but if it’s affecting your daily life or is worrying you or someone you know, you should seek help from your doctor.

But dementia isn’t just about memory loss. It can also affect the way you speak, think, feel and behave.

It’s also important to remember that dementia is not a natural part of ageing.

Although there is no cure for dementia at present, if it’s diagnosed in the early stages, there are ways you can slow it down and maintain mental function.

A diagnosis can help people with dementia get the right treatment and support, and help those close to them to prepare and plan for the future.

With treatment and support, many people are able to lead active, fulfilled lives.

The symptoms of dementia tend to worsen with time. In the much later stages of dementia, people will be able to do far less for themselves and may lose much of their ability to communicate.

Types of amnesia

Childhood amnesia

Childhood amnesia is defined operationally as the forgetting of early life events to a significantly greater degree than is accounted for by “normal” forgetting, which is an increasing recall decrement as time since occurrence increases ¹. The relative paucity of memories from early in life experienced by adults—so-called, childhood amnesia—has been a phenomenon of substantial interest at least since its identification in the late 19th century  and naming in the early 20th century ². Among adults, the average age of earliest memory typically is age 3 to 4 years. There is a gradually increasing number of memories from the ages of 3½ to 7 years, at which time an adult-like distribution of autobiographical memories is assumed ³. Specifically, children 5, 6, and 7 years of age remembered a substantial percentage of events from the age of 3 years. In contrast, children 8 to 9 years of age had lost access to many of their memories of events from the same early age. In addition, in their narrative descriptions of the early-life events, children in the younger age groups provided less total content (5-year-olds only) and less complete narratives (5- and 6-year-olds) relative to children in the older age groups (8- and 9-year-olds). On most measures, children 7 years of age did not differ from either the younger or the older children. These findings are consistent with Wetzler and Sweeney’s ³ designation of age 7 years as the “inflection point” in childhood amnesia, that is, the point in development at which the adult distribution of autobiographical memories begins to take shape.

It is noteworthy that the patterns of remembering and forgetting of early-life events and of narrative completeness were in opposite directions. That is, younger children remembered more of their early-life events than older children, yet their narratives about the events generally were less complete than those of the older children. Among the 5- and 6-year-olds, narratives about early-life events were relatively sparse, typically featuring fewer than half of the categories that make for a “good” narrative account. One of the most salient omissions was information about why events happened as they did. Information that located the events in particular place and time also was relatively rare, as was evaluative information. In contrast, 8- and 9-year-olds remembered fewer early-life events, yet their narratives averaged more than 5 of the 8 categories that make for a good narrative account. They routinely featured the “basics” of who did what to whom and also information that located the events in time and place. Importantly, they also took perspective on the events by providing evaluative information about them.

As observed in research, young children’s event narratives often lack features that are characteristic of autobiographical memory, such as evaluations that indicate a subjective perspective on the event, and temporal and spatial markers that differentiate one event from another and suggest that the narrator is mentally traveling back in time (and space) to the original experience. The relative absence of such features has been interpreted to suggest that early in life, the memories children form are not autobiographical ⁴ or even episodic ⁵. This provides a ready explanation for childhood amnesia—there is no autobiographical record of early-life events because none was formed. The fact that in the present research, older children’s narratives about early-life events located the events in time and place and featured a subjective perspective (evaluations), strongly suggests that the children’s memories of those long-ago events were both episodic and personal.

The fact that the younger children had less complete narratives, relative to the older children, likely has consequences for the continued accessibility of early memories beyond the first decade of life. Narrative retelling affords opportunity for explicit rehearsal and organization of memories. To the extent that children produce more complete and content-filled narratives, they capitalize on this opportunity, thus further strengthening the memory representation.

The hypothesized long-term consequences of less versus more complete narratives about early-life events may help explain age-related differences in consistency of earliest memories in younger and older children. Peterson, Warren, and Short ⁶ interviewed children 4 to 13 years of age about their earliest memories. Two years later, they asked the same children to once again report their earliest memories. Strikingly, among children 4 to 7 years of age at the first interview, there was little overlap in the memories nominated at the two time points: fewer than 20% of the children repeated any memories at the second relative to the first interview. In contrast, 50–60% of the children 8 to 13 years of age repeated at least some memories at the second interview. Moreover, when the memories were the same, more of the specific content of the report was repeated by the older children relative to the younger children. These data suggest age-related increases in the stability of the corpus of early memories, an outcome consistent with the suggestion that memories that survive into the 9th or 10th year of life are likely to continue to be accessible, perhaps even into adulthood.

Dissociative amnesia

Dissociative amnesia is a disorder characterized “one or more episodes of inability to recall important personal information, usually of a traumatic or stressful nature, that is too extensive to be explained by ordinary forgetfulness” ⁷. These gaps involve an inability to recall personal information, usually of a traumatic or stressful nature ⁸. Dissociative amnesia most commonly occurs in the presence of other psychiatric conditions, particularly personality disorders.

Table 1. Diagnostic criteria for dissociative amnesia

1. The predominant disturbance is one or more episodes of inability to recall important personal information, usually of a traumatic or stressful nature, that is too extensive to be explained by ordinary forgetfulness.

2. The disturbance does not occur exclusively during the course of dissociative identity disorder, dissociative fugue, posttraumatic stress disorder, acute stress disorder, or somatization disorder and is not due to the direct physiologic effects of a substance (e.g., drug abuse or medication) or a neurological or other general medical condition (e.g., amnestic disorder due to head trauma).

3. The symptoms cause clinically significant distress or impairment in social, occupational, or other important areas of functioning.

[Source ⁷ ]

Dissociative amnesia can present a very confusing clinical picture ⁹. Differentiating between organic and dissociative memory loss is the first step to accurate diagnosis (Table 2). Unlike dementia, in which an individual may remember personal information but not recall general topics, a common presentation for dissociative amnesia is amnesia for personal identity and traumatic details, but intact memory for general information. Other amnesias, such as transient global amnesia and postconcussion amnesia, present with both retrograde and ongoing anterograde amnesia and demonstrate problems learning new information. In contrast, the amnesia associated with dissociative amnesia is usually only anterograde, restricted to the period following the trauma, and is without problems learning new information. Except for the amnesia, individuals with dissociative amnesia seem cognitively intact and function coherently.

Table 2. Characteristics of organic and dissociative memory loss

Organic Memory Loss

Dissociative Memory Loss

History suggestive of CNS injury Abnormal physical/neurological exam Abnormal laboratory values Abnormal EEG, LP, head CT, and MRI Older age Rare loss of autobiographical information Tends to be irreversible Both retrograde and anterograde Cognitive abilities impaired Difficulty encoding new memories Patient concerned about memory loss Baseline emotional responsiveness

History of an emotional trauma Normal physical/neurological exam Normal laboratory values Normal EEG, LP, head CT, and MRI Younger age Frequent loss of autobiographical information Is mostly reversible Usually anterograde* Cognitive abilities preserved Ability to encode new memories Patient not concerned about memory loss Heightened emotional responsiveness High hypnotizability &dissociative capacity

[Source ⁸]

Recent advances in neurophysiology have clarified the process of memory from a biologic perspective, but dissociative amnesia also has a significant psychological component ¹⁰. There is a large body of literature on peritraumatic dissociation, which is too extensive to be covered here. However, it is worthwhile noting how several experts in the field conceptualize dissociative amnesia. Van der Hart described the Janetian view of dissociation as “the process and the product of psychological and somatic splitting, which result from the impact of trauma emotions” ¹¹. Posttraumatic amnesia can be thought of as faulty ego integrative functioning in the setting of traumatic emotions. Gabbard conceptualizes dissociative amnesia in the following way: “Memories of the traumatized self must be dissociated because they are inconsistent with the everydissociative amnesiay self that appears to be in full control” ¹². Unlike repression, which can be thought of as horizontal split in the memory system, dissociation involves a vertical split ¹³. This results in the loss of memory for discrete periods of time rather than for discrete events.

Nearly all individuals with dissociative amnesia have significant comorbid psychiatric diagnoses, which if not treated will predispose the individual to recurrent eposides of amnesia ¹⁴. Frequently, these diagnoses include personality disorders, which are described in the Diagnostic and Statistical Manual of Mental Disorders-IV-TR as “enduring subjective experiences and behavior that deviate from cultural standissociative amnesiards, are rigidly pervasive with onset in late adolescence or early adulthood, are stable through time, and result in unhappiness and impairment.” The 10 recognized personality disorders are divided into three groups or clusters with Cluster A (paranoid, schizoid, schizotypal) perceived as odd and eccentric; Cluster B (antisocial, borderline, histrionic, narcissistic) being dramatic, emotional, and erratic; and Cluster C (avoidissociative amnesiant, dependent, obsessive compulsive) described as anxious and fearful ⁷.

Dissociative symptomology is most commonly associated with Cluster B personality disorders, presumably because these individuals often have a history of psychic or physical trauma ⁷. However, there is evidence to suggest that the relationship between Cluster C personality disorders, specifically avoidissociative amnesiant and dependent personality disorders, and dissociative amnesia is also prominent.

Psychogenic amnesia

Psychogenic amnesia refers to cases of memory loss presumed to have a psychological, rather than neurological cause, characterized by a sudden memory loss that concerns important personal information and there is usually selective retrograde amnesia too, but this condition is not due to an organic mental disorder. The amnesia may follow severe psychological stress or it may be an unconscious response to an internal conflict or to an intolerable life situation ¹⁵. The patient with psychogenic amnesia usually has difficulties for face recognition and the affective response to faces in relation to the faces’ familiarity during the selective amnesic period ¹⁶.

Patients with psychogenic amnesia fall into four groups that have different clinical characteristics and outcomes. Those who experience fugue states have the best prognosis, a new retrospective case analysis suggests.

In a review of more than 50 cases of psychogenic amnesia, patients in fugue states recovered relatively quickly to near-normal memory recall ― despite severe, blanket memory loss. Surprisingly, patients with psychogenic amnesia were significantly more likely to have experienced head injuries than patients with neurologic memory loss.

Psychogenic amnesia is either ‘global’ or situation-specific ¹⁷. Global psychogenic amnesia is characterized by a sudden loss of autobiographical memories for the whole of a person’s past. In psychogenic fugue, there is a loss of sense of personal identity and a period of wandering (psychogenic fugue), which lasts from a few days to about 4 weeks ¹⁷. In ‘focal retrograde amnesia’, the memory loss is much more persistent ¹⁸. Situation-specific amnesia refers to a gap in memory for a traumatic incident and can arise in a variety of circumstances: for example, post-traumatic stress disorder (PTSD) ¹⁹ or being the victim of an offence ²⁰.

Three factors have been identified as predisposing factors for global psychogenic amnesia ¹⁷: (i) a severe precipitating stress, such as marital or emotional crisis, bereavement, a financial crisis or during war time; (ii) a history of depressed mood and suicidal ideas; and (iii) a previous history of a transient, neurological amnesia. Coons and Milstein ²¹ also identified previous histories of childhood trauma, sexual abuse, and alcohol/ substance misuse problems. However, many previous descriptions of psychogenic amnesias consisted of case reports, making it difficult to generalize about predisposing factors. In cases of focal retrograde amnesia ²², psychogenic factors are often suspected ²³ but may not initially be obvious.

The neuropsychological profile of the memory impairment reported in cases of global psychogenic amnesia is variable. While retrograde autobiographical memory is characteristically impaired, anterograde memory has been described as intact, mildly, or severely impaired. The involvement of semantic memory is disputed: Schacter et al. ²⁴ reported that fugue is an example of an episodic/semantic dissociation, whereas others have reported involvement of both episodic and (personal) semantic memory. Both ‘reversed’ and ‘flat’ temporal gradients have been reported. In general, the literature on recovery from psychogenic amnesia remains sparse: the prognosis for recovery from global psychogenic amnesia has sometimes been reported as good, but in many cases the amnesia persists. When resolution occurs, it is sometimes prompted by chance cues in the environment, but may depend on a variety of factors. However, these observations have again been based on individual case reports or very small case series with few follow-up studies.

Varying patterns of abnormality have been reported in functional imaging studies, including both prefrontal activation and inhibition, temporal lobe changes, posterior cortical changes, or a combination of such findings. This variability may reflect differences in the syndromes described, the time delays until imaging was conducted, and the imaging methods used.

Transient global amnesia

Transient global amnesia is a temporary, acute onset anterograde amnesia that usually occurs in middle-aged and older individuals ²⁵. During an episode of transient global amnesia, your recall of recent events simply vanishes, so you can’t remember where you are or how you got there. In addition, you may not remember anything about what’s happening in the here and now. Consequently, you may keep repeating the same questions because you don’t remember the answers you’ve just been given. You may also draw a blank when asked to remember things that happened a day, a month or even a year ago. With transient global amnesia, you do remember who you are, and you recognize the people you know well. Episodes of transient global amnesia always improve gradually over a few hours. Recovery is usually very rapid and complete. During recovery, you may slowly begin to remember events and circumstances. Transient global amnesia isn’t serious, but it can still be a very frightening experience, both for the affected person and those around them.

Transient global amnesia is often precipitated by particularly strenuous activity, high-stress events, or sexual intercourse, but it can be seen with migraines as well. Studies have been inconclusive as to whether there are risk factors for the development of transient global amnesia, though some have suggested an association with a history of prior heart disease, migraine, or hyperlipidemia. Patients will often present with repetitive questioning and total anterograde memory loss that resolves within 24 hours. While there is disorientation with respect to other people and location, the patients will not lose self-awareness ²⁵. The symptoms, once resolved, rarely recur and no other neurological deficits present with transient global amnesia. The diagnosis is largely a diagnosis of exclusion ²⁶.

Non-cognitive functions are not affected. The presence of other symptoms such as aphasia (impaired ability to communicate), hemiparesis, sensory loss, or coordination problems suggests that other possible diagnoses should be considered ²⁷.

Recurrence is rare and the reported risk of a recurrent attack within 5 years varies between 2.9% and 26.3% ²⁸. A 2005 study with a 7-year follow-up period, which is the longest systematic follow-up period reported, found a recurrence rate of 8% ²⁹. Another study that recruited subjects over a 10-year period (n=142), however, with no designated follow-up period after the first occurrence, found a recurrence rate of 6.3%, if probable episodes were taken into account ²⁸.

Transient global amnesia most commonly presents in the seventh decade of life ³⁰. Across studies, the mean age of an episode ranges from 61 to 67.3 years ³⁰. In a 2006 study, 96% of subjects with transient global amnesia (n=142) presented between the ages of 51 and 80 years. Epidemiological studies fail to identify any subjects under the age of 55 years. Several small-scale studies show a slight female predominance ³¹. However, a study on 5,097 transient global amnesia cases shows gender distribution to be 50.7% females and 49.3% males ³², consistent with one previous analysis ³³.

While transient global amnesia generally does not cause lasting harm, a few studies have looked at the long-term outcome and risk of recurrence ²⁷. Transient global amnesia does not seem to be associated with an increased risk of ischemic stroke or seizures. Several studies have reported complete recovery of cognitive function 5 days to 6 months after the transient global amnesia episode. However, other researchers have noted that memory problems may last longer, although this tends to be in people who have had multiple episodes ²⁷.

Doctors do not know why transient global amnesia happens. Migraine variants and mini-strokes have all been suspected as causes. Transient global amnesia can be precipitated by extreme physical activity, sudden immersion in cold or hot water, accidents or strong emotional experiences. Having had an episode of transient global amnesia does not mean that a stroke becomes more likely or that the person is suffering from any other physical problem.

Transient global amnesia needs to be distinguished from other things which may cause memory loss, some of which may be life-threatening, such as seizures, stroke, fainting episodes and the effect of drugs.

Transient global amnesia symptoms

Generally, patients with transient global amnesia present with acute onset of several hours of memory loss, which is the inability to form new memories and to recall the recent past. People with transient global amnesia will usually keep repeating questions and appear anxious, agitated and perplexed. And they will be fully aware that there is an inexplicable blank period in their memory (they have no recall of how they got where they are or what they did in the time immediately preceding the onset).

• The main sign of transient global amnesia is being temporarily unable to form new memories. This is called prominent anterograde amnesia. During the episode of transient global amnesia, the person will seem disoriented in time and often ask questions about the date or their environment over and over again. This may be described as the person sounding like a “broken record.”
• During the transient global amnesia episode, the person may forget memories from the recent past (retrograde amnesia). The period of memory loss varies and may extend back hours to days or weeks, but only in rare instances, years.
• Other cognitive functions (ability to think) are not affected. In other words, even during the transient global amnesia episode, the person will know who they are and will be able to recognize and name familiar objects and people. The person is able to perform normal complex daily tasks such as driving or cooking.
• No other neurological problems are noticed during an exam. For example, reflexes, balance and coordination are normal.
• The transient global amnesia episode lasts between 1 and 10 hours (6 hours is the average). When the episode is over, the person will be able to make new memories again, but there will be no memories from the time during the episode.
• Duration of no more than 24 hours and generally shorter. Within 24 hours of the end of the transient global amnesia episode, any memories from the past lost during the episode will completely return. This does not include the time during the episode when no new memories could be made. In rare cases, some people may not remember an additional short period of time just before the transient global amnesia episode.
• Other less common symptoms include headache, nausea, dizziness, anxiety, and feelings of tingling and numbness in hands, feet, arms or legs.

Transient global amnesia complications

Transient global amnesia has no direct complications. It’s not a risk factor for stroke or epilepsy. It’s possible to have a second episode of transient global amnesia, but it’s extremely rare to have more than two. But, even temporary memory loss can cause emotional distress. If you need reassurance, ask your doctor to go over the results of your neurological exam and diagnostic tests with you.

Transient global amnesia causes

The underlying cause of transient global amnesia is unknown. Multiple theories exist regarding the true cause of transient global amnesia, but none are proven. These theories have included vascular phenomena, depression, migraines, epilepsy, or psychogenic origins. Transient ischemic attack (TIA), epilepsy, migraine, paradoxical emboli, venous congestion (overfilling of veins with blood due to some sort of blockage or other abnormality with the flow of blood) with consecutive ischemia of memory‐relevant structures and spreading depression of cortical activity have all been mooted as potential causes. Studies have supported and debunked arterial ischemia as a source. Vascular congestion was considered and is still one of the leading hypotheses, although questions regarding the associated with certain age groups and the fact that it is not seen with venous thrombosis have yet to be explained. In addition, transient global amnesia rarely occurs more than a couple of times in a patient’s life. Essentially, the theories generated regarding the cause of transient global amnesia do not explain all of the clinical aspects of transient global amnesia to date ³⁴. There is consensus that areas involved are mediobasal temporal region, the hippocampus and the parahippocampus ³⁵.

The origin of transient global amnesia is thought to arise from the hippocampus, particularly the CA-1 and Sommer sector, and mediobasal temporal lobe ²⁵. The hippocampal region noted is a watershed area of the brain that is especially subject to impact from various metabolic stresses, possibly due to sensitivity to cytotoxic glutaminergic uptake or release. These areas can be affected bilaterally or unilaterally, but are most common on the left side. In functional imaging, however, such as functional MRI, reversible defects were seen bilaterally. The patient transiently develops difficulty forming as well as retrieving new memories.

The presentation seen with transient global amnesia correlates with the affected side of the brain. In bilateral cases, the patient will exhibit both visuospatial and speech-related memory deficits. Dominant brain lesions will demonstrate related speech deficits ³⁶.

Possible mechanisms that have been proposed include ³⁷, ³⁸, ³⁵:

• A vascular etiology, such as venous flow abnormalities
• Hypoxia (deficiency of oxygen supply) and/or ischemia (deficiency of blood supply)
• A relation to migraine (some studies have shown that history of migraine is associated with transient global amnesia)
• Epilepsy
• Psychological factors

However, none of these theories clearly and consistently explain the features of transient global amnesia ³⁸. Because no one theory appears to apply to all people with transient global amnesia, some speculate that transient global amnesia may have multiple different causes ³⁸.

Events that reportedly may trigger an episode of transient global amnesia include ³⁹:

• Sudden immersion in cold or hot water
• Physical exertion
• Emotional distress or psychological stress, as might be provoked by bad news, conflict or overwork
• Pain
• Medical procedures
• Head trauma
• Sexual intercourse
• A Valsalva maneuver

There is a distinct form of transient global amnesia that may occur following excessive alcohol consumption, large sedative doses of barbiturates, the use of several illicit drugs, or sometimes, relatively small doses of benzodiazepines ³⁷.

Transient global amnesia is considered a sporadic disorder (not inherited, occurring in only one person in a family). However, familial cases of transient global amnesia have rarely been reported ⁴⁰. Most familial reports have involved siblings, with only occasional or possible parental involvement. While details of these cases have been incomplete, several of the affected people in these families had a history of migraine ⁴⁰.

Some clinicians believe that transient global amnesia can be a manifestation of a migraine aura, in which a familial predisposition to transient global amnesia may not be surprising. It is also possible that other genetically-influenced developmental factors might predispose only certain families. On the other hand, rare familial cases of transient global amnesia could possibly be coincidental ⁴⁰.

The underlying cause of transient global amnesia is largely unknown, and additional published reports of familial cases are needed to investigate a possible genetic component of the disorder.

Different modalities of neuroimaging have played a significant role in localizing the site of pathology. Single photon emission computed tomography revealed a decrease in cerebral blood flow in the temporal lobe and hippocampal region in most patients with transient global amnesia ⁴¹. Many investigators have used diffusion‐weighted imaging in transient global amnesia and contradictory findings have been reported, possibly because the sensitivity of diffusion‐weighted imaging changes over time. Sedlaczek et al ⁴² showed with serial imaging that diffusion‐weighted imaging changes were rarely noted in the acute phase after attack, but were visible at 48 hours.

The quick onset and recovery of the condition, and its frequent Valsalva triggers, led to the suggestion that it may result from a paradoxical embolus through a patent foramen ovale ⁴³. However, Maalikjy et al ⁴⁴ did not find any significant difference in the prevalence of patent foramen ovale in patients with transient global amnesia. Furthermore, a theory suggesting that transient global amnesia is caused by paradoxical emboli rather than arterial emboli would have difficulty explaining why an arterial embolism would not cause the same clinical sequelae as a venous thrombus taking the same final route.

Epilepsy is thought to be unlikely as a cause of transient global amnesia, as the attacks occur in clear consciousness and have a low recurrence rate. Furthermore, the EEG recording is characteristically normal after the attack and even when EEG was performed during the attack it was unremarkable ⁴⁵. It is likely that the few transient global amnesia patients who later present with epilepsy were initially misdiagnosed as transient global amnesia. One study followed a cohort of presumed patients with transient global amnesia and found that 9% of patients later presented with epilepsy ⁴⁶. However, all of their subsequent seizures culminated with postictal amnesia, and 50% of them had presented initially with an amnesic episode lasting for less than an hour.

The migraine theory proposes that glutamate release (which could be caused by emotional events as seen at the onset of transient global amnesia) in the hippocampus causes a spreading depression with transient dysfunction of the hippocampus ⁴⁷. Although some have reported an association of migraine with transient global amnesia ⁴⁸, others have not found an increased incidence of migraine in transient global amnesia sufferers ⁴⁴. Furthermore, migraine is a condition which generally occurs in the age range 25–55 years ⁴⁹, quite distinct from the transient global amnesia, which is vanishingly rare under the age of 40 years.

Pantoni et al ⁵⁰ suggested that psychological disturbances may play a role in transient global amnesia. They observed that the trigger factors often involve emotional arousal and anxiety, and claimed that 50% of the patients with transient global amnesia demonstrate a phobic personality trait. They compared patients with transient global amnesia with those with TIA, and found a significantly higher rate of psychiatric disease and family history of psychiatric disease in patients with transient global amnesia. They proposed that hyperventilation leading to cerebral vasoconstriction might play a role in the aetiology.

The sudden onset of transient global amnesia might imply an ischemic origin, be it venous or arterial. However, many case‐control studies comparing patients with transient global amnesia with age‐matched controls or with patients with TIA show that patients with transient global amnesia have fewer cardiovascular risk factors and a better prognosis than those with TIA, making thromboembolic arterial ischaemia an unlikely mechanism.

Lewis ⁵¹, however, suggested that transient global amnesia may result from venous ischaemia. Transient global amnesia often begins with a Valsalva maneuver, which allows brief retrograde transmission of high venous pressure to the cerebral venous system. The hippocampus (at least in pigs) is the area of the brain most sensitive to damage by such pressure ⁵², which would help explain why transient global amnesia occurs in the absence of other neurological symptoms. Such an increase in venous pressure would be more significant in the presence of incompetent internal jugular valves. Maalikjy et al ⁴⁴ showed that 90% of those patients who reported Valsalva maneuveres at the onset of their transient global amnesia had incompetent internal jugular valves, compared with 41% (a similar rate to the control group) of those patients with transient global amnesia who did not report such activities. It is tempting to conclude that patients with transient global amnesia can be divided into one group with incompetent valves whose episode was triggered by a Valsalva, and another group with a different aetiology. However, Lewis’s theory ⁵¹ does not explain why the incidence of transient global amnesia is so low given the high prevalence of incompetent jugular valves and Valsalva maneuveres.

Recently, a unifying hypothesis has been put forward by Winbeck et al ⁵³ in that transient global amnesia can result from transient ischemia of memory‐relevant structures either from an arterial emboli or from venous ischemia with Valsalva‐like activities before the onset of symptom. They suggested that diffusion weighted imaging may not be sensitive to pick up abnormalities in all patients with transient global amnesia, particularly when it is due to venous congestion.

Hence, it is possible that transient global amnesia may result from different mechanisms such as venous congestion with Valsalva‐like activities before symptom onset, arterial thromboembolic ischemia and vasoconstriction due to hyperventilation.

Risk factors for transient global amnesia

The clearest risk factors for getting transient global amnesia are:

• Age. People age 50 and older have a higher risk of transient global amnesia than do younger people.
• History of migraines. If you have migraines, your risk of transient global amnesia is significantly higher than that of someone without migraines.

A migraine history is one of the more notable risk factors associated with developing transient global amnesia. In a 2014 population-based study (n=316,602), migraine patients were significantly more likely to develop transient global amnesia than their matched controls, with the incidence rate ratio of 2.48 ⁵⁴. Additionally, of the subjects who developed transient global amnesia after the age of 40 years, those with a history of migraine had a significantly younger age of onset (56.6) compared to the control group (61.4). No associations were found between various migraine subtypes and transient global amnesia ⁵⁴.

Cardiovascular risk factors are also well studied in transient global amnesia. A retrospective case–control study found age- and sex-matched control subjects (n=293) to have significantly decreased odds of having hyperlipidemia and ischemic heart disease when compared with those subjects with transient global amnesia (n=293). Within this same study, 632 transient ischemic attack (TIA) subjects had greater rates of hypertension, diabetes mellitus, ischemic stroke, and atrial fibrillation when compared with transient global amnesia subjects, likely indicating differing risk factors between transient global amnesia and TIA ⁵⁵. Furthermore, a retrospective study of 85 transient global amnesia subjects revealed that those with history of two episodes of transient global amnesia showed a higher frequency of carotid atheromasia and ischemic heart disease than those with a history of just one episode of transient global amnesia ⁵⁶. Also, of note is that cancer diagnosis carries no increased risk of transient global amnesia, according to a prospective cohort study with 5,365,608 subjects running between 2001 and 2009 ⁵⁷.

Transient global amnesia prevention

Because the cause of transient global amnesia is unknown and the rate of recurrence is low, there’s no real way to prevent the condition.

Transient global amnesia diagnosis

The patient with transient global amnesia should be admitted to a hospital setting until the amnesia resolves. Diagnosis of transient global amnesia rests on excluding more-serious conditions — stroke, seizure or head injury, for example — that can cause the same type of memory loss.

A toxicology screen, alcohol level, and basic labs including glucose and electrolytes should be reviewed. Vitals, including oxygen saturation, should be checked. Because of the possibility of similar presentation with Wernicke encephalopathy, consider administering thiamine. If there are features suggestive of repetitive or seizure-like etiology, EEG could be considered, but it is not routinely recommended. MRI with diffusion-weighted imaging is needed to rule out ischemic stroke, which can have a similar presentation in some cases. However, there is no diagnostic test for transient global amnesia; rather, it is a diagnosis of exclusion.

Physical exam

The process begins with a neurological exam, checking reflexes, muscle tone, muscle strength, sensory function, gait, posture, coordination and balance. The doctor may also ask questions to test thinking, judgment and memory.

Brain and imaging tests

The next step is testing to look for abnormalities in the brain’s electrical activity and blood flow. Your doctor might order one or a combination of these tests:

• Magnetic resonance imaging (MRI). This technique uses a magnetic field and radio waves to create detailed, cross-sectional images of the brain. The MRI machine can combine these slices to produce 3D images that may be viewed from many different angles.
• Computerized tomography (CT). Using special X-ray equipment, your doctor obtains images from many different angles and joins them together to show cross-sectional images of the brain and skull. CT scans can reveal abnormalities in brain structure, including narrowed, overstretched or broken blood vessels and past strokes.
• Electroencephalogram (EEG). An EEG records the brain’s electrical activity via electrodes attached to the scalp. People with epilepsy often have changes in their brain waves, even when they’re not having a seizure. This test is usually ordered if you’ve had more than one episode of transient global amnesia or if your doctor suspects that you’re having seizures.

Transient global amnesia treatment

No specific treatment is indicated for a typical transient global amnesia and treatment for transient global amnesia is largely supportive. If there is any possibility of TIA, epilepsy or migraine, that should be treated accordingly.

Patients with transient global amnesia should be examined carefully for any accompanying neurological deficits or evidence of head trauma, both of which would exclude transient global amnesia as the diagnosis. The patient should be observed in the hospital until the memory deficit resolves. Consideration should be given for intravenous thiamine. Recurrences, while they do happen, are rare. The patient does not require any restrictions on driving or other activities once the memory deficits resolve.

People with repeat episodes of transient global amnesia should document the circumstances triggering the event. For some, it may be possible to prevent transient global amnesia by avoiding triggers. However, for many this is not possible. Possible triggers of transient global amnesia include ⁵⁸:

• Sudden immersion in cold or hot water
• Strenuous physical activity
• Sexual intercourse
• Medical procedures, such as angiography or endoscopy
• Mild head trauma
• Acute emotional distress (e.g., from bad news, conflict or being overworked)
• Exposure to high altitudes

Much of what we know about treatment of recurrent transient global amnesia comes from single case reports. These reports emphasize the need to rule out all other possible causes of recurrent transient global amnesia type episodes, such as transient epileptic amnesia, vascular disease, heart conditions, and adverse drug events, as this will affect treatment ⁵⁹.

The cause of transient global amnesia is not known, but migraines seem to be associated in many cases. We found a single report of metoprolol use for treatment of recurrent transient global amnesia in a man with a history of migraine ⁵⁸.

Transient global amnesia prognosis

Transient global amnesia is a temporary event and resolves spontaneously with death being very rare ⁶⁰, ⁶¹. However, the disorder can recur but causes no mortality.

Retrograde amnesia vs Anterograde amnesia

Retrograde amnesia refers to the loss of information that was acquired before the onset of amnesia ⁶².

Anterograde amnesia refers to an impaired capacity for new learning ⁶².

The most comprehensive study of the relationship between anterograde amnesia and retrograde amnesia was carried out in more than 1000 patients who had sustained closed head injury ⁶³. They showed the relationship between the duration of post-traumatic amnesia and the extent of retrograde amnesia for 972 cases. Retrograde amnesia was assessed informally, usually by querying about autobiographical information. They take the duration of anterograde amnesia to be indicated by the time after injury when post-traumatic amnesia resolves. As the duration of anterograde amnesia increased, the number of cases exhibiting pronounced retrograde amnesia also increased. Interestingly, when anterograde amnesia covered one day or less, only a small number of cases (N=19) exhibited substantial retrograde amnesia ⁶³. In fact, out of the 503 cases exhibiting anterograde amnesia of one day or less, 32 had no retrograde amnesia at all. These data describe an orderly relationship between anterograde amnesia and retrograde amnesia and also suggest that anterograde amnesia may need to reach some threshold of severity before retrograde amnesia is observed. In other words, it appears to be easier to disrupt new learning ability and harder to disrupt already acquired information, presumably because some fixation or consolidation of memory has occurred ⁶⁴. Unfortunately, in cases of (non-penetrating) traumatic brain injury, the locus and extent of damage is often difficult to determine. Information is not available about how the severity of anterograde amnesia relates to the severity of retrograde amnesia in patient groups with identified neuroanatomical damage.

In a study of amnesia and people with neuroanatomical damage, researchers found that as the severity of anterograde amnesia increased, so did the severity of retrograde amnesia. Patients with damage to both the hippocampus and parahippocampal gyrus exhibited the most severe anterograde amnesia and the most severe retrograde amnesia. Patients with damage limited largely to the hippocampus exhibited less severe anterograde amnesia and less severe retrograde amnesia. Although there was variability in the severity of retrograde amnesia, the average severity of retrograde amnesia in the two patient subgroups (mean = 10 years, median = 5 years for the hippocampal group and mean = 35 years, median = 35 years for the medial temporal lobe damage group – damage to the hippocampus and parahippocampal gyrus) are in line with previous reports ⁶⁵.

Complications of amnesia

Amnesia varies in severity and scope, but even mild amnesia takes a toll on daily activities and quality of life. The syndrome can cause problems at work, at school and in social settings.

It may not be possible to recover lost memories. Some people with severe memory problems need to live in a supervised situation or extended-care facility.

Amnesia symptoms

The two main features of amnesia are:

• Anterograde amnesia: difficulty learning new information following the onset of amnesia.
• Retrograde amnesia: difficulty remembering past events and previously familiar information that was acquired before the onset of amnesia

Most people with amnesia have problems with short-term memory — they can’t retain new information. Recent memories are most likely to be lost, while more remote or deeply ingrained memories may be spared. Someone may recall experiences from childhood or know the names of past presidents, but not be able to name the current president, know what month it is or remember what was for breakfast.

Isolated memory loss doesn’t affect a person’s intelligence, general knowledge, awareness, attention span, judgment, personality or identity. People with amnesia usually can understand written and spoken words and can learn skills such as bike riding or piano playing. They may understand they have a memory disorder.

Amnesia isn’t the same as dementia. Dementia often includes memory loss, but it also involves other significant cognitive problems that lead to a decline in daily functioning.

A pattern of forgetfulness is also a common symptom of mild cognitive impairment, but the memory and other cognitive problems in mild cognitive impairment aren’t as severe as those experienced in dementia.

Additional signs and symptoms of amnesia

Depending on the cause of the amnesia, other signs and symptoms may include:

• False memories (confabulation), either completely invented or made up of genuine memories misplaced in time
• Confusion or disorientation.

Causes of amnesia

Memory loss can just be a natural part of getting older.

Any disease or injury that affects the brain can interfere with memory.

Amnesia can result from damage to brain structures that form the limbic system, which controls your emotions and memories. These structures include the thalamus, which lies deep within the center of your brain, and the hippocampal formations, which are situated within the temporal lobes of your brain.

Amnesia caused by brain injury or damage is known as neurological amnesia.

Possible causes of neurological amnesia include:

• Stroke
• Transient global amnesia (sudden, temporary loss of memory) of unclear cause
• Transient ischemic attack (TIA) or mini-stroke
• Hydrocephalus (fluid collection in the brain)
• Concussion or head injury
• Brain inflammation (encephalitis) as a result of an infection with a virus such as herpes simplex virus, as an autoimmune reaction to cancer somewhere else in the body (paraneoplastic limbic encephalitis), or as an autoimmune reaction in the absence of cancer e.g. Lyme disease, syphilis, or HIV/AIDS
• Lack of adequate oxygen in the brain, for example, from a heart attack, respiratory distress or carbon monoxide poisoning
• Long-term alcohol abuse leading to thiamin (vitamin B-1) deficiency (Wernicke-Korsakoff syndrome)
• Tumors in areas of the brain that control memory
• Degenerative brain diseases, such as Alzheimer’s disease and other forms of dementia
• Seizures
• Certain medications, such as benzodiazepines or other medications that act as sedatives
• Cancer treatment, such as brain radiation, bone marrow transplant, or chemotherapy

Head injuries that cause a concussion, whether from a car accident or sports, can lead to confusion and problems remembering new information. This is especially common in the early stages of recovery. Mild head injuries typically do not cause lasting amnesia, but more-severe head injuries may cause permanent amnesia.

Another rare type of amnesia, called dissociative (psychogenic) amnesia, stems from emotional shock or trauma, such as being the victim of a violent crime. In this disorder, a person may lose personal memories and autobiographical information, but usually only briefly.

Sometimes amnesia may be caused by something common and treatable, like:

• Stress
• Psychological conditions, such as anxiety, depression or other mental health disorders, such as schizophrenia
• Bipolar disorder
• Sleeping problems

Occasionally, memory loss can be a sign of something more serious, such as dementia.

Don’t try to self-diagnose the cause of your memory loss – always see a doctor.

Amnesia can also be caused by issues that affect the whole brain, such as:

• Dementia
• Drug use
• Some medications, such as sedatives
• After losing the supply of oxygen to the brain, such as with a heart attack or heart surgery
• ECT (electroconvulsive therapy) (most often short-term memory loss)
• Epilepsy that is not well controlled
• Illness that results in the loss of, or damage to brain tissue or nerve cells, such as Parkinson disease, Huntington disease, or multiple sclerosis
• Low levels of important nutrients or vitamins, such as low vitamin B1 or B12
• Major surgery or severe illness, including brain surgery.

Prevention of amnesia

Because damage to the brain can be a root cause of amnesia, it’s important to take steps to minimize your chance of a brain injury. For example:

• Avoid excessive alcohol use.
• Wear a helmet when bicycling and a seat belt when driving.
• Treat any infection quickly so that it doesn’t have a chance to spread to the brain.
• Seek immediate medical treatment if you have any symptoms that suggest a stroke or brain aneurysm, such as a severe headache or one-sided numbness or paralysis.

Amnesia diagnosis

To diagnose amnesia, a doctor will do a comprehensive evaluation to rule out other possible causes of memory loss, such as Alzheimer’s disease, other forms of dementia, depression or a brain tumor.

Medical history

The evaluation starts with a detailed medical history. Because the person with memory loss may not be able to provide thorough information, a family member, friend or another caregiver generally takes part in the interview as well.

The doctor will ask many questions to understand the memory loss. Issues that might be addressed include:

• Type of memory loss — recent or long term
• When the memory problems started and how they progressed
• Triggering factors, such as a head injury, stroke or surgery
• Family history, especially of neurological disease
• Drug and alcohol use
• Other signs and symptoms, such as confusion, language problems, personality changes or impaired ability to care for self
• History of seizures, headaches, depression or cancer

Physical exam

The physical examination may include a neurological exam to check reflexes, sensory function, balance, and other physiological aspects of the brain and nervous system.

Cognitive tests

The doctor will test the person’s thinking, judgment, and recent and long-term memory. He or she will check the person’s knowledge of general information — such as the name of the current president — as well as personal information and past events. The doctor may also ask the person to repeat a list of words.

The memory evaluation can help determine the extent of memory loss and provide insights about what kind of help the person may need.

Diagnostic tests

The doctor may order:

• Imaging tests — including an MRI and CT scan — to check for brain damage or abnormalities
• Blood tests to check for infection, nutritional deficiencies or other issues
• An electroencephalogram to check for the presence of seizure activity
• Cognitive tests (neuropsychological/psychometric tests)
• Cerebral angiography
• Lumbar puncture

Treatment for amnesia

Treatment for amnesia focuses on techniques and strategies to help make up for the memory problem, and addressing any underlying diseases causing the amnesia.

Occupational therapy

A person with amnesia may work with an occupational therapist to learn new information to replace what was lost, or to use intact memories as a basis for taking in new information.

Memory training may also include different strategies for organizing information so that it’s easier to remember and for improving understanding of extended conversation.

Technological assistance

Many people with amnesia find it helpful to use smart technology, such as a smartphone or a hand-held tablet device. With some training and practice, even people with severe amnesia can use these electronic organizers to help with day-to-day tasks. For example, smartphones can be programmed to remind them about important events or to take medications.

Low-tech memory aids include notebooks, wall calendars, pill minders, and photographs of people and places.

Medications or supplements

No medications are currently available for treating most types of amnesia.

Amnesia caused by Wernicke-Korsakoff syndrome involves a lack of thiamin. Treatment includes replacing this vitamin and providing proper nutrition. Although treatment, which also needs to include alcohol abstinence, can help prevent further damage, most people won’t recover all of their lost memory.

Research may one day lead to new treatments for memory disorders. But the complexity of the brain processes involved makes it unlikely that a single medication will be able to resolve memory problems.

Living with amnesia

Living with amnesia can be frustrating for those with memory loss, and for their family and friends, too. People with more-severe forms of amnesia may require direct assistance from family, friends or professional caregivers.

If you have a treatable cause of amnesia, then treatment might allow you to regain your memory.

But if you have ongoing amnesia, then apart from treating whatever is causing it, you will need to developing strategies to improve your memory. This can mean:

• writing down important information using a diary, a notepad, or a smartphone
• telling family and friends about important information you need to remember
• seeing an occupational therapist or a psychologist who can help you develop strategies for remembering information.

It can be helpful to talk with others who understand what you’re going through, and who may be able to provide advice or tips on living with amnesia. Ask your doctor if he or she knows of a support group in your area for people with amnesia and their loved ones.

If an underlying cause for the amnesia is identified, there are national organizations that can provide additional information or support for the individual and their families. Examples include:

• The Alzheimer’s Association ⁶⁶
• The Brain Injury Association of America ⁶⁷

References

1. Childhood amnesia: a conceptualization in cognitive-psychological terms. J Am Psychoanal Assoc. 1986;34(3):663-85. http://journals.sagepub.com/doi/pdf/10.1177/000306518603400307
2. Freud S. Childhood and concealing memories. In: Brill AA, editor. The basic writings of Sigmund Freud. The Modern Library; New York: 1905/1953.
3. Wetzler SE, Sweeney JA. Childhood amnesia: An empirical demonstration. In: Rubin DC, editor. Autobiographical memory. Cambridge University Press; New York: 1986. pp. 191–201.
4. Fivush R. Subjective perspective and personal timeline in the development of autobiographical memory. In: Berntsen D, Rubin DC, editors. Understanding autobiographical memory: Theories and approaches. Cambridge University Press; New York, NY: 2012. pp. 226–245.
5. Wheeler MA. Episodic memory and autonoetic awareness. In: Tulving E, Craik FIM, editors. The Oxford handbook of memory. Oxford University Press; New York: 2000. pp. 597–608.
6. Infantile amnesia across the years: a 2-year follow-up of children’s earliest memories. Peterson C, Warren KL, Short MM. Child Dev. 2011 Jul-Aug; 82(4):1092-105. https://www.ncbi.nlm.nih.gov/pubmed/21557741/
7. American Psychiatric Association. Diagnostic and Statistical Manual of Mental Disorders, Fourth Edition, Text Revision. Washington, DC: American Psychiatric Press, Inc.; 2000.
8. Leong S, Waits W, Diebold C. Dissociative Amnesia and DSM-IV-TR Cluster C Personality Traits. Psychiatry (Edgmont). 2006;3(1):51-55. https://www.ncbi.nlm.nih.gov/pmc/articles/PMC2990548/
9. Miller P, Mycyk M, Leikin J, Ruland S. An unusual presentation of inhalant abuse with dissociative amnesia. Vet Hum Toxicol. 2002;44(1):17–19. https://www.ncbi.nlm.nih.gov/pubmed/11824766
10. Joseph R. The neurology of traumatic “dissociative” amnesia: Commentary and literature review. Child Abuse Neglect. 1999;23(8):715–27. https://www.ncbi.nlm.nih.gov/pubmed/10477233
11. Van der Hart O, Brown P, Graafland M. Trauma-induced dissociative amnesia in World War I combat soldiers. Aust N Z J Psychiatry. 1999;33:37–46. https://www.ncbi.nlm.nih.gov/pubmed/10197884
12. Gabbard G. Psychodynamic Psychiatry in Clinical Practice. Fourth Edition. Washington, DC: American Psychiatric Press, Inc.; 2005. Dissociative disorders.
13. Kluft RP. Multiple personality. In: Tasman A, Goldfinger S, editors. American Psychiatric Press Review of Psychiatry, Volume 10. Washington, DC: American Psychiatric Press; 1991. pp. 161–88.
14. Coons P. The dissociative disorders: Rarely considered and underdiagnosed. Psychiatr Clin North Am. 1998;21(3):637–48. https://www.ncbi.nlm.nih.gov/pubmed/9774801
15. Kaplan HI, Sadock BJ. Comprehensive textbook of psychiatry. 6th ed. New York: William & Wilkins; 1995. pp. 650–653.
16. Pujol M, Kopelman MD. Psychogenic amnesia. Practical Neurology. 2003;3:292–299.
17. Kopelman MD. Disorders of memory. Brain 2002a; 125: 2152–90.
18. Tramoni E, Aubert-Khalfa S, Guye M, Ranjeva JP, Felician O, Ceccaldi M. Hypo-retrieval and hyper-suppresion mechanisms in functional amnesia. Neuropsychologia 2009; 47: 611–24.
19. Brewin CR, Garnett R, Andrews B. Trauma, identity and mental health in UK military veterans. Psychol Med 2011; 41: 1733–40
20. Andrews B, Brewin CR, Rose S, Kirk M. Predicting PTSD symptoms in victims of violent crime: The role of shame, anger, and childhood abuse. J Abnorm Psychol 2000; 109: 69–73.
21. Coons PM, Milstein V. Psychogenic amnesia: a clinical investigation of 25 cases. Dissociation 1992; 5: 73–9.
22. Kapur N. Focal retrograde amnesia and the attribution of causality: an exceptionally benign commentary. Cogn Neuropsychol 2000; 17: 623–37.
23. Kopelman MD. Focal retrograde amnesia and the attribution of causality: an exceptionally critical review. Cogn Neuropsychol 2000: 17: 585–621.
24. Schacter DL, Wang PL, Tulving E, Freedman M. Functional retrograde amnesia: a quantitative case study. Neuropsychologia 1982; 20: 523–32.
25. Nehring SM, Spurling BC, Kumar A. Transient Global Amnesia. [Updated 2021 Jul 21]. In: StatPearls [Internet]. Treasure Island (FL): StatPearls Publishing; 2022 Jan-. Available from: https://www.ncbi.nlm.nih.gov/books/NBK442001
26. Alessandro L, Calandri IL, Suarez MF, Heredia ML, Chaves H, Allegri RF, Farez MF. Transient global amnesia: clinical features and prognostic factors suggesting recurrence. Arq Neuropsiquiatr. 2019 Jan;77(1):3-9. doi: 10.1590/0004-282X20180157
27. Arena JE and Rabinstein AA. Transient global amnesia. Mayo Clin Proc. February, 2015; 90(2):264-272. https://www.ncbi.nlm.nih.gov/pubmed/25659242
28. What does transient global amnesia really mean? Review of the literature and thorough study of 142 cases. Quinette P, Guillery-Girard B, Dayan J, de la Sayette V, Marquis S, Viader F, Desgranges B, Eustache F. Brain. 2006 Jul; 129(Pt 7):1640-58. https://www.ncbi.nlm.nih.gov/pubmed/16670178/
29. Clinical features, risk factors, and prognosis in transient global amnesia: a follow-up study. Pantoni L, Bertini E, Lamassa M, Pracucci G, Inzitari D. Eur J Neurol. 2005 May; 12(5):350-6. https://www.ncbi.nlm.nih.gov/pubmed/15804264/
30. Spiegel DR, Smith J, Wade RR, et al. Transient global amnesia: current perspectives. Neuropsychiatric Disease and Treatment. 2017;13:2691-2703. doi:10.2147/NDT.S130710. https://www.ncbi.nlm.nih.gov/pmc/articles/PMC5661450/
31. Long-Term Outcome in Patients With Transient Global Amnesia: A Population-Based Study. Arena JE, Brown RD, Mandrekar J, Rabinstein AA. Mayo Clin Proc. 2017 Mar; 92(3):399-405. https://www.ncbi.nlm.nih.gov/pubmed/28185658/
32. Zhu J, Lu D, Sveinsson O, et al. Is a cancer diagnosis associated with subsequent risk of transient global amnesia? PLoS One. 2015;10(4):e0122960. https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4388478/
33. Quinette P, Guillery-Girard B, Dayan J, et al. What does transient global amnesia really mean? Review of the literature and thorough study of 142 cases. Brain. 2006;129(pt 7):1640–1658. https://www.ncbi.nlm.nih.gov/pubmed/16670178
34. Yi M, Sherzai AZ, Ani C, Shavlik D, Ghamsary M, Lazar E, Sherzai D. Strong Association Between Migraine and Transient Global Amnesia: A National Inpatient Sample Analysis. J Neuropsychiatry Clin Neurosci. 2019 Winter;31(1):43-48. doi: 10.1176/appi.neuropsych.17120353
35. Owen D, Paranandi B, Sivakumar R, Seevaratnam M. Classical diseases revisited: transient global amnesia. Postgraduate Medical Journal. 2007;83(978):236-239. doi:10.1136/pgmj.2006.052472. https://www.ncbi.nlm.nih.gov/pmc/articles/PMC2600033/
36. Lanzone J, Ricci L, Assenza G, Ulivi M, Di Lazzaro V, Tombini M. Transient epileptic and global amnesia: Real-life differential diagnosis. Epilepsy Behav. 2018 Nov;88:205-211. doi: 10.1016/j.yebeh.2018.07.015
37. Juebin Huang. Transient Global Amnesia. Merck Manual. http://www.merckmanuals.com/professional/neurologic-disorders/function-and-dysfunction-of-the-cerebral-lobes/transient-global-amnesia
38. Sarah Kremen. Transient Global Amnesia. UpToDate. Waltham, MA: UpToDate; November, 2016
39. Transient global amnesia. MayoClinic. https://www.mayoclinic.org/diseases-conditions/transient-global-amnesia/symptoms-causes/syc-20378531
40. R. Rhys Davies and A.J. Larner. Familial Transient Global Amnesia. Case Rep Neurol. September-December, 2012; 4(3):236-239.
41. Sander K, Sander D. New insights into transient global amnesia: recent imaging and clinical findings. Lancet Neurol 20054437–444. https://www.ncbi.nlm.nih.gov/pubmed/15963447
42. Sedlaczek O, Hirsch J G, Grips E. et al Detection of delayed focal MR changes in the lateral hippocampus in transient global amnesia. Neurology 2004622165–2170. https://www.ncbi.nlm.nih.gov/pubmed/15210876
43. Klotzsch C, Sliwka U, Berlit P. et al An increased frequency of patent foramen ovale in patients with transient global amnesia. Analysis of 53 consecutive patients. Arch Neurol 199653504–508. https://www.ncbi.nlm.nih.gov/pubmed/8660151
44. Maalikjy N, Agosti C, Anzola G. et al Transient global amnesia: a clinical and sonographic study. Eur Neurol 20034967–71. https://www.ncbi.nlm.nih.gov/pubmed/12584412
45. Cole A J, Gloor P, Kaplan R. Transient global amnesia: the electroencephalogram at onset. Ann Neurol 198722771–772. https://www.ncbi.nlm.nih.gov/pubmed/3435087
46. Hodges J R, Warlow C P. Syndromes of transient amnesia: towards a classification. A study of 153 cases. J Neurol Neurosurg Psychiatry 199053834–843. https://www.ncbi.nlm.nih.gov/pmc/articles/PMC488242/
47. Lewis S L. Aetiology of transient global amnesia. Lancet 1998,352;397–399.
48. Frederiks J A. Transient global amnesia. Clin Neurol Neurosurg 199395265–283 https://www.ncbi.nlm.nih.gov/pubmed/8299284
49. Lipton R B, Stewart W F. The epidemiology of migraine. Eur Neurol 199434(Suppl 2)6–11. https://www.ncbi.nlm.nih.gov/pubmed/7835383
50. Pantoni L, Bertini E, Lamassa M. et al Clinical features, risk factors, and prognosis in transient global amnesia: a follow‐up study. Eur J Neurol 200512350–356. https://www.ncbi.nlm.nih.gov/pubmed/15804264
51. Lewis S L. Aetiology of transient global amnesia. Lancet 1998352397–399. https://www.ncbi.nlm.nih.gov/pubmed/9717945
52. Ye J, Yang L, Del Bigio M R. et al Neuronal damage after hypothermic circulatory arrest and retrograde cerebral perfusion in the pig. Ann Thorac Surg 1996611316–1322. https://www.ncbi.nlm.nih.gov/pubmed/8633934
53. Winbeck K, Etgen T, von Einsiedel H G. et al DWI in transient global amnesia and TIA: proposal for an ischaemic origin of TGA. J Neurol Neurosurg Psychiatry 200576438–441. https://www.ncbi.nlm.nih.gov/pmc/articles/PMC1739538/pdf/v076p00438.pdf
54. Migraine is associated with a higher risk of transient global amnesia: a nationwide cohort study. Lin KH, Chen YT, Fuh JL, Li SY, Chen TJ, Tang CH, Wang SJ. Eur J Neurol. 2014 May; 21(5):718-24. https://www.ncbi.nlm.nih.gov/pubmed/24520813/
55. Different risk factor profiles between transient global amnesia and transient ischemic attack: a large case-control study. Jang JW, Park SY, Hong JH, Park YH, Kim JE, Kim S. Eur Neurol. 2014; 71(1-2):19-24. https://www.ncbi.nlm.nih.gov/pubmed/24281363/
56. Recurrency in transient global amnesia: a retrospective study. Agosti C, Akkawi NM, Borroni B, Padovani A. Eur J Neurol. 2006 Sep; 13(9):986-9. https://www.ncbi.nlm.nih.gov/pubmed/16930365/
57. Is a cancer diagnosis associated with subsequent risk of transient global amnesia? Zhu J, Lu D, Sveinsson O, Wirdefeldt K, Fall K, Piehl F, Valdimarsdóttir U, Fang F. PLoS One. 2015; 10(4):e0122960. https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4388478/
58. Berlit P. Successful prophylaxis of recurrent transient global amnesia with metoprolol. Neurology. 2000 Dec 26; 55(12):1937-8. http://www.ncbi.nlm.nih.gov/pubmed11134409
59. Tsai MY1, Tsai MH, Yang SC, Tseng YL, Chuang YC. Transient global amnesia-like episode due to mistaken intake of zolpidem: drug safety concern in the elderly. J Patient Saf. 2009 Mar; 5(1):32-4. http://www.ncbi.nlm.nih.gov/pubmed19920437
60. Sophocles, A., Chen, L., Lin, D., & Liu, R. (2014). Postoperative amnesia in a patient undergoing general anesthesia for electro-physiologic (EP) catheter ablation of an irritable atrial focus. Translational perioperative and pain medicine, 1(2), 35–38.
61. Michel P, Beaud V, Eskandari A, Maeder P, Demonet JF, Eskioglou E. Ischemic Amnesia: Causes and Outcome. Stroke. 2017 Aug;48(8):2270-2273. doi: 10.1161/STROKEAHA.117.017420
62. Smith CN, Frascino JC, Hopkins RO, Squire LR. The nature of anterograde and retrograde memory impairment after damage to the medial temporal lobe. Neuropsychologia. 2013;51(13):10.1016/j.neuropsychologia.2013.09.015. doi:10.1016/j.neuropsychologia.2013.09.015. https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3837701/
63. Traumatic amnesia. RUSSELL WR, NATHAN PW. Brain. 1946 Dec; 69(4):280-300. https://www.ncbi.nlm.nih.gov/pubmed/20287646/
64. Memory–a century of consolidation. McGaugh JL. Science. 2000 Jan 14; 287(5451):248-51. https://www.ncbi.nlm.nih.gov/pubmed/10634773/
65. The fate of old memories after medial temporal lobe damage. Bayley PJ, Hopkins RO, Squire LR. J Neurosci. 2006 Dec 20; 26(51):13311-7. https://www.ncbi.nlm.nih.gov/pmc/articles/PMC2424208/
66. Alzheimer’s Association. https://www.alz.org/
67. Brain Injury Association of America. https://www.biausa.org/