Transient global amnesia

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Transient global amnesia
Transiente globale Amnesie MRT DWI axial.png
Areas of hypoperfusion, seen above in the left sided hippocampus (seen as white punctate lesions on diffusion weighted MRI) are a characteristic finding in Transient Global Amnesia
Specialty Neurology
Symptoms Memory impairment
Complications Usually no long term sequelae
Usual onsetSudden
DurationLess than 24 hours
CausesUnknown
Diagnostic method Clinical diagnosis, imaging may aid in diagnosis
TreatmentReassurance
Medication None
Prognosis Good

Transient global amnesia (TGA) is a neurological disorder whose key defining characteristic is a temporary but almost total disruption of short-term memory with a range of problems accessing older memories. A person in a state of TGA exhibits no other signs of impaired cognitive functioning but recalls only the last few moments of consciousness, as well as possibly a few deeply encoded facts of the individual's past, such as their childhood, family, or home perhaps. [1] [2]

Contents

Both TGA and anterograde amnesia deal with disruptions of short-term memory. However, a TGA episode generally lasts no more than 2 to 8 hours before the patient returns to normal with the ability to form new memories.

Signs and symptoms

A person having an attack of TGA has almost no capacity to establish new memories, but generally appears otherwise mentally alert and lucid, possessing full knowledge of self-identity and identity of close family, and maintaining intact perceptual skills and a wide repertoire of complex learned behavior. The individual simply cannot recall anything that happened outside the last few minutes, while memory for more temporally distant events may or may not be largely intact. [1] [2] The degree of amnesia is profound, and, in the interval during which the individual is aware of his or her condition, is often accompanied by anxiety. [3] The diagnostic criteria for TGA, as defined for purposes of clinical research, include: [2]

Progression of a TGA event

This onset of TGA is generally fairly rapid, and its duration varies but generally lasts between 2 and 8 hours. [2] A person experiencing TGA has memory impairment; with an inability to remember events or people from the past few minutes, hours or days (retrograde amnesia) and has working memory of only the past few minutes or less, thus they cannot retain new information or form new memories beyond that period of time (anterograde amnesia). [4] One of its bizarre features is perseveration, in which the victim of an attack faithfully and methodically repeats statements or questions, complete with profoundly identical intonation and gestures "as if a fragment of a sound track is being repeatedly rerun." [5] This is found in almost all TGA attacks and is sometimes considered a defining characteristic of the condition. [2] [6] [7] The individual experiencing TGA retains social skills and older significant memories, almost always including knowing his or her own identity and the identity of family members, and the ability to perform various complex learned tasks including driving and other learned behavior; one individual "was able to continue putting together the alternator of his car." [2] Also, during episodes of TGA, a person's personality remains intact and the episode is not associated with loss of consciousness, a decreased level of consciousness or cognitive deficits (other than memory impairment). [4] Though outwardly appearing to be normal, a person with TGA is disoriented in time and space, perhaps knowing neither the year nor where they reside. Although confusion is sometimes reported, others consider this an imprecise observation, [7] but an elevated emotional state (compared to patients experiencing Transient Ischemic Attack, or TIA) is common. [8] In a large survey, 11% of individuals in a TGA state were described as exhibiting "emotionalism" and 14% "fear of dying". [9] The attack lessens over a period of hours, with older memories returning first, and the repetitive fugue slowly lengthening so that the victim retains short-term memory for longer periods. This characteristic of TGA, where the length of time affected by retrograde amnesia shortens (i.e. older memories return first, followed by more recent memories) is commonly seen. [4] In the majority of cases there are no long-term effects other than a complete lack of recall for this period of the attack and an hour or two before its onset. [2] [10] However, while seemingly back to normal within 24 hours, there are subtle effects on memory that may persist longer. [11] [12] There is emerging evidence for observable impairments in a minority of cases weeks or even years following a TGA attack. [11] [13] [14]

Causes

The underlying cause of TGA remains enigmatic. The leading hypotheses are some form of epileptic event, a problem with blood circulation around, to or from the brain, or some kind of migraine-like phenomenon. [8] [15] [16] [17] The differences are sufficiently meaningful that transient amnesia may be considered a heterogeneous clinical syndrome [2] with multiple etiologies, corresponding mechanisms, and differing prognoses. [9]

Precipitating events

TGA attacks are associated with some form of precipitating event in at least one-third of cases. [18] The most commonly cited precipitating events include vigorous exercise (including sexual intercourse), swimming in cold water or enduring other temperature changes, and emotionally traumatic or stressful events. [2] There are reports of TGA-like conditions following certain medical procedures and disease states. [16] One study reports two cases of familial incidence (in which two members of the same family experienced TGA), out of 114 cases considered. [2] This indicates the possibility that there could be a slight familial incidence.

If the definition of a precipitating event is widened to include events days or weeks earlier, and to take in emotionally stressful burdens such as money worries, attending a funeral or exhaustion due to overwork or unusual childcare responsibilities, a large majority, over 80%, of TGA attacks are said to correlate with precipitating events. [9]

The role of psychological co-factors has been addressed by some research. It is the case that people in a state of TGA exhibit measurably elevated levels of anxiety and/or depression. [3] Emotional instability may leave some people vulnerable to stressful triggers and thus be associated with TGA. [9] Individuals who have experienced TGA, compared with similar people with TIA, are more likely to have some kind of emotional problem (such as depression or phobias) in their personal or family history [19] or to have experienced some kind of phobic or emotionally challenging precipitating event. [20]

Vascular hypotheses

Cerebral ischemia is a frequently disputed possible cause, at least for some segment of the TGA population, and until the 1990s it was generally thought that TGA was a variant of transient ischemic attack (TIA) secondary to some form of cerebrovascular disease. [8] [17] Those who argue against a vascular cause point to evidence that those experiencing TGA are no more likely than the general population to have subsequent cerebral vascular disease. [8] In fact, "in comparison with TIA patients, TGA patients had a significantly lower risk of combined stroke, myocardial infarct, and death." [19]

Other vascular origins remain a possibility, however, according to research of jugular vein valve insufficiency in patients with TGA. In these cases TGA has followed vigorous exertion. One current hypothesis is that TGA may be due to venous congestion of the brain, [21] leading to ischemia of structures involved with memory, such as the hippocampus. [22] It has been shown that performing a Valsalva maneuver (involving "bearing down" and increasing breath pressure against a closed glottis, which occurs frequently during exertion) may be related to retrograde flow of blood in the jugular vein, and therefore, presumably, cerebral blood circulation, in patients with TGA. [21] [23] [24] [25] [26]

Migraine

A history of migraine is a statistically significant risk factor for the development of TGA. [8] [9] [4] "When comparing TGA patients with normal control subjects… the only factor significantly associated with an increased risk for TGA was migraine." [17] Fourteen percent of people with TGA had a history of migraine in one study, [18] and approximately a third of the participants in another clinical study reported such a history. [2]

However, migraine does not appear to occur simultaneously with TGA nor serve as a precipitating event. Headache frequently occurs during TGA, as does nausea, both symptoms often associated with migraine, but it appears that these do not indicate migraine in patients during a TGA event. The connection remains conceptual, and muddied further by a lack of consensus about the definition of migraine itself, and by the differences in age, gender, and psychological characteristics of migraine sufferers when compared to those variables in the TGA cohort. [9]

Epilepsy

Amnesia is often a symptom in epilepsy, and for that reason people with known epilepsy are disqualified from most studies of TGA. In a study where strict criteria were applied to TGA diagnosis, no epileptic features were seen in EEGs of over 100 patients with TGA. [9] However, despite the fact that EEG readings are usually normal during a TGA attack, and other usual symptoms of epilepsy are not observed with TGA, [17] it has been speculated that some initial epileptic attacks present as TGA. [2] The observation that 7% of people who experience TGA will develop epilepsy calls into question whether those case are, in fact, TGA or transient epileptic amnesia (TEA). [8] TEA attacks tend to be short (under one hour) and tend to recur, so that a person who has experienced both repeated attacks of temporary amnesia resembling TGA and if those events lasted less than one hour is very likely to develop epilepsy. [2]

There is additional speculation that atypical cases of TEA in the form of nonconvulsive status epilepticus may present with duration similar to TGA. [27] This may constitute a distinct subgroup of TGA. TEA, as opposed to "pure" TGA, is also characterized by "two unusual forms of memory deficit …: (i) accelerated long-term forgetting (ALF): the excessively rapid loss of newly acquired memories over a period of days or weeks and (ii) remote autobiographical memory loss: a loss of memories for salient, personally experienced events of the past few decades." [6]

Whether an amnestic event is TGA or TEA thus presents a diagnostic challenge, [16] especially in light of the recently published descriptions of possible long-term cognitive deficits with (presumably correctly diagnosed) TGA.

Diagnosis

There is no universally accepted diagnostic criteria for TGA, however proposed diagnostic criteria include: the absence of seizures, the absence of a head injury, symptoms that resolve within 24 hours, and the dysfunction or impairment being limited to amnesia (both retrograde and anterograde). [4] TGA is a clinical diagnosis and brain imaging or other testing is not required for the diagnosis. [4] However, brain imaging is often obtained to rule out other serious causes of sudden amnesia, including a stroke. Brain imaging is usually normal during and immediately after an episode of TGA. However delayed diffusion weighted MRI (obtained 12–48 hours after the episode) can sometimes show punctate lesions in the hippocampus (one of the areas of the brain responsible for memory) or adjacent areas of the brain. These lesions are transient; often persisting for several days after the episode. [4]

Functional MRI may show bitemporal hypoperfusion during an episode of TGA. Other areas affected include the hippocampus, parahippocampal gyrus, and amygdala. [4]

Other than memory impairment, the neurological exam is usually normal and without focal deficits. [28]

Laboratory tests may be obtained to rule out other causes of sudden amnesia such as a complete blood count, electrolytes, kidney function, liver function, inflammatory markers (such as C reactive protein and erythrocyte sedimentation rate), ammonia level (often elevated in hepatic encephalopathy), urine toxicology screening, alcohol level and thyroid stimulating hormone level. [28]

Differential diagnosis

A differential diagnosis should include: [29]

If the event lasts less than one hour, transient epileptic amnesia (TEA) might be implicated. [2] [30]

If the condition lasts longer than 24 hours, it is not considered TGA by definition. A diagnostic investigation would then probably focus on some form of undetected ischemic attack or cranial bleed. [31] [32]

Prognosis

The prognosis of "pure" TGA is very good, as by definition, symptoms resolve within 24 hours. It does not affect mortality or morbidity [29] There is no treatment specific to TGA. [4] "The most important part of management after diagnosis is looking after the psychological needs of the patient and his or her relatives. Seeing a once competent and healthy partner, sibling or parent become incapable of remembering what was said only a minute ago is very distressing, and hence it is often the relatives who will require reassurance." [33]

It is unclear if episodes of TGA increase the future risk of a stroke. Some population based studies show no increased risk of a stroke after an episode of TGA, while other population based studies show a slightly increased risk. [34] [35] [4]

Recurrence rates of TGA are variously reported, with one systematic calculation suggesting the rate is under 6% per year. [19] Fifteen percent of people who have had an episode of TGA have multiple episodes, with an average interval of 2 years between episodes. [4]

TGA may have multiple etiologies and prognoses. [9] Atypical presentations may masquerade as epilepsy [8] and be more properly considered TEA. In addition to such probable TEA cases, some people experiencing amnestic events diverging from the diagnostic criteria articulated above may have a less benign prognosis than those with "pure" TGA. [2]

Recently, moreover, both imaging and neurocognitive testing studies question whether TGA is as benign as has been thought. MRI scans of the brain in one study showed that among people who had experienced TGA, all had cavities in the hippocampus, and these cavities were far more numerous, larger, and more suggestive of pathological damage than in either healthy controls or a large control group of people with tumor or stroke. [13] Verbal and cognitive impairments have been observed days after TGA attacks, of such severity that the researchers estimated the effects would be unlikely to resolve within a short time frame. [14] A large neurocognitive study of patients more than a year after their attack has shown persistent effects consistent with amnestic mild cognitive impairment (MCI-a) in a third of the people who had experienced TGA. [36] In another study, "selective cognitive dysfunctions after the clinical recovery" were observed, suggesting a prefrontal impairment. [12] These dysfunctions may not be in memory per se but in retrieval, in which speed of access is part of the problem among people who have had TGA and experience ongoing memory problems. [11]

Epidemiology

The estimated annual incidence of TGA varies from a minimum of 2.9 cases per 100,000 population (in Spain) and 5.2 per 100,000 (in the US), [29] but among people aged over 50, the rate of TGA incidence is reported to range from approximately 23 per 100,000 (in a US population) to 32 per 100,000 (in a population in Scandinavia). [18] [37]

TGA is most common in people between age 56 and 75, [9] with the average age of a person experiencing TGA being approximately 62. [8]

See also

Related Research Articles

<span class="mw-page-title-main">Epilepsy</span> Group of neurological disorders causing seizures

Epilepsy is a group of non-communicable neurological disorders characterized by recurrent epileptic seizures. An epileptic seizure is the clinical manifestation of an abnormal, excessive, and synchronized electrical discharge in the brain cells called neurons. The occurrence of two or more unprovoked seizures defines epilepsy. The occurrence of just one seizure may warrant the definition in a more clinical usage where recurrence may be able to be prejudged. Epileptic seizures can vary from brief and nearly undetectable periods to long periods of vigorous shaking due to abnormal electrical activity in the brain. These episodes can result in physical injuries, either directly such as broken bones or through causing accidents. In epilepsy, seizures tend to recur and may have no immediate underlying cause. Isolated seizures that are provoked by a specific cause such as poisoning are not deemed to represent epilepsy. People with epilepsy may be treated differently in various areas of the world and experience varying degrees of social stigma due to the alarming nature of their symptoms.

A transient ischemic attack (TIA), commonly known as a mini-stroke, is a minor stroke whose noticeable symptoms usually end in less than an hour. TIA causes the same symptoms associated with strokes, such as weakness or numbness on one side of the body, sudden dimming or loss of vision, difficulty speaking or understanding language, slurred speech, or confusion.

A convulsion is a medical condition where the body muscles contract and relax rapidly and repeatedly, resulting in uncontrolled shaking. Because epileptic seizures typically include convulsions, the term convulsion is often used as a synonym for seizure. However, not all epileptic seizures result in convulsions, and not all convulsions are caused by epileptic seizures. Non-epileptic convulsions have no relation with epilepsy, and are caused by non-epileptic seizures.

In neurology, anterograde amnesia is the inability to create new memories after an event that caused amnesia, leading to a partial or complete inability to recall the recent past, while long-term memories from before the event remain intact. This is in contrast to retrograde amnesia, where memories created prior to the event are lost while new memories can still be created. Both can occur together in the same patient. To a large degree, anterograde amnesia remains a mysterious ailment because the precise mechanism of storing memories is not yet well understood, although it is known that the regions of the brain involved are certain sites in the temporal cortex, especially in the hippocampus and nearby subcortical regions.

A headache is often present in patients with epilepsy. If the headache occurs in the vicinity of a seizure, it is defined as peri-ictal headache, which can occur either before (pre-ictal) or after (post-ictal) the seizure, to which the term ictal refers. An ictal headache itself may or may not be an epileptic manifestation. In the first case it is defined as ictal epileptic headache or simply epileptic headache. It is a real painful seizure, that can remain isolated or be followed by other manifestations of the seizure. On the other hand, the ictal non-epileptic headache is a headache that occurs during a seizure but it is not due to an epileptic mechanism. When the headache does not occur in the vicinity of a seizure it is defined as inter-ictal headache. In this case it is a disorder autonomous from epilepsy, that is a comorbidity.

In neurology, retrograde amnesia (RA) is the inability to access memories or information from before an injury or disease occurred. RA differs from a similar condition called anterograde amnesia (AA), which is the inability to form new memories following injury or disease onset. Although an individual can have both RA and AA at the same time, RA can also occur on its own; this 'pure' form of RA can be further divided into three types: focal, isolated, and pure RA. RA negatively affects an individual's episodic, autobiographical, and declarative memory, but they can still form new memories because RA leaves procedural memory intact. Depending on its severity, RA can result in either temporally graded or more permanent memory loss. However, memory loss usually follows Ribot's law, which states that individuals are more likely to lose recent memories than older memories. Diagnosing RA generally requires using an Autobiographical Memory Interview (AMI) and observing brain structure through magnetic resonance imaging (MRI), a computed tomography scan (CT), or electroencephalography (EEG).

Cognitive disorders (CDs), also known as neurocognitive disorders (NCDs), are a category of mental health disorders that primarily affect cognitive abilities including learning, memory, perception, and problem-solving. Neurocognitive disorders include delirium, mild neurocognitive disorders, and major neurocognitive disorder. They are defined by deficits in cognitive ability that are acquired, typically represent decline, and may have an underlying brain pathology. The DSM-5 defines six key domains of cognitive function: executive function, learning and memory, perceptual-motor function, language, complex attention, and social cognition.

<span class="mw-page-title-main">Aura (symptom)</span> Symptom of epilepsy and migraine

An aura is a perceptual disturbance experienced by some with epilepsy or migraine. An epileptic aura is a seizure.

Psychogenic non-epileptic seizures (PNES), which have been more recently classified as functional seizures, are events resembling an epileptic seizure, but without the characteristic electrical discharges associated with epilepsy. PNES fall under the category of disorders known as functional neurological disorders (FND), also known as conversion disorders. These are typically treated by psychologists or psychiatrists. PNES has previously been called pseudoseizures, psychogenic seizures, and hysterical seizures, but these terms have fallen out of favor.

Acephalgic migraine is a neurological syndrome. It is a relatively uncommon variant of migraine in which the patient may experience some migraine symptoms such as aura, nausea, photophobia, and hemiparesis, but does not experience headache. It is generally classified as an event fulfilling the conditions of migraine with aura with no headache. It is sometimes distinguished from visual-only migraine aura without headache, also called ocular migraine.

Memory disorders are the result of damage to neuroanatomical structures that hinders the storage, retention and recollection of memories. Memory disorders can be progressive, including Alzheimer's disease, or they can be immediate including disorders resulting from head injury.

Dissociative amnesia or psychogenic amnesia is a dissociative disorder "characterized by retrospectively reported memory gaps. These gaps involve an inability to recall personal information, usually of a traumatic or stressful nature." In a change from the DSM-IV to the DSM-5, dissociative fugue is now subsumed under dissociative amnesia.

Alternating hemiplegia of childhood (AHC) is an ultra-rare neurological disorder named for the transient episodes, often referred to as "attacks", of hemiplegia that those with the condition experience. It typically presents before the age of 18 months. These hemiplegic attacks can cause anything from mild weakness to complete paralysis on one or both sides of the body, and they can vary greatly in duration. Attacks may also alternate from one side of the body to the other, or alternate between affecting one or both sides during a single attack. Besides hemiplegia, symptoms of the disorder include an extremely broad range of neurological and developmental impairments which are not well understood. Normally, hemiplegia and other associated symptoms cease completely with sleep, but they may recur upon waking.

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.

Transient epileptic amnesia (TEA) is a rare but probably underdiagnosed neurological condition which manifests as relatively brief and generally recurring episodes of amnesia caused by underlying temporal lobe epilepsy. Though descriptions of the condition are based on fewer than 100 cases published in the medical literature, and the largest single study to date included 50 people with TEA, TEA offers considerable theoretical significance as competing theories of human memory attempt to reconcile its implications.

Amnesia is a deficit in memory caused by brain damage or brain diseases, but it can also be temporarily caused 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.

<span class="mw-page-title-main">Epilepsy in children</span>

Epilepsy is a neurological condition of recurrent episodes of unprovoked epileptic seizures. A seizure is an abnormal neuronal brain activity that can cause intellectual, emotional, and social consequences. Epilepsy affects children and adults of all ages and races, it is one of the most common neurological disorders of the nervous system. As well as, this condition is more common among children than adults affecting about 6 out of 1000 US children that are between the age of 0 to 5 years old. The epileptic seizures can be of different types depending on the part of the brain that was affected, seizures are classified in 2 main types partial seizure or genralized seizure.

Musical hallucinations describes a neurological disorder in which the patient will hallucinate songs, tunes, instruments and melodies. The source of these hallucinations are derived from underlying psychotic illness or hearing impairment. These hallucinations are often rare and are followed by mental decline. A majority of patients who have symptoms of musical hallucinations are older and have onset conditions predisposing them to the disease. While there is no set form of treatment, research has discovered medications and alternative therapies to be successful in alleviating the hallucinations.

People with epilepsy may be classified into different syndromes based on specific clinical features. These features include the age at which seizures begin, the seizure types, and EEG findings, among others. Identifying an epilepsy syndrome is useful as it helps determine the underlying causes as well as deciding what anti-seizure medication should be tried. Epilepsy syndromes are more commonly diagnosed in infants and children. Some examples of epilepsy syndromes include benign rolandic epilepsy, childhood absence epilepsy and juvenile myoclonic epilepsy. Severe syndromes with diffuse brain dysfunction caused, at least partly, by some aspect of epilepsy, are also referred to as epileptic encephalopathies. These are associated with frequent seizures that are resistant to treatment and severe cognitive dysfunction, for instance Lennox-Gastaut syndrome and West syndrome.

Semantic amnesia is a type of amnesia that affects semantic memory and is primarily manifested through difficulties with language use and acquisition, recall of facts and general knowledge. A patient with semantic amnesia would have damage to the temporal lobe.

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  25. ↑ Nedelmann; Eicke, BM; Dieterich, M (2005). "Increased incidence of jugular valve insufficiency in patients with transient global amnesia". Journal of Neurology. 252 (12): 1482–6. doi:10.1007/s00415-005-0894-9. PMID   15999232. S2CID   25268484.
  26. ↑ Akkawi NM, Agosti C, Rozzini L, Anzola GP, Padovani A (2001). "Transient global amnesia and venous flow patterns". The Lancet . 357 (9256): 639. doi:10.1016/S0140-6736(05)71434-3. PMID   11558519. S2CID   5978618.
  27. ↑ Vuilleumier, P.; Despland, P; Regli, F (1996). "Failure to recall (but not to remember): Pure transient amnesia during nonconvulsive status epilepticus". Neurology. 46 (4): 1036–9. doi:10.1212/wnl.46.4.1036. PMID   8780086. S2CID   40835407. Archived from the original on 2005-11-14. Retrieved 2009-10-18.
  28. 1 2 Sealy, David; Tiller, Robert J.; Johnson, Katherine (January 2022). "Transient Global Amnesia". American Family Physician. 105 (1): 50–54. ISSN   1532-0650. PMID   35029951.
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  30. ↑ Engmann, Birk; Reuter, Mike (2003). "A case history of sudden memory dysfunction – caused by transient epileptic amnesia". Aktuelle Neurologie. 30 (7): 350–353. doi:10.1055/s-2003-41889. S2CID   59264426.
  31. ↑ Landres B: UCLA Department of Medicine Clinical Vignette: Transient Global Amnesia. Last Revised: Sun, 13-Apr-2003. "UCLA Department of Medicine - wfsection-Transient Global Amnesia". Archived from the original on 2012-03-09. Retrieved 2012-07-03. accessed 9/26/09
  32. ↑ Monzani; Rovellini, A; Schinco, G; Silani, V (2000). "Transient global amnesia or subarachnoid haemorrhage? Clinical and laboratory findings in a particular type of acute global amnesia". European Journal of Emergency Medicine. 7 (4): 291–3. doi:10.1097/00063110-200012000-00007. PMID   11764138. S2CID   2450356.
  33. ↑ Magnus Harrison; Mark Williams (2007). "The diagnosis and management of transient global amnesia in the emergency department". Emerg Med J. 24 (6): 444–445. doi:10.1136/emj.2007.046565. PMC   2658295 . PMID   17513554.
  34. ↑ Lee, Sang Hun; Kim, Keon-Yeup; Lee, Jeong-Woo; Park, So-Jeong; Jung, Jin-Man (1 April 2022). "Risk of ischaemic stroke in patients with transient global amnesia: a propensity-matched cohort study". Stroke and Vascular Neurology. 7 (2): 101–107. doi:10.1136/svn-2021-001006. ISSN   2059-8688. PMC   9067272 . PMID   34702748.
  35. ↑ Mangla, Atul; Navi, Babak B.; Layton, Kelly; Kamel, Hooman (February 2014). "Transient Global Amnesia and the Risk of Ischemic Stroke". Stroke. 45 (2): 389–393. doi:10.1161/STROKEAHA.113.003916. PMC   3946840 . PMID   24309586.
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  37. ↑ Koski; Marttila, RJ (1990). "Transient global amnesia: incidence in an urban population". Acta Neurologica Scandinavica. 81 (4): 358–60. doi: 10.1111/j.1600-0404.1990.tb01571.x . PMID   2360405. S2CID   32980858.
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