Transient global amnesia
Transient global amnesia | |
---|---|
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 onset | Sudden |
Duration | Less than 24 hours |
Causes | Unknown |
Diagnostic method | Clinical diagnosis, imaging may aid in diagnosis |
Treatment | Reassurance |
Medication | None |
Prognosis | Good |
Transient global amnesia (TGA) is a
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]
- The attack was witnessed by a capable observer and reported as being a definite loss of recent memory (anterograde amnesia).
- There was an absence of clouding of consciousness or other cognitive impairment other than amnesia.
- There were no focal neurological signs or deficits during or after the attack.
- There were no features of epilepsy, or active epilepsy in the past two years, and the patient did not have any recent head injury.
- The attack resolved within 24 hours.
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.
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
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
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
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]
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
Differential diagnosis
A differential diagnosis should include:[29]
- Thrombosis of the basilar artery
- Cardioembolic stroke
- Complex partial seizures
- Frontal lobe epilepsy
- Lacunar syndromes
- Migraine variants
- Posterior cerebral artery stroke
- paroxysmalspells
- Temporal lobe epilepsy
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
References
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