A neurological disorder characterized by a temporary, but almost total, disruption of short-term memory with a range of problems accessing older memories.
It is an alarming, sudden onset syndrome of reversible antegrade and shrinking retrograde memory dysfunction, lasting several hours and occurring in otherwise healthy adults.
Typically, is characterized by sudden, complete, inability to retain new information, lasting for several hours, in a middle age, or older person, with preservation of alertness and all of the cognitive functions.
With an episode, there is anterograde amnesia, with an inability to retain new information for more than a few seconds, and retrograde amnesia, extending backward for several hours, days, or longer.
Frequently there is repetitive stereotyped questions, sometimes ask hundreds of times, at regular intervals of approximately 30 seconds – how did I get here?, where are we?, what happened?
All cognitive functions or otherwise normal.
Several disorders simulate transient global amnesia, and the diagnosis is doubtful if there are atypical features, such as global confusion, seizures, ataxia, vertigo, or deficits in cognition beyond memory.
The estimated annual incidence varies from a minimum of 2.9 cases per 100,000 population and 5.2 per 100,000.
Among people aged over 50, the incidence ranges from approximately 23 per 100,000 to 32 per 100,000.
TGA is most common in people between age 56 and 75,
Average age of a person experiencing TGA being approximately 62.
Predominately affects middle-age or elderly individuals.
Annual incidence between 3.4-10.4 per hundred thousand people.
In population older than 50 years the incidence is 23.5 per hundred thousand per year.
More common in individuals with migraine.
Episodes last a mean of six hours, with most lasting 2 to 12 hours.
In most series, approximately 15% of patients have had more than one episode with an average interval between episodes of approximately two years.
Episodes may be preceded by a physical or mental shock or extreme exertion, but in most instances, there is no obvious trigger.
Some patients report medications used for anesthesia seizure or drugs of abuse may have triggered the event.
Patients exhibit no other signs of impaired cognitive functioning but recall only the last few moments of consciousness, and deeply encoded facts of the individual’s past.
During an attack the patient has almost no capacity to establish new memories.
Patients appear otherwise mentally alert and lucid, possessing full knowledge of self-identity, maintaining intact perceptual skills and a complex of learned behavior.
Patients cannot recall anything that happened outside the last few minutes.
During the event there is retrograde memory loss encompassing a period of many hours or days before the event, gradually shrinking to just hours and minutes as the episode ends.
Distant memories that preceded the event by hours or days are accessible and personal identity is not lost.
Memory for more distant events may or may not be largely intact.
The episode ceases in hours and the patient regains new memories.
Some patients experience, a mild headache, afterward, and nausea and dizziness have been reported in frequently.
The neurologic examination is normal during and after the incident and brain imaging is initially normal.
A permanent gap in memory for the episode, and for the hours before it exists.
A memory circuit include the hippocampus on each side of the brain projecting to the septal areas via the fornix, then to the mammillary bodies, and subsequently to the anterior nucleus of the thalamus, and from there it projects to the cingulate gyrus of the frontal lobe and back to the hippocampus, completing the short- term Papez memory circuit.
Amnesia is caused by destruction of the above pathways.
Disruption of the hippocampus can cause anterograde amnesia and is characterized by the inability to lay down new information.
Unconventional vascular, or ischemic mechanisms affecting the medial temporal lobes and thalamus with the posterior cerebral circulation that supplies these regions are suspected to be affected.
Studies of neural networks during an episode show reduced connectivity of the hippocampi and parahippocampal gyri bilaterally, as well as reduced connectivity of other structures, such as the amygdala and portions of the lateral temporal lobe.
Confirmation that the hippocampus is the nexus of memory formation, and retrieval, and that widespread networks are disrupted in transient global amnesia.
The degree of amnesia is profound.
The process is often accompanied by anxiety.
The diagnostic criteria for TGA, include a definite loss of recent memory, and an absence of impaired consciousness or other cognitive impairment.
There are no focal neurological signs or deficits during or after the attack.
There are no features of epilepsy, or active epilepsy in the past two years, and the patient did not have any recent head injury.
This onset is generally fairly rapid, and generally lasts between 2 to 8 hours.
Patients typically have memory only of the past few minutes or less.
Patients cannot retain new information beyond a few minutes.
Perseveration, in which repeat statements or questions is found in almost all attacks and is sometimes considered a defining characteristic of the condition.
Patients retain social skills and older significant memories.
Patients know their identity and those of family members.
Patients retain the ability to perform complex learned tasks.
Patients outwardly appearing normal, but are disoriented in time and space.
An elevated emotional state is common, as is the fear of dying.
The attack lessens over a period of hours.
Older memories return first.
With time the repetitive fugue slowly lengthens so that there is retention of short-term memory for longer periods.
By 24 hours patients seem normal, but effects on memory that can persist.
In the majority of cases there are no long-term effects, but there is evidence for impairments in a minority of cases weeks or even years following an attack
There is a complete lack of recall for this period of the attack and an hour or two before its onset.
Patient’s are aware that something is not quite right, feeling they just lost their memory, believing they had a stroke, and not aware of the other signs that they are displaying repetitive actions.
Differential diagnosis includes:
Thrombosis of the basilar artery
Cardioembolic stroke
Complex partial seizures
Frontal lobe epilepsy
Lacunar syndromes
Migraine variants
Posterior cerebral artery stroke
Syncope and related paroxysmal spells
Temporal lobe epilepsy
If the event lasts less than one hour, transient epileptic amnesia (TEA) might be implicated.
If the condition lasts longer than 24 hours, it is not considered TGA by definition.
Cause unknown, but hypotheses include an epileptic event, a brain circulation impairment, or some kind of migraine-like phenomenon.
Associated with some form of precipitating event in at least one-third of cases
In females may be related to emotional reaction, while in males it is more often related to physical exertion.
Precipitating events include sexual intercourse, swimming in cold water and emotionally traumatic or stressful events.
Familial incidence is low at approximately 2%.
More than 80%, of TGA attacks are said to correlate with precipitating events.
Previously thought to be a variant of transient ischemic attack (TIA) secondary to some form of cerebrovascular disease, but such patients are no more likely than the general population to have subsequent cerebral vascular disease, and in fact have a significantly lower risk of combined stroke, myocardial infarct, and death.
TGA in men may be due to venous congestion of the brain, leading to ischemia of structures involved with memory, such as hippocampus.
In many cases, especially among men, TGA, can follow vigorous exertion.
Hypothetically TGA may be due to venous congestion of the brain, that can lead to ischemia of structures involved with memory, such as the hippocampus.
The Valsalva maneuver which occurs during exertion and may be related to retrograde flow of blood in the jugular vein, and therefore, presumably, cerebral blood circulation, in patients with TGA
A history of migraine is a statistically significantly associated with an increased risk for TGA, but they do not occur simultaneously, and it does not serve as a precipitating event.
Headache frequently occurs during TGA, as does nausea.
Not associated with epileptic features on EEG.
7% of people who experience TGA will develop epilepsy.
Prognosis of TGA is very good, not affecting mortality or morbidity, and is not a risk factor for stroke or ischemic disease.
Rates of recurrence is under 6% per year.
Approximately 15% of patients have recurrence years later.
Requires no further treatment except for reassurance.
Recent imaging and neurocognitive testing studies question whether TGA is as benign as has been previously considered: MRI scans of the brain in patients who have experienced TGA have cavities in the hippocampus suggestive of pathological damage.
Most affected patients have one or more punctate lesions in the hippocampus or adjacent structures on the fusion weighted MRI, but the appearance of these lesions is delayed and transient.
Previous studies did not detect changes because imaging was done soon after the episode:70% of lesions are not apparent until 12 to 48 hours after the episode.
Verbal and cognitive impairments have been observed after TGA attacks: A neurocognitive study of patients more than a year after their attacks has shown persistent effects consistent with amnestic mild cognitive impairment in a third of the patients.
Patients may have retrieval dysfunction in which speed of access is part of the problem in those who experience ongoing memory problems.