Transient Global Amnesia
Transient global amnesia
Transient global amnesia (TGA) is a temporary short-term memory loss that may result from the deactivation of the brain's temporal lobes and/or thalamus (the part of the brain that serves as a center for the relay of sensory information). Usually occurring in otherwise healthy persons, TGA triggers memory loss from external stresses such as strenuous exertion, high levels of anxiety, sexual intercourse, immersion in water, and other similar conditions. The event may also be triggered by a condition called the Valsalva maneuver. During this maneuver, a person performs the "breathe-in-bear-down" movement that is automatically performed during strenuous exercise . It is thought that this maneuver temporarily siphons blood from the temporal lobes of the brain. The temporal lobes are where the memories are stored. This loss of blood may induce the loss of memory by persons experiencing TGA. While this hypothesis is still under review, it has been accepted as a logical explanation for a condition that currently has no generally accepted causal explanation.
Transient global amnesia was first identified and described around 1960. Since that time, there have been extensive writings and studies about the condition, but its etiology (causation) is still not clearly known or understood.
TGA affects memory function. People experiencing TGA can register information and there is no loss of social skills and sense of identity, but their ability to retain information is severely impaired. One of the puzzling associations with TGA is that many people who experience this disorder are also migraine headache sufferers. However, there is no report of a migraine prior to onset, nor is there any reported nausea, sensitivity to light or sound, or headache.
There are no race or inherited conditions associated with TGA. Men experience the condition more often than women. In addition, the occurrence of this type of amnesia rarely happens before middle age, with about 12 out of 100,000 people ever experiencing the condition before age 50. The most likely ages in which to experience TGA are the 50s and 60s. About 3% of people who experience one episode of TGA will experience another episode sometime during their lifetime, but it is very rare for a person to experience more than three episodes of TGA.
The reason people in their 50s and 60s are more likely to experience TGA is not understood. No definitive links to any particular pathology or reaction to medication have been discovered. It is an elusive medical experience. For example, the connection of TGA with exposure to cold water cannot be explained in any convincing way. However, the condition has, as one of its major triggers, the exposure to cold water as in swimming, or prolonged exposure to cold rain or snow.
Causes and symptoms
The causes of this disorder are not yet fully understood. The hypotheses that the event is triggered by a temporary loss of blood to certain regions of the brain are most popular. In some cases, there is evidence of small strokes and local evidence of minor depressions on the surface of the brain. A well-accepted hypothesis suggests that blood is reduced to the temporal region of the brain during Valsalva, or weight-bearing movement.
People who have experienced TGA are also screened for current use of medications. Some drug interactions have been known to cause other types of amnesia, although not the type associated with TGA.
Another suggestion as a cause for TGA is that venous congestion (congested blood flow in the veins) inhibits blood flow to the thalamic or temporal regions of the brain. The support for this hypothesis is that increases in sympathetic nervous system activity and/or pressure within the thorax may exert pressure on the jugular veins. This, in turn, may disrupt arterial blood flow within the brain, resulting in ischemia (lack of oxygen) to memory centers or other areas of the brain. While the common precipitating factors have been discussed, why these events might trigger a TGA episode are not well understood.
TGA is sometimes a difficult condition to diagnose. It is extremely helpful for an observer to contribute information to the physician. Some of the criteria for identifying the event are the impairment of memory, both newly learned and past. There is no loss of consciousness or personal identity. There must be no recent experience of head trauma. Patients must not be epileptics nor can they have experienced any form of a seizure in the last two years.
The episode usually lasts for only a few hours and is usually completely resolved by the end of 24 hours. However, rare cases have been documented in which the patient experiences the amnesia for up to a month.
Anterograde amnesia, which sometimes also follows head trauma, is a component of TGA. With the anterograde types of amnesia, the person experiences a memory loss of recent experiences, however, long-term memory persists. Persons with anterograde amnesia often ask questions and, after receiving a response, immediately ask the same question again. Physicians examining a person with amnesia will rule out retrograde amnesia, which is not a part of TGA. Retrograde amnesia is somewhat the opposite of anterograde amnesia, whereby the affected person can remember events that occur after the head trauma, but not before.
With TGA, a person experiences temporary confusion and lack of memory. The person is disoriented and confused, but no loss of personal identity occurs and long-term memories are intact. The person may be frightened and sometimes mildly delusional, but this passes soon and the incidence of recurrence is rare.
The initial kinds of tests a physician will request are those that rule out infection, stroke , brain injury, and other physiological conditions.
Blood tests such as a CBC with differential help to rule out infection. Another test often performed is running an electrolyte panel. Eletrolytes are common salt minerals such as potassium, calcium, magnesium, etc. Most professional and amateur athletes are aware of how important proper electrolyte balances are for proper body functioning. A lowering of electrolytes may cause some of the symptoms described by a person experiencing TGA. Other types of blood tests, including the search for clotting potentials, are often performed. To determine whether the patient may be prone to blood clotting, a physician may request a pothrombin time (PT) and activated partial thromboplastin time (aPTT). Quick clotting times could indicate a propensity towards thrombosis (blood clotting), which could lead to stroke.
Part of the diagnosis involves conducting several types of imaging tests. The uses of positron emission tomography (PET) and diffusion-weighted magnetic resonance imaging (MRI-DWI) have shown a small degree of ischemia (lack of blood flow) to certain areas of the brain with TGA. However, these same tests have shown conflicting results in other patients. No definitive tests have been suggested to diagnose the condition.
Initially, most persons with TGA receive care from a physician in a hospital emergency department. A neurologist usually provides diagnosis and treatment. Both physicians usually order tests to differentiate TGA from other acute neurological events such as a stroke. As there is really no specific treatment for TGA, diagnosis and re-assurance by a physician are important for a person experiencing TGA, as well as for family members.
After ruling out trauma to the brain from accident, disease, or stroke, most people who have experienced TGA receive very little treatment because the condition is benign. A follow-up appointment with the neurologist is usually recommended.
Recovery and rehabilitation
Expected average times for recovery are within hours. A TGA patient rarely experiences the symptoms any longer than 24 hours. For most people, the condition lasts only 4–8 hours. Many people even report a shorter duration of one or two hours of disorientation and confusion. They may become frightened, but this is often alleviated with diagnosis and an explanation of the condition.
The prognosis for TGA patients is excellent. There are no debilitating side effects or any permanent loss of memory. TGA does not portend a serious stroke or similar condition involving the circulatory system. This is one of the reasons that TGA is such a perplexing syndrome for researchers; it is impossible to predict who will experience it. Because repeat occurrences are rare, numerous re-evaluations by a physician are usually not necessary.
It is important for people to be aware of the possibility of TGA. Seeking medical help, personal protection, and reassurance are the beneficial to offer someone displaying TGA symptoms.
Adams, R. D., M. Victor, and A. H. Ropper. "Transient Global Amnesia." In Principles of Neurology. New York: McGraw-Hill, 1997.
Simons, Jon S. and John R. Hodges. "Previous Cases: Transient Global Amnesia." Neurocases (2000): 6, 211–230.
Tuen, Charles. Neuroland. Transient Global Amnesia. January 4, 2004 (March 24, 2004). <http://neuroland.com/sands/tga.htm>.
National Institute for Neurological Disorders and Stroke. P.O. Box 5801, Bethesda, MD 20824. (301) 496-5761 or (800) 352-9424. <http://www.ninds.nih.gov>.
Brook Ellen Hall
"Transient Global Amnesia." Gale Encyclopedia of Neurological Disorders. . Encyclopedia.com. (August 18, 2018). http://www.encyclopedia.com/science/encyclopedias-almanacs-transcripts-and-maps/transient-global-amnesia
"Transient Global Amnesia." Gale Encyclopedia of Neurological Disorders. . Retrieved August 18, 2018 from Encyclopedia.com: http://www.encyclopedia.com/science/encyclopedias-almanacs-transcripts-and-maps/transient-global-amnesia