Transient global amnesia (TGA) is a benign neurological condition in which the prominent deficit is a temporary organic amnesic syndrome. The episode of TGA is stereotyped. It usually begins suddenly, lasts for at least several hours, and resolves gradually over several hours to a day. Careful examination duringan episode of TGA shows that the patient has a relatively isolated amnesic syndrome. Vision, hearing, sensation, strength, and coordination are normal. Language, spatial abilities, and general intellectual function also are normal, and the TGA patient can repeat a list of numbers or words. In contrast, the patient can recall little of any verbal or nonverbal material presented minutes before. The TGA patient often repeats the same question many times because of an inability to remember the answer that was just given. Frequently repeated questions include, "Is there something the matter with me?" and "What's wrong, have I had a stroke?" During TGA the patient has a patchy loss of recall for events dating from several hours to many years before the attack. Older memories are spared, and the patient does not lose personal identity. TGA patients examined carefully after the episode are normal except for an inability to recall the episode.
TGA generally occurs in persons over the age fifty, and 75 percent of patients are fifty to sixty-nine years old. Men and women are affected with nearly equal frequency. The estimated incidence is 5.2 per 100,000 per year for persons of all ages and 23.5 per 100,000 per year for persons older than fifty. A third to a half of TGA attacks are precipitated by physical or psychological stress, including strenuous exertion, sexual intercourse, intense emotion, pain, exposure to intense heat or cold, and minor or major medical procedures. TGA has a recurrence rate of 3 to 5 percent per year for at least five years after the initial episode. However, the patient with TGA does not appear to have an increased risk of developing significant permanent memory deficit or other cognitive dysfunction, and TGA patients have an incidence of subsequent stroke equal to the incidence of a comparable population.
Few laboratory abnormalities are associated with TGA. Blood, urine, and spinal fluid examination, electrocardiogram, electroencephalogram, and brain computerized tomography are normal. Some investigators have noted abnormalities, particularly in one or both medial temporal lobes, on single-photon emission computerized tomography (SPECT) brain scans and on diffusion-weighted magnetic resonance imaging (MRI) brain scans performed during the episode of TGA, which resolve following the episode.
Only a small number of patients have been examined with formal neuropsychological tests during TGA. Of these, eleven were studied with a single battery of memory tests that also had been given to patients with chronic organic amnesia. All of the eleven patients had severe anterograde amnesia (i.e., inability to learn new material) for verbal and nonverbal material, and their test scores were similar to scores obtained by well-studied patients with chronic organic amnesia. The severity of the anterograde amnesia appeared to correlate with the time since onset of TGA. There was no evidence for material-specific, or partial, amnesia—no TGA patient had a significant disparity between the degree of anterograde amnesia for verbal and nonverbal material. The patients also had a temporally graded retrograde amnesia (i.e., inability to recall events that occurred before the onset of amnesia) covering at least twenty years prior to TGA onset. Again, their test scores were similar to the scores of many well-studied patients with chronic organic amnesia. The retrograde amnesia was patchy—all patients were able to recall some events that occurred within the time interval affected by retrograde amnesia. Indeed, during TGA some memories were recalled, albeit incompletely, that were less than one to two months old. The temporally graded retrograde amnesia was similar for both public and personal events. During the episode, TGA patients performed normally on almost all other formal neuropsychological tests.
TGA is likely caused by temporary dysfunction of either bilateral medial temporal lobe structures, including field CA1 of the hippocampus and adjacent, anatomically related, structures; or bilateral medial diencephalic structures, including the dorsomedial nucleus of the thalamus, the mammillothalamic tract, and the mammillary bodies. The exact cause of TGA is not known, although it appears to be a benign condition that requires no medical treatment.
Bibliography
Hodges, J. R. (1998). Unraveling the enigma of transient global amnesia. Annals of Neurology 43, 151-153.
Kritchevsky, M. (1987). Transient global amnesia: When memory temporarily disappears. Postgraduate Medicine 82, 95-100.
—— (1989). Transient global amnesia. In F. Boller and J. Graffman, eds., Handbook of neuropsychology, Vol. 3, pp. 167-182. Amsterdam: Elsevier.
This is the complete article, containing 752 words
(approx. 3 pages at 300 words per page).
