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Acute transient memory loss
From American Family Physician, 5/1/89 by Daniel C. Vinson

Acute Transient Memory Loss Anterograde amnesia refers to the inability to form new memories. Alcoholic blackout, benzodiazepine-induced amnesia and transient global amnesia are three disorders that result in acute transient memory loss. These disorders may be difficult to recognize, because the memory loss is not usually accompanied by other symptoms of neurologic impairment. Family physicians frequently encounter patients with memory disorders. In many cases, the problem, such as Alzheimer's disease, is chronic and involves much more than memory impairment. There are, however, several acute transient disorders that affect little besides memory. Three of these--alcoholic blackout, benzodiazepine-induced amnesia and transient global amnesia--may be challenging conditions.

Anterograde Amnesia

Anterograde amnesia is defined as an inability to form new memories. This inability to learn new material, even simple sequences of numbers or single words, is common to the amnestic disorders discussed in this article. Although some degree of retrograde amnesia (loss of past memories) is often present in these disorders, anterograde amnesia is the central, diagnostically important element.

Other disturbances of cognitive functioning, such as disorientation, clouding of judgment or decreased level of consciousness, do not usually occur in transient anterograde amnestic disorders. This distinguishes them from more common conditions, such as acute delirium, in which other disturbances of cognitive functioning are often more prominent than memory loss.

Detailed psychometric testing may be needed to differentiate among some memory disorders, such as early Alzheimer's disease, Korsakoff's syndrome and depression.(1) In acute anterograde amnesia, however, the patient's memory impairment can usually be detected easily. To do this, the physician gives the patient three simple, unrelated words, such as "window, apple, chair." After a few minutes, the patient with anterograde amnesia will be unable to recall the words.


Rather than denoting a loss of consciousness, as the term is commonly understood, alcoholic blackout refers to a state of anterograde amnesia. Although intoxicated, the patient is not unconscious or even stuporous. The memory deficit often goes unnoticed until later and then is mistakenly viewed as retrograde amnesia.

Some remarkable accounts of alcoholic blackouts have been recorded. Goodwin and colleagues(2) related the story of a man who awoke one morning in an unfamiliar hotel. Although the man did not know where he was, he had apparently shaved the day before and his clothes were neatly hung. The desk clerk told the man that nothing had appeared out of the ordinary when the man had checked into the hotel on the previous evening. In response to the man's questions, the desk clerk informed him that it was Saturday morning and that he was in Las Vegas. The man's last memory was of being in a bar in St. Louis on Monday evening. He could not recall, and never did remember, how he got to the Las Vegas hotel or what had happened between Monday evening and Saturday morning.

Wolf(3) studied five men accused of homicide who claimed alcoholic amnesia for the event. Wolf was able to reproduce the anterograde amnesia under controlled conditions in the hospital by allowing the men to become intoxicated rapidly. While intoxicated, the men were unable to form new memories and were subsequently unable to recall what happened, even though some of them became violent during the experiment.

The acute alcoholic amnesia that family physicians usually encounter is likely to be much less dramatic. An example is an intoxicated patient who comes to the emergency department with a laceration and repeatedly asks, "When are you going to sew me up, Doc?" Although the physician may answer the question each time it is asked, the patient continues to repeat the question every few minutes, without remembering the answer. The patient is in an alcoholic blackout and therefore is unable to form new memories.

This situation emphasizes the importance of talking to a family member or other person who will be taking care of the patient until the intoxication clears. The patient may not be able to recall even simple instructions (such as the date to return for suture removal) minutes after hearing them. Certainly, more involved efforts, such as attempts to initiate counseling, are better left until the patient is sober.

Studies of hospitalized male alcoholics(4,5) have shown an association between a history of blackouts and the more severe manifestations of alcoholism. A correlation between the rapid drinking of a large amount of alcohol and the development of amnesia has also been found.(6) Most of the patients in these studies had a history of blackouts. Surprisingly, a history of one or more episodes of anterograde amnesia has also been reported by nonalcoholic men.(4-6) The amnesia often occurred at a younger age in these men than in alcoholics, and the memory loss was often related to isolated episodes of binge drinking, such as at fraternity initiation parties.

Goodwin and colleagues(4) concluded that blackouts are not necessarily a sign of alcoholism and are not always a sign of advanced disease. However, there is a correlation between the number of blackouts an individual has in a year and the number of times the person becomes intoxicated each month.(7) For this reason, determining the frequency of blackouts may be helpful in clarifying a diagnosis of alcoholism.

Whether alcohol-induced acute memory problems are related to chronic permanent alcoholic amnesia (Korsakoff's syndrome) is unknown. A study by Zucker and associates(5) showed no significant association between a history of blackouts and mild to moderate memory impairment in patients while they were sober, although the study gave few details on how memory was measured in these subjects.

Family physicians should be alert to the possibility of anterograde amnesia in intoxicated patients. As discussed previously, confirmation of the memory impairment requires only a simple test to evaluate word recall.


Anterograde amnesia has been reported in association with several benzodiazepines, especially triazolam (Halcion), lorazepam (Ativan) and alprazolam (Xanax).(8) As was recently reported in a small case series,(9) neuroscientists who traveled to Europe and took triazolam in an attempt to minimize jet lag were able to go through customs, exchange money and carry on coherent conversations. Several hours later, they did not remember those events. The memory deficit appeared to involve the recording of new memories and, as with alcoholic blackout, spared intellectual functioning. For example, after taking triazolam, lecturers have given two-hour slide presentations and physicians have made hospital rounds uneventfully, only to "come to" a few hours later with no recollection of what they had done.(10) Whether similar pathophysiologic mechanisms are involved in both benzodiazepine-induced amnesia and alcoholic blackout is unknown.

Physicians sometimes take advantage of the anterograde amnesia induced by benzodiazepines. Drugs such as diazepam (Valium) and midazolam (Versed) are administered intravenously as premedication to impair a patient's ability to remember an unpleasant procedure, such as endoscopy. Since this anterograde amnesia may last for several hours, postprocedure instructions should be given to a family member or written out for the patient. Discussions of test results should take place hours later or, preferably, on the next day.

Less profound degrees of anterograde amnesia may occur with oral doses of benzodiazepines, especially in the elderly and in patients with significant illness. In these patients, the benzodiazepine-induced memory impairment may be confused with dementia or delirium. Physicians and family members should watch for memory problems in patients taking this class of drugs. If memory is impaired out of proportion to other cognitive deficits, benzodiazepine therapy should be discontinued.


Transient global amnesia was first named by Fisher and Adams(11) in 1964, although it was described ten years earlier as a complication of angiography.(12) In 1985, Caplan(13) advised that patients should be diagnosed as having transient global amnesia only in the following circumstances: (1) if information about the beginning of the attack is available from a capable observer who witnessed the onset; (2) if the patient is examined during the attack and there are no important accompanying neurologic signs and (3) if the memory loss is transient.

In a case I encountered, a 56-year-old hospital employee was brought to the emergency department by co-workers who noted that she seemed confused. She repeatedly said, "I know I'm in the emergency room, but why am I here?" Each time, her question was answered and she seemed to be reassured. After two or three minutes, however, she would repeat the question, using the same words with the same inflection. Neurologic examination was normal, and the memory deficit cleared after a few hours. This patient met Caplan's criteria for the diagnosis of transient global amnesia.

There is some disagreement about Caplan's criteria,(14) and many case reports in the literature describe a more broadly defined disorder. Furthermore, patients with amnesia that appears to meet Caplan's criteria still may have a drug- or alcohol-related problem, a tumor(15) or a seizure disorder.(16) Yet, Caplan's diagnostic criteria were usually used in the cases reported in the literature, and cases that could be ascribed to some other problem were not included.

The cause of transient global amnesia remains unknown, although three major etiologic theories have been advanced. First, it has been suggested that this disorder is a form of transient ischemic cerebrovascular disease.(17) However, several case series indicate that patients with transient global amnesia but no other signs of transient cerebrovascular ischemia or stroke have the same risk of stroke as healthy patients of the same age.(18-20) One case-control series(21) found a significant association between cerebrovascular disease and transient global amnesia; however, four of the 18 patients in the series had suffered a previous stroke, and four others presented with neurologic deficits (other than memory deficit) at the time of the episode of transient global amnesia.

From these studies, it is reasonable to conclude that ischemic disease can cause transient anterograde amnesia, perhaps in as many as half of the cases of transient global amnesia. However, if patients with other neurologic signs, such as hemiparesis, are excluded, patients with transient global amnesia are probably no more likely to have cerebrovascular disease than are age-matched patients in the general population.

A second possible cause of transient global amnesia is seizure disorder, but this appears to be uncommon. In patients with transient global amnesia, the electroencephalogram (EEG) is usually normal, and only a few patients benefit from anticonvulsants. In 13 of 277 patients reported on by Miller and colleagues,(16) EEGs were obtained during the episode of transient global amnesia; none of the EEGs showed seizure discharges. In at least one patient,(22) an EEG was being obtained when the amnesia began; the EEG showed no change. After excluding patients with obvious motor manifestations of seizure, Miller and colleagues(19) found that the amnesia was caused by a seizure disorder in only two of the 277 patients.

Seizures may be the cause of some episodes of transient global amnesia, even if patients with obvious seizures are excluded by a stricter definition of the disorder. In particular, a diagnosis of seizure disorder should be considered if the amnesia is first noted on waking or if the onset is not witnessed.

Third, an association between transient global amnesia and migraine has been described in many case reports, including that of a nine-year-old child.(23) However, migraine is not a common cause of this memory disorder. Physicians from the Mayo Clinic found that a history of migraine is not common in patients with transient global amnesia and pointed out that the clinical courses of transient global amnesia and migraine are different.(19) Furthermore, the average age of patients with transient global amnesia is about 60,(13,17-19) which is considerably older than most patients with migraines.

There may be a common underlying pathophysiologic mechanism in migraine and transient global amnesia--Leao's spreading depression. This term describes a depolarization of neurons that spreads to adjacent neurons at 2 to 4 mm per minute. This depolarization has been elicited experimentally in animals and humans. In animals, chemically induced spreading depression in the hippocampus causes behavior cosistent with amnesia. It has been suggested that this mechanism plays a role in migraine and in transient global amnesia.(24)

The risk of recurrence of transient global amnesia is about 5 percent per year, with about one-fourth of patients having one or more recurrences within the next few years.(18,19) Permanent memory loss from transient global amnesia alone appears unlikely.(25)

Anterograde amnesia caused by ischemic events, seizures, migraine, tumors, drugs, alcohol or trauma can usually be distinguished from "pure" transient global amnesia by the history or physical examination, by computed tomographic (CT) scanning or by EEG examination. Since patients with transient global amnesia usually have some degree of retrograde amnesia, information must be sought from family members and from witnesses present at the onset of the patient's difficulties.

The physical examination should include a thorough neurologic examination, with particular attention to other signs of ischemic deficits. A CT scan may disclose evidence of a tumor or previous stroke, and the EEG helps identify seizure disorder. Theraphy should be directed at the underlying condition in patients with abnormal test results. If the test results are all unremarkable, more invasive tests probably are not necessary, and the patient can be reassured that the condition is benign.

In my experience, patients without neurologic deficits other than amnesia do not require hospitalization and can safely be managed at home. In the absence of other signs of ischemia, transient global amnesia probably requires no therapy,(19) although this issue has not been subjected to rigorous study.

Final Comment

Alcoholic blackout, benzodiazepine-induced amnesia and transient global amnesia are all characterized by the inability to form new memories. Physicians who are knowledgeable about these disorders can more easily recognize them, whether the symptoms are subtle, as in alcoholic blackout, or startling, as in transient global amnesia. Early recognition facilitates appropriate evaluation and management of these generally benign disorders.

REFERENCES (1)Kopelman MD. Clinical tests of memory. Br J Psychiatry 1986; 148:517-25. (2)Goodwin DW, Crane JB, Guze SB. Phenomenological aspects of the alcoholic "blackout." Br J Psychiatry 1969; 115:1033-8. (3)Wolf AS. Homicide and blackout in Alaskan natives: a report and reproduction of five cases. J Stud Alcohol 1980; 41:456-62. (4)Goodwin DW, Crane JB, Guze SB. Alcoholic "blackouts": a review and clinical study of 100 alcoholics. Am J Psychiatry 1969; 126:191-8. (5)Zucker DK, Austin FM, Branchey L. Variables associated with alcoholic blackouts in men. Am J Drug Alcohol Abuse 1985; 11:295-302. (6)Connors GJ, O'Farrell TJ, Cutter HS, Thompson DT. Dose-related effects of alcohol among male alcoholics, problem drinkers and nonproblem drinkers. J Stud Alcohol 1987; 48:461-6. (7)Poikolainen K. Blackouts increase with age, social class and the frequencyof intoxication. Acta Neurol Scand 1982;66:555-60. (8)Scharf MB, Fletcher K, Graham JP. Comparative amnestic effects of benzodiazepine hypnotic agents. J Clin Psychiatry 1988;49:134-7. (9)Morris HH 3d, Estes ML. Traveler's amnesia. Transient global amnesia secondary to triazolam. JAMA 1987;258:945-6. (10)You don't have to be a neuroscientist to forget everything with triazolam--but it helps [Letter]. JAMA 1988;259:350-2. (11)Fisher CM, Adams RD. Transient global amnesia. Acta Neurol Scand 1964;40(Suppl 9):1-83. (12)Hauge T. Catheter vertebral angiography. Acta Radiol 1954;109(Suppl):61-71. (13)Caplan LB. Transient global amnesia. In: Frederiks JA, ed. Handbook of clinical neurology. Vol 1 rev. Amsterdam: Elsevier, 1985:205-18. (14)Shuaib A. TGA criteria: what's in a name? [Letter] Neurology 1986;36:1625-6. (15)Meador KJ, Adams RJ, Flanigin HF. Transient global amnesia and meningioma. Neurology 1985;35:769-71. (16)Miller JW, Yanagihara T, Petersen RC, Klass DW. Transient global amnesia and epilepsy. Electroencephalographic distinction. Arch Neurol 1987;44:629-33. (17)Colombo A, Scarpa M. Transient global amnesia: pathogenesis and prognosis. Eur Neurol 1988;28:111-4. (18)Hinge HH, Jensen TS, Kjaer M, Marquardsen J, de Fine Olivarius B. The prognosis of transient global amnesia. Results of a multicenter study. Arch Neurol 1986;43:673-6. (19)Miller JW, Petersen RL, Metter EJ, Millikan CH, Yanagihara T. Transient global amnesia: clinical characteristics and prognosis. Neurology 1987;37:733-7. (20)Jensen TS, de Fine Olivarius B. Transient global amnesia--its clinical and pathophysiological basis and prognosis. Acta Neurol Scand 1981;63:220-30. (21)Kushner MJ, Hauser WA. Transient global amnesia: a case-control study. Ann Neurol 1985;18:684-91. (22)Cole AJ, Gloor P, Kaplan R. Transient global amnesia: the electroencephalogram at onset. Ann Neurol 1987;22:771-2. (23)Amit R, Shapira Y, Flusser H, Aker M. Basilar migraine manifesting as transient global amnesia in a 9-year-old child. Headache 1986;26:17-18. (24)Olesen J, Jorgensen MB. Leao's spreading depression in the hippocampus explains transient global amnesia. A hypothesis. Acta Neurol Scand 1986;73:219-20. (25)Stracciari A, Morreale A. Memory performances before and after transient global amnesia [Letter]. Stroke 1987;18:813-4.

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