"Forgettable" Sex: A Case of Transient Global Amnesia Presenting to the Emergency Department

Kevin Maloy, MD; Jonathan E. Davis, MD


J Emerg Med. 2011;41(3):257-260. 

In This Article


Transient global amnesia is characterized by the sudden development of dense anterograde amnesia, without alteration in level of consciousness and in the absence of focal neurologic deficits or seizure activity.[1] It is a benign, self-limited condition. Numerous precipitating causes have been identified, including strenuous physical activity, severe pain, and physiological or psychological stress.[2–4] It has an overall annual incidence of 3.4–5.2 per 100,000 individuals, with increased frequency in those over 50 years of age (reported incidence of 23.5 per 100,000).[5] Theories regarding the pathophysiology of TGA have focused on migraine, seizure discharge, arterial ischemia, and venous congestion of the brain leading to ischemia (resulting from a Valsalva response), although the precise mechanisms remain unclear.[6] The hallmark of TGA is anterograde amnesia, although TGA may also present with retrograde amnesia, with most recently acquired memories at greatest risk.[5] Long-term (distant) memories, the meaning of words and objects, as well as an awareness of what one should know, are typically preserved.[5] Repetitive questioning is frequently reported during an episode of TGA, likely secondary to the inability to learn new information coupled with retrograde memory loss.[7] In a case series of TGA, the majority (90%) of patients experienced repetitive questioning.[4] Patients suffering from TGA typically return to baseline within a few hours, except for a dense, residual amnesic gap for events occurring during the attack.[8]

Helpful in making the diagnosis of TGA is the common occurrence of a precipitating event. Up to 90% of TGA episodes have an identifiable physical or psychological precipitating factor.[3] Sexual intercourse (including orgasm) has been reported as a precipitant of TGA.[9–11] In sex-induced TGA, the precipitating activity may not be remembered, including only hazy recollections of foreplay in some cases.[12] Fisher and Adams in 1964 reported a case of a man whose episode began during orgasm when he suddenly exclaimed "Where am I? What's happened?".[13] Recurrent episodes of TGA induced by sexual activity have also been reported.[12] However, the overall recurrence rate is very low and in most patients, TGA strikes only once.[3]

Hodges and Warlow in 1990 devised clinical criteria for the diagnosis of isolated TGA (Figure 1).[1] The utility of these diagnostic criteria to the acute care provider has been questioned. For example, requiring resolution within 24 h to fulfill the diagnostic criteria of TGA is impractical in the ED setting.[5] Indeed, these diagnostic criteria are more helpful in hindsight, after complete resolution of the episode. Furthermore, several emergent conditions requiring prompt action may be confused with TGA (as discussed below), hampering the utility of the "wait and see" approach.[14]

Figure 1.

Clinical criteria for the diagnosis of transient global amnesia. Adapted from (1): Hodges JR, Warlow CP. The aetiology of transient global amnesia. A case-control study of 114 cases with prospective follow-up. Brain 1990;113:639–57.

The differential of acute total amnesia includes TGA, TIA, subarachnoid hemorrhage (SAH), complex partial seizures, transient epileptic amnesia, psychogenic amnesia, and drug-related confusional states, among others.[5,14–17] SAH is a particularly important consideration, as headache is frequently reported in TGA patients (up to 40% in one series).[3] In one small case series of sex-induced acute amnesia presenting to an ED, SAH was identified in one of 10 cases, with TGA comprising the remaining cases. However, in contrast to TGA, the patient with SAH demonstrated clear focal (cerebellar) findings on neurological examination.[14] It is important to note that the headache associated with SAH may be quite distinctive (sudden, severe) contrasted with that of TGA, which is generally mild and not the patient's primary complaint.[3]

An equally important differential consideration is a TIA. Distinguishing TIA from TGA may be particularly challenging. In fact, some authors argue that the pathogenesis of TGA is actually transient ischemia of brain structures responsible for memory function (i.e., medial temporal lobe).[18] This evidence comes from MRI abnormalities noted in some, but not all, TGA patients.[18] A risk factor making TGA more likely than TIA is a history of migraine headache.[1,15] Ischemic heart disease, smoking, peripheral artery disease, or other "cardiovascular" risk factors, on the other hand, make TIA more likely.[1,15]

Important to its accurate diagnosis, TGA does not affect consciousness.[5] In TGA, self-identity and attention (as manifested by the ability to perform "serial sevens" or spell WORLD backwards) are preserved.[5,17] This is in contrast to acute delirium, where patients may present with altered level of consciousness (LOC) or attention deficits. In addition, patients with toxin-mediated acute confusional states are often able to learn new data (anterograde memory) if given sufficient time.[5] As noted in the anesthesia literature, intoxication with benzodiazepines can be distinguished from TGA by the lack of retrograde memory loss in the former.[19]

Routine laboratory testing (i.e., complete blood count, serum chemistry panel) adds little to aid in diagnosis, particularly when a patient presents to the ED after complete resolution of amnestic symptoms.[5] Lumbar puncture is unwarranted unless central nervous system infection or SAH are suspected.[5] A non-contrast head CT scan does not show abnormalities in TGA patients.[5] The CT scan may reveal an alternative diagnosis, especially when neurologic findings are present on examination.[14] MRI has been used to evaluate TGA with conflicting results; usually negative, it may reveal an alternate diagnosis.[3] Electroencephalography is not recommended in TGA, except for attacks of exceptionally brief duration (minutes) or repeat attacks, which are suspicious for seizure activity.[5] Single-photon emission CT may reveal transient dysfunction of the medial temporal lobe in many patients during the acute phase of TGA, although such specialized testing is not available in the ED setting.[3]

The natural course of TGA is typically benign and self-limited. In a case-control study comparing long-term outcomes of patients diagnosed with TGA and TIA, patients in the TIA group exhibited 7.4 times greater standardized mortality as compared with the TGA group at 7-year follow-up. Similarly, the incidence of stroke at follow-up was less in the TGA group (1.7% vs. 15% in the TIA group).[1]

In the case presented, the episode was witnessed, with clear identification of a distinct precipitating event. In addition, the patient maintained her consciousness throughout the episode, had a normal neurological examination, and exhibited a spontaneous return to baseline level of functioning during a brief period of ED observation. Ultimate patient disposition in this case was, therefore, straightforward. With more prolonged amnestic symptoms, determining the appropriate ED management and disposition would be more difficult. Some authorities have suggested that only a careful history and physical examination focused on identifying neurological deficits are needed for a first-time, isolated episode of TGA that is not exceptionally brief.[5] In patients with unclear circumstances, altered LOC, focal neurologic findings, and persistent (or very brief) amnestic symptoms, it is prudent to exclude alternative diagnoses such as SAH, TIA, or seizure with appropriate studies.