![]() ![]() A single board-certified neurologist (A.M.) reviewed the medical records from these 50 encounters while blinded to their ICD-9-CM diagnoses, and adjudicated cases of TGA based on its standard definition as the sudden onset of anterograde and retrograde memory lasting <24 hours and unaccompanied by other neurological deficits. To do so, we identified 25 ED visits or hospitalizations from 2008 through 2012 with a primary ICD-9-CM discharge diagnosis of 437.7, as well as 25 discharges with other primary cerebrovascular diagnosis codes (e.g., TIA) and no TGA code. Since the accuracy of the International Classification of Diseases, 9 th Edition, Clinical Modification ( ICD-9-CM) code for TGA (437.7) has not been validated, we first performed a retrospective chart review at our institution to determine its sensitivity and specificity. ![]() 7 Therefore, to build on prior studies and confirm that TGA confers a low risk of subsequent stroke, we performed a retrospective cohort study using statewide administrative claims data from across California. ![]() It is important to clearly resolve whether TGA is a benign entity or a stroke risk factor, because uncertainty about the etiology and prognosis of TGA drives potentially unnecessary stroke evaluations, especially when vascular risk factors are present. 23 Furthermore, the majority of studies on the outcome of TGA have had low statistical power, with an average of approximately 70 patients among the studies cited above and a maximum sample size of 236. 19– 22 Many of these studies were done decades ago, and the diagnosis of vascular events such as stroke or TIA has improved since then due to better imaging and clearer definitions. While many studies have supported the benign nature of TGA, 6, 8– 17 others have suggested that TGA may be a vascular prelude 18 that confers the same risk of stroke as transient ischemic attack (TIA). 7Īlthough neurologists generally view TGA as a benign entity, its exact prognosis remains unclear. 4– 6 Most episodes (75%) occur in people between 50 and 70 years of age, and TGA rarely occurs in patients younger than 40 years of age. 2, 3 The incidence of TGA ranges from 3 to 8 per 100,000 people per year. 1 Fisher and Adams introduced the term in 1964, 1 although Bender and separately Guyotat and Courjon had initially described a syndrome consistent with TGA in 1956. ![]() Epilepsy may mimic TGA in a minority of cases.Transient global amnesia (TGA) is characterized by a sudden deficit of anterograde and retrograde memory that usually lasts for a few hours and is not accompanied by other focal neurological symptoms or signs. The significant positive association between migraine and TGA may support this hypothesis. Since half of our patients had a precipitating event in their history, it is reasonable to hypothesize that spreading depression may play a role in TGA. The results of our case-control and longitudinal studies point to the conclusion that TGA and TIA do not share the same etiology. In three patients (4.5%), the TGA was eventually considered to be of epileptic origin. Migraine was more common in TGA patients than in both normal and TIA control subjects. In contrast to TIA control subjects, no TGA patient suffered stroke, myocardial infarction, or TIA during the follow-up period. We did not find evidence of an increased risk of TGA associated with any vascular risk factor. Then we compared the outcome of the two groups using actuarial analysis based on survival curves. We prospectively studied the vascular events and mortality rates of the TGA cases and of the TIA control subjects. In a case-control study, we compared the prevalence of vascular risk factors in 64 TGA patients with 64 first-ever transient ischemic attack (TIA) control subjects and 108 normal community-based control subjects matched for age and sex. The purpose of the present study was to make an attempt to ascertain the etiology of transient global amnesia (TGA), which is still disputed more than 30 years after the first description of this clinical entity. ![]()
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