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• W4281736602 abstract "Transient global amnesia (TGA) is an idiopathic acute neurological disorder that presents with sudden onset anterograde memory loss. It was first described as a syndrome in 1956 by Courjon and Guyotat1 and also by Bender.2 Fisher and Adams formally described TGA in 1964.3 The usual presentation is a patient between 50 and 70 years of age who is cognitively and neurologically intact but asking repetitive questions and unable to form new memories. Symptoms are short-lived and resolve within 24 h. The incidence has been reported as 23.5 per 100,000 people per year and is more common in people who get migraine headaches.4, 5 TGA is often precipitated by physical or emotional stressors, pain, the Valsalva maneuver, hot or cold water immersion, or sexual intercourse.6 The criterion standard of TGA diagnosis combines seven clinical criteria: the attack is witnessed, there is clear anterograde amnesia, the absence of other neurological symptoms during the attack, the absence of abnormal neurological examination findings, memory loss is less than 24 h, there are no epileptic features or history of same, and there is no recent head injury.7 The workup of TGA can include laboratory testing, EEG, ECG, echocardiography, and advanced neuroimaging. This is a systematic review of observational studies of TGA. It included adult patients with a diagnosis of TGA based on existing clinical criteria who were evaluated with diffusion-weighted magnetic resonance imaging (DW-MRI) at varying time intervals (e.g., 0–12 h, 12–24 h) after symptom onset. The primary outcome was the sensitivity of DW-MRI in diagnosis of TGA. DW-MRI had low sensitivity for TGA early after symptom onset, but the sensitivity increased over time. The authors concluded that obtaining a DW-MRI in patients with a clinical diagnosis of TGA in the acute setting is likely a low-yield test. This was a good quality systematic review with a relevant diagnostic question, a detailed search strategy, and appropriate assessment of primary studies for common forms of bias. The major limitations of the included studies were the lack of precision (i.e., wide confidence intervals [CIs]) and high heterogeneity for estimates of DW-MRI sensitivity in diagnosing TGA. Heterogeneity as measured by the I2 test was very high at 72%–96% for most measured time points after symptom onset. Another limitation is that all studies included in this systematic review were observational in nature, with no randomized trials allocating patients to any time frame. Furthermore, although there were almost 1700 patients included in this review, there were still very few patients in some of the time points at which MRI was performed. This study also suffered from partial verification bias, also known as referral or workup bias. This occurs when only a certain set of patients who underwent the index test are verified by the reference standard. In this case, only those who met the clinical criteria for TGA had a DW-MRI performed, while patients who did not meet clinical criteria did not have an MRI. This could increase the overall sensitivity reported in the study. Finally, to get an accurate measure of sensitivity and specificity, we need a criterion standard to measure against. TGA is a clinical diagnosis, and the criterion standards used were the defined clinical criteria for the disease. This may be a somewhat uncertain criterion standard. Furthermore, if the criterion standard is clinical, the bedside physician already has access to the criterion standard diagnosis, and it is reasonable to ask what value an MRI could possibly add. Overall, 23 studies with a total of 1688 patients met inclusion criteria. All studies were case series of adult patients who were diagnosed with TGA clinically and who underwent DW-MRI. In the first 12 h from symptom onset, sensitivity of DW-MRI is 15.6%. Sensitivity improves thereafter to ranges as high as 83%, but there are very wide CIs for all point estimates and significant heterogeneity between studies. The Table 1 summarizes sensitivity of DW-MRI as a function of time interval from symptom onset. This study emphasizes the value of clinical criteria in the diagnosis of TGA and the low yield of DW-MRI testing. This is valuable information as it will reduce the unnecessary use of an expensive and time-consuming test in the acute setting. It is possible but unlikely that future prospective and randomized trials will change this. @shawnkdowling: Assuming there are no red flags, I do some basic labs and non-contrast CT head. I'd never considered ordering a DW-MRI and glad I do not need to based on this study. I typically consult neuro if the amnesia has not resolved at 12 h. @iwwalker: Textbook TGA does not need a neuro consult so consulting early likely keeps them unnecessarily in the ED for that, but cannot send them home until resolved regardless. If TGA is going on and on, I would also question the diagnosis, thus the referral. @Kapur_AK: Similar approach here. Our neurologists suggest we refer all as outpatients, which I'm okay with doing. I refer atypical or prolonged presentations in the ED (closer to 4–6 h). Ultimately the conclusion of emergency physicians weighing in on Twitter was not to order MRIs, while outpatient neurology consultation practices were variable. Clinical criteria remain the criterion standard in diagnosis of transient global amnesia. Early imaging with DW-MRI is a low-yield test and should not be performed in the emergency department. The authors declare no potential conflict of interest." @default.
• W4281736602 created "2022-06-13" @default.
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• W4281736602 date "2022-06-19" @default.
• W4281736602 modified "2023-09-26" @default.
• W4281736602 title "Hot off the press: <scp>MRI</scp> sensitivity for transient global amnesia" @default.
• W4281736602 cites W2003281625 @default.
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• W4281736602 doi "https://doi.org/10.1111/acem.14540" @default.
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