NEUROLOGY  Editorial What causes transient global amnesia New insights from DWI David C

NEUROLOGY Editorial What causes transient global amnesia New insights from DWI David C - Description

Tong MD and Murray Grossman MD Transient global amnesia TGA is a dramatic event Without warning the patient suddenly experiences antegrade memory loss 12 As quickly as the amnesic syndrome appears it resolves usually within 24 hours There are no app ID: 35459 Download Pdf

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NEUROLOGY Editorial What causes transient global amnesia New insights from DWI David C

Tong MD and Murray Grossman MD Transient global amnesia TGA is a dramatic event Without warning the patient suddenly experiences antegrade memory loss 12 As quickly as the amnesic syndrome appears it resolves usually within 24 hours There are no app

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NEUROLOGY Editorial What causes transient global amnesia New insights from DWI David C

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NEUROLOGY 2004;62:2154–2155 Editorial What causes transient global amnesia? New insights from DWI David C. Tong, MD; and Murray Grossman, MD Transient global amnesia (TGA) is a dramatic event. Without warning, the patient suddenly experiences antegrade memory loss. 1,2 As quickly as the amnesic syndrome appears, it resolves, usually within 24 hours. There are no apparent long-term sequelae, and recurrence is uncommon. What causes TGA? For years this question has been debated. Various proponents have advocated ischemic, migrainous, and epileptic causes. Even a

neuropsychological cause has been proposed. Unfor- tunately, definitive evidence supporting any of these mechanisms has been lacking. More recently, Lewis hypothesized that TGA was related to venous congestion due to retrograde ve- nous cerebral blood flow, because of the commonly reported association between TGA and situations that result in reduced venous return and retrograde venous blood flow (e.g., sexual activity, stress, Val- salva maneuver). Interestingly, there is some sup- port for this hypothesis. The same group has reported that a significantly higher percentage of TGA patients

possess jugular venous backflow with Valsalva compared with controls. 5,6 Can MRI help provide answers? The profound na- ture of the memory deficit has encouraged specula- tion that memory-related structures such as the hippocampus are involved. Until recently, this has been difficult to prove since TGA has not been asso- ciated with any findings on CT or MRI. More re- cently, diffusion-weighted imaging (DWI) has detected high signal abnormalities in the medial temporal lobe and possibly other structures impli- cated in memory functioning. 7-9 However, these re- ports have been conflicting,

with some investigators reporting no detectable DWI abnormalities, while others report these findings in a high percentage of cases. 7-11 Until now, the reason for this marked dis- crepancy has been unknown. In this issue of Neurology , an explanation for this discrepancy is presented. 12 Sedlaczek et al. report a high frequency of DWI positivity in TGA patients, but primarily ( 90%) in individuals who were scanned more than 24 hours after symptom onset. Overall, DWI abnormalities were detected in 36/59 (61%) TGA patients. The lesions were small and lo- cated in the hippocampal and thalamic

regions—a finding consistent with previous works using SPECT and PET that showed hypoperfusion in these same areas. Is TGA really a TIA? Both recover within 24 hours, and now both have been associated with DWI abnormalities. However, there are differences. The apparent time course of TGA-detected DWI findings is unusual for conventional arterial ischemia. Al- though rare reports describe ischemic DWI lesions after a significant time delay, these lesions typically appear very soon after ischemia onset. In contrast, according to the authors, DWI changes associated with TGA regularly occur

following a 24-hour delay. TIA-associated DWI lesions also tend to be larger than TGA (although still small), and have lower ap- parent diffusion coefficient (ADC) values than TGA- associated lesions. Moreover, the correlation between vascular risk factors and TGA is weak, making the relationship of TGA to an ischemic cause even more suspect. Status epilepticus, hypercellular tumors, bacterial abscesses, hemiplegic migraine, and acute multiple sclerosis lesions also may result in DWI positivity, although these causes are quite uncommon. 13,14 Fo- cusing on the significantly higher ADC values

that they observed in TGA, the authors speculate that this condition may be explained by venous conges- tion, consistent with Lewis’ venous backflow hypoth- esis. A lower ADC is associated with a more severe degree of tissue injury, they argue, and this would have suggested more pronounced ischemic insult such as is seen in arterial disease. While this is a possible explanation, less severe reductions in ADC have been reported with small lesions, such as those identified in TIA patients. A venous explanation also would not explain why TGA does not recur more See also page 2165 From the

Department of Neurology and Neurological Sciences (Dr. Tong), Stanford University School of Medicine, CA; and University of Pennsylvania S chool of Medicine (Dr. Grossman), Philadelphia. Address correspondence and reprint requests to Dr. David C. Tong, Associate Professor, Department of Neurology and Neurological Sciences, Stanfor University School of Medicine, Stanford, CA ; e-mail: 2154 Copyright  2004 by AAN Enterprises, Inc.
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frequently in a previously affected patient, since pre- sumably anatomic factors predisposing to retrograde flow do not

diminish over time. Moreover, given the high frequency of situations that result in dimin- ished venous return such as sexual activity, stress, and Valsalva maneuvers, TGA should be more fre- quent in the population if this were the explanation. Should the presence of these new DWI findings change patient management? This depends on whether there is a plausible reason to believe that the patient should be considered for antithrombotic therapy. The individuals described in the present study had many risk factors, in contrast to other studies that reported a low incidence of vascular risk

factors in TGA. 1,2 Therefore, in individuals with vas- cular risk factors, antiplatelet therapy should be con- sidered. One approach would be to add antiplatelet therapy to patients with DWI abnormalities particu- larly if they possess conventional cerebrovascular risk factors. Further studies evaluating stroke occur- rence in TGA patients who are DWI positive vs neg- ative might be useful in clarifying this question. The relative rarity of TGA makes such studies problem- atic, and it is unlikely we will have a definitive an- swer in the near future. The study by Sedlaczek et al may point the

way for better understanding TGA. Using this work as a stepping stone, perhaps we can further clarify the mechanism of this condition by combining these find- ings with perfusion weighted MRI, functional neuro- imaging such as PET or SPECT, and possibly venography using MR and Doppler techniques. The current study provides tantalizing new information regarding the nature of TGA. We can only hope that further studies can more definitively clarify the etiol- ogy of this enigmatic process. References 1. Hodges JR, Warlow CP. Syndromes of transient amnesia: towards a classification. A study of 153

cases. J Neurol Neurosurg Psychiatry 1990;53:834 843. 2. Hodges JR, Warlow CP. The aetiology of transient global amnesia. A case-control study of 114 cases with prospective follow-up. Brain 1990; 113(Pt 3):639 657. 3. Pantoni L, Lamassa M, Inzitari D. Transient global amnesia: a review emphasizing pathogenic aspects. Acta Neurol Scand 2000;102:275 283. 4. Lewis SL. Aetiology of transient global amnesia. Lancet 1998;352(9125):397 399. 5. Akkawi NM, et al. Transient global amnesia and venous flow patterns. Lancet 2001;357(9256):639. 6. Sander D, et al. Disturbance of venous flow patterns in

patients with transient global amnesia. Lancet 2000;356(9246):1982 1984. 7. Strupp M, et al. Diffusion-weighted MRI in transient global amnesia: elevated signal intensity in the left mesial temporal lobe in 7 of 10 patients. Ann Neurol 1998;43:164 170. 8. Ay H, et al. Diffusion-weighted MRI characterizes the ischemic lesion in transient global amnesia. Neurology 1998;51:901 903. 9. Woolfenden AR, et al. Diffusion-weighted MRI in transient global am- nesia precipitated by cerebral angiography. Stroke 1997;28:2311 2314. 10. Huber R, et al. Transient global amnesia. Evidence against vascular

ischemic etiology from diffusion weighted imaging. J Neurol 2002;249: 1520 1524. 11. Gass A, et al. Lack of evidence of acute ischemic tissue change in transient global amnesia on single-shot echo-planar diffusion-weighted MRI. Stroke 1999;30:2070 2072. 12. Sedlaczek O, Hirsch JG, Grips E, et al. Detection of delayed focal MR changes in the lateral hippocampus in transient global amnesia. Neu- rology 2004;62:2165 2170. 13. Roberts TP, Rowley HA. Diffusion weighted magnetic resonance imag- ing in stroke. Eur J Radiol 2003;45:185 194. 14. Connelly A, et al. Diffusion weighted magnetic resonance

imaging of compromised tissue in stroke. Arch Dis Child 1997;77:38-41. June (2 of 2) 2004 NEUROLOGY 62 2155