Transient Global Amnesia Attacks Are Not TIAs
Abstract & Commentary
By John J. Caronna, MD Professor of Clinical Neurology, Weill Cornell Medical College, New York, NY. Dr. Caronna reports no financial relationships relevant to this field of study.
Synopsis: Patients with transient global amnesia (TGA), with or without DWI+ (positive diffusion weighted images) on MRI, do not have an increase in any vascular risk factors compared to healthy age and sex matched controls.
Source: Enzinger C, Thimary F, Kapeller P, et al. Transient global amnesia: diffusion-weighted imaging lesions and cerebrovascular disease. Stroke 2008;39:2219-2225.
Before the report of Fisher and Adams,1 sudden attacks of memory loss usually were diagnosed as seizures or fugue states. Fisher and Adams drew attention to the mysterious nature of amnesia attacks occurring in middle age and to the striking similarity from case to case. Patients lost memory suddenly, perception and personal identity remained normal throughout, and there were no other neurological abnormalities during or after the attacks. The retrograde amnesia, which initially might last for days, weeks, or even years, shrank gradually during the subsequent 30 minutes to 24 hours, until at the end of the attack it remained only for the period between onset and full recovery. Fisher and Adams rejected both epilepsy and hysteria as explanations for what they called "transient global amnesia." Even today, consensus as to its etiology and pathogenesis is lacking, although cerebral ischemia and migraine are the main pathogenic hypotheses.2
Recent reports of infarct-like, diffusion-weighted imaging abnormalities on MRI in the mesio-temporal region of TGA patients suggest that either acute focal cerebral ischemia3 or delayed ischemia4 are possible causes of the syndrome.
Enzinger and colleagues in Austria tested the hypothesis that TGA has a hypoxic-ischemic cause. They compared vascular risk factors, MRI markers of cerebral vascular disease, and other evidence of a cerebrovascular disorder in TGA patients with (DWI+) and without (DWI-) DWI lesions, and in normal community-based controls.
The authors retrospectively identified 86 patients hospitalized for TGA at the Medical University of Graz hospital between January 2002 and December 2006 in whom an MRI of the brain, including DWI, was available. The mean age ± SD was 66 ± 11 years; 62% were women. Vascular risk factors and findings from ECG (n=86), duplex sonography of the extracranial cerebral arteries (n=86), transthoracic echocardiography (n=46), EEG (n=83), chest x-ray, and routine laboratory tests were recorded. TGA patients were compared to a randomized selected age- and sex-matched sample of 172 control subjects. In the TGA cohort, 10 patients had 14 DWI+ lesions in the mesiotemporal region (9 left, 5 right hemisphere). The vascular risk profile of TGA patients and concomitant changes on brain MRI were comparable to those of healthy controls and showed no significant differences between DWI+ and DWI- subjects. There was no evidence for a higher rate of cerebrovascular disorder-related abnormalities in either the total group of TGA patients or TGA DWI+ patients.
The authors conclude that their results argue against an association between cerebrovascular disease and TGA, and that the cause of the DWI+ lesions in the context of TGA remains speculative.
Commentary
This retrospective analysis of 86 TGA patients discovered DWI lesions in only 11%, a relatively low percentage compared with previous reports. A review of existing MRI studies in acute TGA found that 52% of 99 patients had DWI+ abnormalities.2 Sedlaczek et al,4 by repeating MRI scans at later time intervals, found that 84% of TGA patients had DWI+ abnormalities. The present authors might have achieved a higher rate of detection of DWI+ lesions had they used dedicated protocols and follow-up MRI scans. Nevertheless, in their study, the DWI+ cohort did not have more vascular risk factors or a greater burden of cerebrovascular disease than the DWI- cohort or the controls. The benign acute and long-term prognosis of TGA argues against its identity with stroke or TIA. Similarly, the myriad of eliciting events (physical exercise, sexual intercourse, swimming and diving, driving, emotional upset, watching a sports event, neck hyperextension, vertebral angiography, Valsalva maneuver, etc.) and the plethora of postulated mechanisms (paradoxical embolism, migraine, arterial thromboembolism, venous ischemia, jugular vein incompetency, and more) suggest a cause other than cerebrovascular disease. Fifty years after Fisher and Adams described it, the cause of TGA remains a mystery.
References
1. Fisher CM, Adams RD. Trans Am Neurol Ass 1958;83:143-145.
2. Sander K, Sander D. Lancet Neurol 2005;4:437-444.
3. Ay H, Furie KL, Yamada K, et al. Neurology 1998; 51:901-903.
4. Sedlaczek O, Hirsch JG, Grips E, et al. Neurology 2004;62:2165-2170.
Patients with transient global amnesia (TGA), with or without DWI+ (positive diffusion weighted images) on MRI, do not have an increase in any vascular risk factors compared to healthy age and sex matched controls.You have reached your article limit for the month. Subscribe now to access this article plus other member-only content.
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