(TGA) as first described by Bender 1 is characterized by a sudden onset of the inability to acquire new information and the loss of memory for recent events while immediate recall is preserved.1 "
3The patient remains alert, maintains self identity, and usually demonstrates concern by asking the same questions repeatedly. There are usually no concomitant neurologic deficits, and the disorder resolves within 24 hours, with residual amnesia for the event.1 " 3 Many etiologies have been proposed for TGA, including cerebrovascular disease, 4 -3 seizure disorder, 67 stress, 8 focal cerebral mass lesions, 9 cardiac disorders, 10 and migraine. 1112 However, no definite association between cerebral ischemia 11314 or ictal events 67 has been documented. Since many of these patients are considered to have cerebrovascular disease equivalent to patients with focal cerebral transient ischemic attacks (TIAs), 56 patients with symptoms of TGA were evaluated with noninvasive carotid artery testing to determine if there was a relation between TGA and the presence of extracranial atherosclerotic cerebrovascular disease.
Subjects and MethodsFifty-six consecutive patients with symptoms fulfilling the criteria for a diagnosis of TGA '" 3 were evaluated by a neurologist soon after the episode, usually within 1 day and always within 1 week. Most of the patients had been referred with the diagnosis of TGA by a neurologist. Their mean age was 67 years, with a 18 was performed on all 56 patients. This battery of tests has been shown to identify nearly all carotid lesions with a stenosis of > 5 0 % on angiography 19 and is also capable of identifying small atheromas in the carotid sinus not readily visualized on angiography.18 A hemodynamically obstructive lesion at the carotid artery bifurcation was identified when an atherosclerotic plaque was visualized at the carotid bifurcation associated with high-frequency turbulence on Doppler flow 19 or reduction in the ophthalmic artery pressure to 10% below the contralateral side or to < 6 5 % of the brachial artery pressure. 13 ' 20 Pneumooculoplethysmography was performed with a Life Sciences PVR (Boston, Mass.). Supraorbital directional Doppler and Doppler velocity wave form analysis of carotid flow was performed with a Parks 908 continuous-wave directional Doppler (Beaverton, Ore.) at 9.5 mHz. Real-time B-mode ultrasonography was performed with a High Stoy SP100B and duplex scanning with 4-and 8-mHz Sonomed continuouswave directional Dopplers (Lake Success, N.Y.). Statistical analysis was performed by Fisher's exact test with the Epistat program (Tracy Gustafson, Round Rock, Tex.) on an IBM PC XT computer.
ResultsOnly 1 of the 56 patients with TGA in this series had a history of neurologic disturbance, an episode of cerebellar ataxia, which probably represented a TIA in the vertebrobasilar distribution. The remaining 55 patients had no other history suggestive of cerebrovascular disby guest on