Transient global amnesia and transient topographical amnesia

Abstract

Sirs: I have previously focused attention on episodes of transient topographical amnesia (TTA) occurring in healthy elderly women, in the absence of overt brain disease or damage [5–7]. A TTA attack is characterized by sudden failure to find the way, in spite of a spared recognition of the environment. The nature of TTA is not clear; the only reasonable conjecture in most cases is that it reflects a transient dysfunction of unknown origin of the right occipitotemporal region. Similarities with the more common transient global amnesia (TGA) have been noted [5, 6]. Here I describe a patient who experienced two episodes of TGA, one of which ended in a typical TTA attack. This observation supports the idea of a common pathogenetic mechanism underlying both TGA and TTA. A 56-year-old right-handed healthy woman was seen for acute amnesia. On 14 March 1996, while swimming in a swimming pool with two friends, she suddenly lost her memory. She got out of the water, appeared astonished, asking the friends about why they had decided to go to the swimming pool (it was their regular activity every week). She repeated the same questions, showing a blank for the previous months. She dried herself, showing no problems in reaching the dressing room, in using towels and hair dryer, or dressing herself. She remained 90 minutes in the swimming pool area, during which the amnesic disturbance gradually subsided. Then, she decided to go home, driving her car by herself. She performed all the procedures to turn on the car engine and started. While driving, she suddenly lost her way, even though the route was familiar to her. After twenty minutes of driving around close to the swimming pool building and asking for help from passers by, she returned to the swimming pool and was taken to hospital. I saw the patient the next day. She appeared alert and fully oriented. Her medical history was unremarkable. In particular, no history of migraine, seizures, cerebrovascular disease or psychiatric disorders was reported. General and neurological examination were normal. Concerning the previous day, the patient had a blank from the moment she had begun to swim, until when she was outside in the car park (a period of about two hours), ready to get into her car to go home. She remembered having tried to drive along the usual route, but without being able to find her way, even though she recognized streets and buildings perfectly. Blood parameters, including thyroid function, and ECG proved normal. Search for alcohol and drugs was negative. EEG disclosed isolated theta activity on the temporal regions. Brain CT and ultrasound Doppler echotomography proved normal. A neuropsychological examination gave normal findings. Two months later cerebral SPECT was normal. On 6 February 1997, the patient experienced a 40 minute long antero-retrograde amnesia, again triggered by swimming. Neurological examination, EEG and brain MRI were normal. No other neurological problems emerged during four years of follow-up. This patient experienced two episodes of amnesia, fulfilling the criteria for TGA [3]. On one occasion, the TGA attack ended in an episode of TTA. These appeared as two distinct features, one leading to the other, but each maintaining its own characteristics. During TGA, the patient had a preserved spatial orientation. The topographical disorientation began once the TGA attack subsided and developed the typical course of TTA, with a maintained ability to record the events during the attack. Similarities between TGA and TTA have been previously noted [5, 6]. Both consist of transient memory dysfunction occurring in healthy middle aged or elderly people. Both have a good outcome, leaving at most a mild frailty on circumscribed cognitive performances, such as verbal memory in TGA [1] and geographical orientation in TTA [7]. This observation reinforces the idea of a possible common pathogenesis for TGA and TTA. Current pathogenetic hypotheses for TGA favor functional changes in cerebral metabolism more than structural damage. Leao’s spreading depression, suggested by Olesen and Jorgensen in 1986 [4] to explain TGA, has been recently reconsidered [2]. It is possible that stress, emotional and/or physical experiences may induce biochemical changes in the hippocampus, triggering a spreading depression, leading to a decreased local metabolism as well as a reversible functional ablation of the structures critical for memory. This mechanism could be invoked both for TGA and TTA. Both disorders may be due to the effect of spreading depression, which, propagating in different parts of the brain, may induce varied types of amnesia based on the affected region. LETTER TO THE EDITORS

DOI: 10.1007/s00415-003-1064-6

Cite this paper

@article{Stracciari2003TransientGA, title={Transient global amnesia and transient topographical amnesia}, author={Andrea Stracciari}, journal={Journal of Neurology}, year={2003}, volume={250}, pages={633-634} }