Brain Injury ISSN: 0269-9052 (Print) 1362-301X (Online) Journal homepage: http://www.tandfonline.com/loi/ibij20 Transient global amnesia and cerebral infarct: A case report R. Raffaele, C. Tornali, A. A. Genazzani, I. Vecchio & L. Rampello To cite this article: R. Raffaele, C. Tornali, A. A. Genazzani, I. Vecchio & L. Rampello (1995) Transient global amnesia and cerebral infarct: A case report, Brain Injury, 9:8, 815-818, DOI: 10.3109/02699059509008237 To link to this article: http://dx.doi.org/10.3109/02699059509008237 Published online: 03 Jul 2009. Submit your article to this journal Article views: 4 View related articles Citing articles: 1 View citing articles Full Terms & Conditions of access and use can be found at http://www.tandfonline.com/action/journalInformation?journalCode=ibij20 Download by: [McMaster University] Date: 01 April 2016, At: 11:37 BRAIN INJURY, 1995, VOL. 9, NO. 8, 815-818 Transient global amnesia and cerebral infarct: a case report R. RAFFAELE, C. TORNALI, A. A. GENAZZANI, I. VECCHIO and L. RAMPELLO Institute of Neurological Sciences, University of Catania Medical School, Italy Downloaded by [McMaster University] at 11:37 01 April 2016 (Received 2 4 March 1994; accepted 22 February 1995) Transient global amnesia refers to a sudden and isolated dysfunction of memory for recent events, lasting a few hours. The pathogenesis of this neurological disorder is s t i l l uncertain. The most accepted hypotheses concern ischaemic, epileptic and migraine causes. We now report a case of transient global amnesia associated with computed tomography evidence for a hypodense area in the left thalamus 10 days after the transient memory dysfunctions. Introduction The term transient global amnesia (TGA) refers to a sudden and isolated dyshnction of memory for recent events, lasting a few hours [l]. The following criteria were recently set by Caplan for the correct diagnosis of T G A (1) the attack onset should be witnessed; (2) dysfunction during the attack should be limited to repetitive queries and amnesia; (3) there should be no other major neurological signs or symptoms; (4) the memory loss should be transient, lasting no more than 48 hours [2]. Attacks generally last fiom 20 minutes to a few hours, and only occasionally have repetitive attacks been reported [3]. The aetiology of this disease is unclear at present, and vascular [4,5], epileptic [6] and migraine [7] mechanisms have been proposed. Moreover, TGA has also been described in association with brain tumours [8,9] and head trauma [lo]. We now describe a patient with TGA in whom computed tomography (CT) showed a cerebral infarct in the left thalamus 10 days after the transient memory dysfunctions. Case report A 58-year-old right-handed, diabetic and dyslipidaemic housewife with no history of neurological diseases suddenly started asking her daughter repetitive questions about a ‘family argument’ although she had already dscussed this matter on various occasions. She could also not remember what she had been doing since breaKast the same day. The woman &d not complain of headache or any other neurological symptom. The housewife was admitted to the Institute of Neurosciences of Catania 2 days after this acute episode. Neurological and general examinations were normal. Clinical history revealed that the patient had suffered no prior traumatic injury, and had never suffered psychiatric diseases or other acute neurological dyshnctions, including disturbances of conscious level or cognitive dysfunction. The clinical evidence for the diagnosis of TGA Correspondence to: R. RafEaele, Institute of Neurological Sciences, University of Catania Medical School, Vide A. Dona 6 , Italy 95125. 0269-9052/95 $10.00 0 1995 Taylor & Francis Ltd. 816 R . Raffaele et al. comprised reversibility ofthe syndrome, inability to lay down new memories during the attack, variable retrograde amnesia, amnesic lacuna persisting after the episode and resolution within 24 hours. Downloaded by [McMaster University] at 11:37 01 April 2016 Table 1 . Neuropsychological studies Wechsler Adult Intelhgence Scale, revised Temporal Orientation Test Rey Auditory Verbal Learning Test Wechsler Memory Scale Boston Famous Faces Test Rey’s 15 Words Digit Corsi’s Cube Test Barrage Attention Test Benton Visual; Retention Test (Adm. A, Form C) Orientation on a Geographic Map Stroop Test Figure 1. Patient with focal lesion consisting . f a l$t thalamic lacuna. Transient global amnesia and stroke 817 Various neuropsychological tests (listed in Table 1)were administered to the patient on the following day, and showed no peculiar findings. ECG was normal and Doppler ultrasounds of the extracranial vessels showed no evidence of stenosis. The EEG showed theta and delta waves over the left hemisphere. A brain CT scan performed 10 days after the admission showed a focal lesion consisting of a left thalamic lacuna (Figure 1). A follow-up CT was executed 3 months after the event and showed no visible lesions. The patient was discharged on ticlopidine (250mg/day) and followed as an outpatient for 6 months. During this follow-up period the patient had no recurrence. Downloaded by [McMaster University] at 11:37 01 April 2016 Discussion There are various hypotheses concerning the pathogenesis of TGA. The most valuable suggestions are migraineous, epileptogenic and ischaemic. The migraineous hypothesis, that states that TGA is a manifestation of an abnormal redstribution of cerebral flow during the vasodilatory phase of migraine, has been suggested by various authors [7,11] but Kushner and Hauser found no association between TGA and migraine in their case-control analysis [12]. Miller et al., in a retrospective study on 277 patients, found that 14.1%had a history of migraine [13]. The abruptness, shortness and reversibility of the disturbance, and the findng of some EEG anomalies, supports the epileptic origin ofTGA [6]. Miller et al. found that only 2.9% ofpatients with TGA had seizure disorders [ 131. The ischaemic theory suggests that TGA is due to a transient vascular deficit, mainly of the posterior cerebral arteries, in the brain regions serving memory. In the above-cited paper by Miller et al. the patients with cerebrovascular diseases comprised 11.7% [13]. The case we now report meets the requirements set by Caplan for the dagnosis of TGA, since the attack onset was witnessed, the dysfunction was transient and limited to amnesia and repetitive queries, with no other neurological signs or symptoms. The CT scan showed a cerebrovascular lesion consisting of a left thalamic lacuna, and suggests that, of the above hypotheses, the ischaemic one is most consistent with our case report. The thalamic lesion is consistent with the amnesia since diencephalic structures, and the dorsomedial nucleus in particular, appear to play an important role in memory dysfunctions. Since not all the lesions of the medial thalamus are associated with amnesia it is argued that, to produce a memory deficit, either the amount of the dorsomedial nucleus damaged must be above a certain threshold or a second region, such as the mammillothalamic tract or the anterior nucleus, must also be damaged [14]. In conclusion, TGA can be the isolated manifestation of a cerebrovascular event involving dencephahc structures. References 1. FISHER,C. M. and ADAMS,R. V.: Transient global amnesia. Acta Neurologica Scandinavica, 9): 1-83, 1964. 4O(~~ppl. 2. CAPLAN, L. R.: Transient global amnesia: criteria and classification. Neurology, 36: 441, 1986. 3. Lou, H.: Repeated episodes of transient global amnesia. Acta Neurologica Scandinavica, 44: 612-618, 1968. 4 BOGOUSSLAVSKY, J. and REGLI, F.: Transient global amnesia and stroke. European Neurology, 28: 106-110, 1988. 5. MATHEW, N. T. and ~ Y E RJ. ,S.: Pathogenesis and natural history oftransient global amnesia. Stroke, 5 : 303-311, 1974. 818 R.RaJaele e t al. 6. DEISENHAMMER, E.: Transient global amnesia as an epileptic manifestation.Joumal OfNeurology, 225: 289-292, 1981. 7. CAPLAN, L., CHEDRU, F., LHERMITT, F. el al.: Transient global amnesia and migraine. Neurology, 31: 1167-1170, 1981. 8. LISAK,R. P. and ZIMMEKMA",R. A.:Transient global amnesia due to a dominant hemisphere tumour. Archives ofNeurology (Chicago), 34: 317-318, 1977. Downloaded by [McMaster University] at 11:37 01 April 2016 9. MEADOR,K.J., ADAMS, R.J. and FLANIGIN, H. F.: Transient global amnesia and meningioma. Neurology, 35: 769-771, 1985. 10. F~SHER,C. M.: Concussion amnesia. Neurology, 16: 826-830, 1966. 11. CROWELL, G. F., STUMP,D. A,, BILLER, J. et al.: The transient global amnesia-migraine connection. Archives of Neurology (Chicago), 41: 75-79, 1984. 12. KUSHNER, M.J. and HAUSER, W. A,: Transient global amnesia: a case-control study. Annals OfNeurology, 18: 684-691, 1985. 13. MILLER, J. W., PETERSEN, R. C., METTER,E. J. et al.: Transient global amnesia: clinical characteristics and prognosis. Neurology, 37: 733-737, 1987. 14. KRITCHEVSKY, M., GRAFF-REDFORD, N. R. and DAMASIO, A. R.: Normal memory after damage to medial thalamus. Archives L$ Neurology, 44: 959-962, 1987.