Prolonged reversible amnesia: A case report

Case Report

Prolonged Reversible Amnesia: A Case Report Ming-Chyi Pai, MD

A 55-year-old woman sustained an acute amnesia that lasted for 8 days. The results of a cerebral magnetic resonance imaging scan and an electroencephalogram were normal. A Wechsler Memory Scale-Revised (WMS-R) test performed 6 days after the event showed global impairment in every domain, except for attention/concentration. A single photon emission computed tomography (SPECT) scan taken 8 days after the event showed hypoperfusion in the left temporal and frontal areas. The results of a follow-up SPECT scan on the 40th day after the episode were normal. A second WMS-R test showed some improvement on the 40th day after the event and considerable improvement on the 176th day. The clinical feature of the patient meets the criteria of transient global amnesia (TGA), except for her protracted course. It was not amnesic stroke, however, because of its reversibility and because there were no accompanying neurological signs. This case raises some implications of the pathogenesis of TGA and the clinical applicability of research criteria. Key Words: Amnesic stroke--Neuropsychological test--Transient global amnesia.

Transient global amnesia (TGA) is a clinical syndrome characterized b y the abrupt onset of severe anterograde amnesia (AA), usually accompanied by repetitive questioning. 1 It usually occurs in middle-aged or elderly patients and lasts a few hours. Although thousands of TGA cases have been reported, its definitive cause remains unknown. A m o n g the most widely believed causes of TGA include cerebrovascular disease, epilepsy, and migraine. Other conditions related to TGA include cerebral angiography, 2 cerebral tumor, 3 and cerebral hemorrhage. 4 One of the criteria for the diagnosis of TGA is that the patient must recover from the attack within 24 hours. 5 Some patients, however, suffer transient amnesia, lasting longer than a day, from which From the Division of Behavioral Neurology, Department of Neurology, National Cheng Kung University Hospital, Tainan, Taiwan, Republic of China. Received July 28, 1999; accepted October 1,1999. Supported in part by a grant (NHRI-GT-EX89P707C) from the National Health Research Institute, Republic of China. Address reprint requests to Ming-Chyi Pai, MD, Department of Neurology, National Cheng Kung University Hospital, 138 Shen Li Road, Tainan, Taiwan 704, Republic of China. Copyright 9 2000 by National Stroke Association 1052-3057/00/0902-000753.00/0 86

they ultimately fully recover. This makes stringent criteria for the diagnosis of transient amnesia impractical.

Case Report Clinical Course A 55-year-old, right-handed w o m a n was in excellent general health without any past history of vascular disease, migraine, or psychiatric disorder before suffering an acute onset of protracted amnesia. At about 6 AM on April 12, 1997, she went out to perform her regular leisure activities. First, she m a d e an appointment with her friends for a singing contest to be heId several days later. She behaved quite normally until suddenly, at 7:30 AM, she repetitively asked when the contest was going to be held. Meanwhile, she did not know that she had already sung 3 songs. She complained of a headache and rode home b y herself, taking the usual time from the p a r k to her house. " W h y am I here?", " H o w did I get back?", "What h a p p e n e d to m y left hand?", and "Why am I wearing this jogging suit?", the patient asked repeatedly after arriving at home. She told her family about her dizziness and then went to bed. She awoke at 3 PM and was astonished at the jogging suit she was wearing. In addition, she told her

Journal of Stroke and Cerebrovascular Diseases, Vol. 9, No. 2 (March-April), 2000: pp 86-88

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daughter that she had dreamed of having gone to a park and then riding a bicycle home. She recovered her memory gradually and began to learn new things in the evening, but never fully recovered. Before she had left to exercise in the morning, she had prepared a Chinese herbal treatment for tendinitis of her left thumb. She denied making it, however, when her husband asked her in the evening if she wanted to take the medicine. She also could not remember a receipt she had been given by a friend the same morning. There were no known immediate precipitants before the episode, such as cold weather, sexual intercourse, vigorous exercise, stress, or emotional disturbance. On the next day, she performed her activities as usual, except for looking bemused and retarded. She went to her neighbors' house and had a long talk with them, but her memory seemed to be a complete blank. At one point she said, "I haven't seen you for ages" to a friend with w h o m she had just spoken the day before. Three days after her episode of TGA, she was admitted to the hospital. She was found to have no neurological deficits, except for the memory deficit and a dreamlike feeling. She had no history of epilepsy, hypertension, diabetes mellitus, hyperlipidemia, or other systemic disease. She had experienced menopause 6 months previously and had been taking 0.625 mg of Premarin (WyethAyerst, Philadelphia, PA) daily since then. The patient was discharged from the hospital 6 days after her TGA episode. At that time, she had fully recovered her memory and was able to lead a normal life. There had been no recurrence of TGA after 27 months. If asked, the patient could describe her TGA episode in detail, but could not remember anything that occurred that day from 6 AMto 3 PM. She said that she had a strange feeling soon after the onset of the attack, when she was singing on the first day. Assessments

The results of investigation for a stroke, which included carotid duplex sonography, a scalp electroencephalogram

Figure 1. The first SPECT scan, performed 8 days after the patient's TGA episode, showing a focus of decreased uptake in the region of the left medial temporal lobe.

(EEG) and a cerebral magnetic resonance imaging (MRI) scan, were normal. The cerebral MRI scan showed no abnormal signal, especially in the mesial temporal regions, thalamus, or fornix. The laboratory data were within normal limits. The patient did not feel recovered from her memory impairment until 8 days after the event. On that day, a cerebral Technetium 99m hexylmethypropylene amineotine single photon emission computed tomography (SPECT) perfusion study was performed, showing hypoperfusion in the left mesial temporal and frontal areas (Fig 1). The patient has an elementary school education. She repeated 5 digits forward and 4 backward. Her general intelligence was preserved. The Wechsler Memory Scale-Revised (WMS-R) 6 test was administered 6 days after the patient's TGA event and yielded abnormal results in every subset, except for immediate memory. The follow-up WMS-R test performed 40 days after the TGA event revealed improvement, and the results of a follow-up SPECT scan were normal. The third and fourth WMS-R tests performed 176 and 264 days after the TGA episode, respectively, showed further improvement and stability (Table 1).

Discussion

Although this patient stopped asking repetitive questions and began to gain new memory within hours, her memory impairment lasted a protracted period, based on the findings of her behavior, the results of neuropsychological tests and SPECT examinations. Judging from the follow-up WMS-R test and the SPECT scan, however, it was reversible. The protracted course of the memory deficit defied the criteria of TGA, s and the reversibility of the memory deficit defied the definition of an amnesic stroke. 7 If this patient had neither TGA nor amnesic stroke, what was her diagnosis? Obviously, from a clinical viewpoint, there is a gray zone between TGA and amnesic stroke. Except for the protracted course, the clinical features of this patient were identical to TGA. Although TGA may be a syndrome of varied etiology, the neural

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Table 1. Neuropsychological tests results Days after TGA event Test

3

Digit span (forward/backward) CCFA SPMSQ HDS-R WMS-R General memory Attention/concentration Verbal memory Visual memory Delayed memory

5/4 10/10 9/10 27.5/30 ------

6 40

176

264

8/5 10/10 9/10

62 92 69 75 74

89 96 91 88 94

99 100 97 108 109

95 90 89 110 105

Abbreviations: CCFA, Chinese version of Cortical Function Assessment16; SPMSQ, Short Portable Mental State Questionnairet7; HDS-R, Hasegawa Dementia Scale-Revised~S; WMS-R, Wechsler Memory Scale-Revised.6 substrates accounting for declarative memory would transiently dysfunction. Although most cases of TGA last for 5 to 6 hours, their ranges are diverse and sometime difficult to estimate, s-l~ Clinical researchers divide TGA into subgroups according to duration to predict the prognosis. Some authors consider that attacks with a duration of less than 1 hour harbor a tendency to recur and favor an epileptic origin,s although all do not support this viewpoint. 9 At the other extreme, TGA lasting more than 24 hours is related to cerebral ischemic episodes and has a poor prognosis. Very few patients, however, develop a cerebral ischemic stroke immediately after an episode of TGA. 11-12If we consider TGA an ischemic phenomenon, the manifestation of the patient in this report resembled the condition of reversible ischemic neurological deficit. From the results of investigation and long-term follow-up, however, there was no strong evidence relating this episode to a stroke. Reversible amnesic syndromes may occur in rare instances of infarction involving the mesial temporal regions or the thalamus. The clinical manifestation, the finding of the cerebral MRI scan, and the results of follow-up SPECT examination of the patient, however, made this unlikely. From the neuropsychological viewpoint, there was a discrepancy between the patient's awareness and her actual memory function. Serial follow-up neuropsychological tests for patients with TGA revealed prolonged subclinical deficits that continued to improve even for several months after the attack. 13 Patients with TGA always have a profound AA; the degree of retrograde amnesia (RA) is extremely variable. Consolidation may be the most obvious interpretation of RA in TGA. 13 Others suggest that the problem may be one of retrieval rather than failure to consolidate. 14 This patient had a dreamy

sensation about events that occurred shortly before and during her memory gap. This implies that at least some memory traces continued to register, albeit incomplete, after the TGA episode began. It is difficult, however, to differentiate between memories intact from the beginning and those relearned. 15 In conclusion, when encountering a patient with acute amnesia, especially in the early period of the disorder, one should not stick to the strLngent criteria of the duration because a research criterion is different from a clinical one.

References 1. Fisher CM, Adams RB. Transient global amnesia. Acta Neurol Scand 1964;40:1-83 (suppl 9). 2. Schamschula RG, Soo MY. Transient global amnesia following cerebral angiography with non-ionic contrast medium. Australas Radiol 1994;38:196-198. 3. Po HL, Hseuh IH. Transient global amnesia associated with a right sphenoid ridge meningioma: A case report. Chin Med J 1990;46:113-116. 4. Chen WH, Liu JS, Wu SC, et al. Transient global amnesia and thalamic hemorrhage. Clin Neurol Neurosurg 1996; 98:309-311. 5. Hodges JR. Transient global amnesia: Clinical and neuropsychological aspects. London: Saunders, 1991. 6. Wechsler D. Wechsler memory scale-revised. New York: The Psychological Corporation, 1984. 7. Benson DF, Marsden CD, Meadows JC. The amnesic stroke. Neurology 1973;23:400 (abstr). 8. Hodges JR, Warlow CP. Syndromes of transient amnesia: Towards a classification. A study of 153 cases. J Neurol Neurosurg Psychiatry 1990;53:834-843. 9. Melo TP, Ferro JM, Paiva T. Are brief or recurrent transient global amnesias of epileptic origin? J Neurol Neurosurg Psychiatry 1994;57:622-625. 10. Pai MC, Yang SS. Transient global amnesia: A retrospective study of 25 patients. Chin Med J 1999;62:140-145. 11. Bogousslavsky J, Regli F. Transient global amnesia and stroke. Eur Neurol 1988;28:106-110. 12. Zorzon M, Antonutti L, Mase G. Transient global amnesia and transient ischemic attack. Natural history, vascular risk factors, and associated conditions. Stroke 1995;26: 1536-1542. 13. Hodges JR, Ward CD. Observation during transient global amnesia. Brain 1989;112:595-620. 14. Understanding amnesia. In: Baddeley A, ed. Human memory. Hove, UK: Lawrence Erlbaum, 1990:412-413. 15. Kapur N. How can we best explain retrograde amnesia in human memory disorder? Memory 1997;5:115-129. 16. Pai MC, Lai ML, Tsai JJ, et aL A brief cortical function assessment in cerebral damage. Acta Neurol Sin 1994;3:813. 17. Pfeiffer E. A short portable mental status questionnaire for the assessment of organic brain deficit in elderly patients. J Am Geriatr Soc 1975;10:433-441. 18. Hasegawa K. The clinical assessment of dementia in the aged: A dementia screening scale for psychogeriatric patients. In: Bergener M, Lehr U, Lang E, SchmitzScherzer R, eds. Aging in the eighties and beyond. New York: Springer, 1983:207-218.