Introduction
The transitory memory disturbance known
as Transient Global Amnesia (TGA) remains an enigma from a pathogenic point of view. It manifests as a paroxysmal transient loss of memory function. Inspite of its typical benign prognosis, transient global amnesia is frightening experience for the patients and their relatives. More over an episode of TGA usually leads to extensive investigation of patient in search of organic alternatives that might be responsible for the event. The syndrome of transient global amnesia affects the middle age and elderly. Attack usually last for 1-24 hrs.¹

Case Report
Case 1
A 42 year old female, hypertensive since 4 yrs. on treatment presented one evening, at 6 pm with sudden onset of confusion, amnesia with one episode of vomiting. There had been no physical exertion or travel. There was no migrainous attack, headache, fever or seizures. There had been no similar episode before. She had been upset over her son who was not studying for his exams. She recognised the attending doctor (who was known to her) and her relatives during the episode. She was oriented in place and person but she was bewildered and repeatedly kept asking questions about present and recent events like where were the children, why was she at the hospital, when did she reach the hospital, etc.

On examination she was afebrile, had a regular pulse rate of 72/min, blood pressure of 150/110 mmHg. On neurological examination speech, cranial nerves were normal. There was no sensory motor deficit. On mental status examination the patient appeared to be well kept, she was co-operative and communicative, appeared perplexed; there was no tics or mannerisms noted. Speech was relevant and coherent, but revealed stereotyped questions regarding events of that day. Psychomotor activity was normal. She was oriented to place and person but disoriented to time and date. Immediate memory was intact - patient was able to recall digit forward 5, backwards 4. Recent memory was impaired, was not able to recall events of that whole day including tea that she had 2 hours previously. She was able to do simple calculations, attention was rousable and sustained, affect was anxious, there were no perceptual disturbances, judgement was intact. Remote memory was intact, able to recall all past events. There was no evidence of seizures; biorhythms were normal. Neuropsychological testing using the 1st three tests of Wechsler memory scale was done on admission, 4 hours post admission. The score was 13/20 both times. Cardiovascular system examination was normal. Investigations revealed normal biochemical parameters, ECG, EEG, CT scan brain, MRI brain. The dosage of her antihypertensive medication was stepped up and she was given mild sedation. By next morning nearly after 14 hrs she recovered fully. Wechsler memory scale test was repeated; the score was 19/20. Till todate, she is amensic for that day, has no recall of the events whatsoever.

Case 2
A 60 year old man was brought by his wife with complaints of sudden loss of memory. While he accused her of not giving him breakfast and lunch that day, she said that he was telling lies and had gone crazy. There was no headache, nausea, vomiting, fever. There was no physical or emotional stress, no migrainous attack, seizures or similar episode in the past. There was no history of hypertension/diabetes/ischaemic heart disease/stroke. Patient was not an alcoholic. On examination he was afebrile, pulse was 72/min, regular; blood pressure 130/70 mmHg. On neurological examination there was no sensory motor deficit, cranial nerves were normal. On mental status examination, he had a stereotyped speech, was repeatedly blaming his wife for not giving him meals. Affect was angry and irritable. He was disoriented to time. Registration and recall could not be tested as patient was illiterate and unable to understand the requirements of the test. Recent memory was impaired - he said he had not had meals and that his son had not visited him (though actually he was with the parents that morning). Remote memory was intact. Rest of the systemic examination was normal. Investigations revealed normal biochemical parameters and a single interpolated ventricular ectopic in rhythm strip of the ECG. CT scan brain, MRI brain, EEG were normal. Patient was kept under observation and recovered completely after 10 hrs. After recovery, mental status examination revealed that he was amnesic for that day - no recall of being taken to hospital, but all other parameters were normal.

Discussion
TGA is a well described phenomenon for many years, and is characterized by sudden onset of complete anterograde loss of memory and learning abilities usually occurring in middle age and elderly persons.1 Onset of memory loss may occur in context of emotional stimulus or physical exertion.2 During the attack, the individual is alert and communicative. There are no neurological signs and symptoms. Loss of memory is accompanied by repetitive questioning about present events.1 Immediate recall ability is usually preserved as is remote memory. But patients can experience a striking loss of memory for recent events and an impaired ability to retain new information. The attack lasts for 1-24 hrs, after which the patient is absolutely normal but there is total amnesia for the episode and those 24 hours (or less) are forever erased from the patient's life. Recurrences are rare but do occur in small proportion. Aetiopathogenesis is not clear.¹ TGA has been particularly related to migraine, epilepsy and cerebral vascular pathology, although its aetiology has not been fully determined.³ A Mayo clinic review of 277 patients with TGA found a past history of migraine in 14%, cerebrovascular disease in 11% and epilepsy in 7%.² Studies have shown bilateral mesial temporal lobe hypoperfusion on SPECT scan in TGA that partially resolved after 24 hrs and return to normal at 3 months.⁴ Imaging studies have also shown hippocampus and thalamic hypoperfusion.⁵ In a review by Santos S et al, the authors have concluded that the most generally accepted theory is vascular in origin; TGA is probably a transient ischaemic phenomenon triggered (or not) following an attack of migraine. Risk factors for TGA are arterial hypertension, dyslipaemia and migraine.⁶

We decided to report these two cases to bring out the importance of this entity. It is imperative to know that it really exists. These cases, because of their transient nature and paucity of clinical signs are often mistaken for episodes of hysteria/psychosis. In a lighter tone, it is an ideal escape window in tight situations. In one of our patient's words to his wife - "At my age, if you're healthy and something out of the blue hits you, amnesia is the perfect affliction. I now have the perfect excuse for forgetting our anniversary or birthday".

References

1. Rossor M. Neuropsychological disorders, dementia and behavioural neurology. In : Brain's Diseases of the Nervous System. Michael Donaghy (Ed). 11th Ed. Oxford University Press Inc. New York, 2001; 736-74.
2. Bird TD. Memory loss and dementia. In : Harrison's Principles of Internal Medicine. Braunwald E, Hauser SL, Fauci AS, Longo DL, Kasper DL, Jamson JL (Eds.) 15th ed. McGraw-Hill, New York, 2001; 148-55.
3. Tuduri I, Carneado J, Fragoso M, Ortiz P, Jimenez - Ortiz C. Amnesia global transitoria factores de riesgo vascular. Revista de Neurologia 2003; 30 (5) : 418-21.
4. Jovin TG, Vitti RA. McCluskey LF. Evolution of temporal lobe hypoperfusion in transient global amnesia : a serial single photon emission computed tomography study. J Neuroimaging 2000; 10 (4) : 238-41.
5. Masson C. Ictus amnisique. Press Medicale 2000; 29 (30) : 1677-82.
6. Santos S, Lopez J, Tejero C, Iniguez C, Lalana JM, Morales F. Amnesia global transitoria : revion de 58 cases. Revista de Neurologia 2000; 30 (12) : 1113-7.