SHORT COMMU NCATION Acta Neurol Scand., 1988:77:331-334 Key words: transient global amnesia; hypertensive haematoma; lefl thalamus; epileptic discharges. Left thalamic hypertensive haemorrhage presenting as transient global amnesia Majaz Moonis’, S.Jainl, K. Prasadl, N. K. Mishra2, R. K. Goulatia2, M. C. Maheshwaril Departments of lNeurology and 2Neuro-Radiology, Neurosciences Centre, All India Institute of Medical Sciences, New Delhi, India ABSTRACT - A case is described which presented as transient global amnesia (TGA) due to a critically placed intracerebral hypertensive haematoma in the left thalamic region, with epileptic discharges arising from the same area. It is proposed that intracerebral haematomas may occasionally present as a clinically well-defined neurological syndrome. The deficit in such cases is probably not due to the underlying direct tissue damage but secondary to indirect pressure or ischaemic insults. Accepted f o r publication October 12, 1987 Transient global amnesia (TGA) has been defined as a clinical syndrome consisting of an episode of the inability to assimilate new information for a period of time while retaining remote memory (1). TGA usually lasts for less than 24 h, leaving the patient amnesic of events occurring during the attack and there is usually no other deficit. Ischaemia in the posterior cerebral artery territory affecting the mesial temporal lobe and hippocampal regions has been attributed to be the most common cause for TGA (2). An epileptiform aetiology has been implicated in other reports (3, 4). Various unusual causes of TGA have been reported and include cardiac dysrhythmia in digitalis toxicity (9,embolism complicating coronary angiography (6), cerebral neoplasm (7), migraine (1, 8), toxic metabolic disturbances (9),complication of selective cerebral angiography (1013) and arterial DSA (14), and a left temporal lobe abscess (15). A single case of subarachnoid haemorrhage presenting as TGA has also been reported (16). Our report describes a TGA-like presentation in a patient who had a hypertensive intracerebral left thalamic haemorrhage. Case report On September 28, 1986 at 10.00 a.m., a 53-year-old hypertensive right-handed man felt a sudden severe generalised headache which was not associated with altered sensorium, vomiting, visual disturbances, motor weakness or any sensory dysfunction. The headache subsided after one hour with analgesic tablets. After 4 h, while involved in a conversation with a friend, he was noted to be confused. On being questioned, he told that he could not remember the topic of their conversation. His wife was called and he recognised her immediately. He complained that his mind had gone blank and he could not recall, anything. He became a little agitated. At 4.30 p.m. he was admitted to the neurological services of the All India Institute of Medical Sciences. After admission his blood pressure was recorded to be 150/110 mmHg. The neurological examination was normal except that he was disoriented about time and had dyscalculia with astereogonosis on the right side of his body. He had been mildly hypertensive for one year but was not under any treatment. He had no history of migraine. When examined the next day he had amnesia of the previous 24 h and still had dyscalculia and rightsided asterogonosis. His blood pressure was controlled with Metoprolol tablets. His routine blood chemistry and ECG was normal. An unenhanced CT scan done on the day after his admission revealed a well-circumscribed area of high attenuation (mean value: 63 Hounsfield units) in the left thalamic area (Fig. la). The volume of this haematoma was estimated to be 4.4 332 MAJAZ MOONIS ET AL Fig. l a . Unenhanced CT Scan done on the day after admission showing a well-circumscribed area of high attenuation (mean value:63 Hounsfield units) in the left thalamic area. Fig. Ib. A repeat unenhanced CT scan done on January 30, 1987 which shows the total resolution of the haematoma. ml. This was interpreted as a hypertensive intracerebral haematoma. An EEG done on the same day revealed bifrontal slow waves at 4-5 Hz and sharp wave discharges from the left central area (C3: Fig. 2). Cerebral Angiography was not done. When examined at 6 weeks and about 9 months after discharge he was normal except for amnesia of all events during those 24 h (10 am; September 28 to 10 am September 29, 1986). He had no dyscalculia or astereogonosia. The EEG’s repeated twice on follow up and a repeat unenhanced CT scan (Fig. Ib) done on January 30, 1987, were normal. patient a clinical presentation as TGA was associated with acalculia and right-sided astereogonosia. The C. T. scan revealed a haematoma in the left thalamic region, which was probably responsible for his symptoms. The previous case reports of TGA due to a dominant hemisphere tumor (7) and left temporal abscess (15) support our hypothesis that a critically placed lesion such as haematoma can also give rise to a clinical picture of TGA. The EEG done soon after he was admitted revealed sharpwave discharges arising from the left central region with bifrontal slowing. These EEG findings are interesting and have support in various reports where an epileptogenic disturbance has been implicated as a cause for TGA (3, 4). Of further interest is a report of 7 patients with TGA, 5 of whom had epileptogenic discharges that originated from the medial temporal lobes during sleep (17). In our patient, we postulate that the haematoma lying in the left thalamic region triggered the epileptogenic EEG discharges arising from the same area and was ultimately responsible for his clinical presentation like TGA. His other clinical findings of acalculia and right sided anosogonosia and Discussion TGA as a clinical entity is now well recognized but its pathogenesis is not well understood (13). TGA is commonly believed to be due to dysfunction of or damage to the hippocampal, parahippocampal and mamillary body system. In most cases an ischaemic insult to these areas supplied by the posterior cerebral arteries is thought to be the trigger for TGA (2, 13). In our HYPERTENSIVE HAEMORRHAGE AS TGA 333 Acknowledgement The authors thank Mr. R. Sharma for his secretarial assistance. References 1 Fisher C M, Adams R D. Transient global amnesia. Acta Fig. 2. The EEG done on the day after admission showing bifrontal slow waves at 4-5 Hz and sharp wave discharges from the left central area (CJ. the EEG changes improved on follow up as would be expected with the resolution of the haematoma. Intracranial haemorrhage as a cause for TGA is extremely unusual. Only 2 reports of acute amnesia due to intracranial haemorrhage have been abstracted in the English literature which mention a haematoma of the third ventricle and the fornix (18). and a haematoma of the left cerebral hemisphere (19) as the possible cause of acute amnesia. Our patient had the unusual and interesting combination of left thalamic hypertensive haematoma with epileptogenic focus in the same area as the possible underlying mechanism for his TGA-like presentation. The rarity of similar reports prompted us to report this case. Our previous exprience of having seen 2 cases of pure motor hemiparesis due to hypertensive and nonhypertensive putaminal haemorrhaye with very good prognosis (20, 21) lends support to our belief that, occasionally, intracerebral haematomas may present as specific clinical syndromes. The neurological deficit in such cases is due to pressure effects and/or secondary ischaemia rather than direct tissue damage due to the haematoma itself. 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Acute amnesia caused by a haematoma of the third ventricle and the fornix. Acta Neurol Belg 1984:84(5):243-253 (Engl abstr.). 19. Matias-Guiu J et al. Amnesic ictus due to a haematoma of the left cerebral hemisphere (letter). Rev Clin Esp 1985:177(5):237. 334 MAJAZ MOONIS ET AL 20. Jain S , Maheshwari M C , Dhamija R M. Mishra N K. Pure motor hemiparesis due to hypertensive putaminal haemorrhage. Eur Neurol 1985:24:205-207. 21. Jain S, Mishra N K , Maheshwari M C. Pure motor hemiparesis due to non-hypertensive putaminal haemorrhage. J Neurol 1985232381-382. Address Dr. Sarish Jain Department of Neurology AIIMS New Delhi - 110029 India