Hyponatremia Mimicking Transient Global Amnesia

Abstract

Dear Editor, Transient global amnesia (TGA) is a clinical syndrome characterized by temporary loss of anterograde memory, followed by retrograde amnesia, with preserved consciousness, attention and awareness. It usually lasts 1-8 hours and recovers without need for treatment. TGA usually occurs as a single attack and does not recur. The annual recurrence rate is reported to be 6-10%. Time and place orientation may be impaired and patients may repeat the same questions, leading to anxiety and agitation. However, consciousness is not affected and higher cortical activities such as driving and talking are preserved. TGA is often seen in patients aged over 50 years and is equally common in both sexes.Although TGA was first described in 1956, no definite pathogenesis has been revealed. Ischemic, epileptic, metabolic, migrainous, and psychological factors are thought to be responsible. The affected brain regions are memory-related structures such as the thalamus, hippocampus (especially CA1 domain), splenium of the corpus callosum, fornix, and cingulate gyrus (1,2). In contrast, there are usually no etiologic factors in patients. Ischemia (vasospasm, venous congestion) or changes in neurotransmitter concentrations are usually listed among the causes of TGA. To the best of our knowledge, TGA accompanied by hyponatremia has never been identified in the literature.A man aged 56 years was admitted to our neurology clinic with memory loss lasting 5-6 hours. He did not remember where he lived and how he had been brought to the hospital during this time. He was asking the same questions again and again. The patient was fully conscious, he could recognize his relatives and could fulfill instructions given by the physician. It was observed that he could solve mathematical problems and count backwards from 100 by 7 (93, 86…) in serial 7 examination. It was learned that there had had no such previous attacks, and that he only had arterial hypertension in his medical history; he was not on any antihypertensive drugs. The patient's wife said that the patient was on salt restriction and he drank about 6 liters of water that day. His blood pressure was normal and the neurologic examination was normal except for the amnestic situation. The other blood tests were within normal limits except that the serum sodium level, which was 120 mEq/L. No lesions were detected in computed tomography and diffusion-weighted magnetic resonance imaging (MRI) scans. Electroencephalography (EEG) of the patient was reported as normal. After sodium replacement, the patient returned to normal, recalling events that occurred before the attack, but he could not remember the 8-hour symptomatic period. The patient was diagnosed as having sodium electrolyte imbalance mimicking TGA.Ad dress for Cor res pon den ce/Ya z›fl ma Ad re si: Babürhan Güldiken MD,

Syndrome of inappropriate anti‐diuretic hormone secondary to transient global amnesia

“…The amnesia resolved after the correction of hyponatraemia and the eventual diagnosis was 'sodium electrolyte imbalance mimicking TGA'. 6 The case described here raises an alternative possibility of SIADH caused by transient global amnesia (TGA). Here, severe hyponatraemia developed after the onset of TGA, biochemical testing was diagnostic of SIADH and no alternative cause for SIADH was identified.…”