LAUSR

A 68-year-old woman with no significant past medical history presented to our emergency department with a 6-h history of confusion and repetitive questioning of sudden onset. On assessment, she was amnestic but oriented to place, time and person. Neurological examination was otherwise unremarkable and a plain computed tomography of the head reported as normal. Initial blood tests included a serum sodium of 132 mmol/L (135– 145), but otherwise no abnormality of consequence. No recent serum sodium level (prior to presentation) was available. She was referred to general medicine, where a clinical diagnosis of transient global amnesia was made and she was admitted for observation. Eight hours later, she had witnessed a generalised tonic–clonic seizure. Blood tests immediately thereafter showed hyponatraemia to have worsened, serum sodium 118 mmol/L (135–145), with low serum osmolality of 241 mmol/kg (280–300). She was clinically euvolaemic and urine biochemistry included sodium of 69 mmol/L and osmolality of 399 mmol/kg (300–1200), consistent with the syndrome of inappropriate antidiuretic hormone (SIADH). Urgent cerebrospinal fluid obtained by lumbar puncture was normal, as was plasma cortisol (1019 nmol/L at 0721 h, normal 170–500) and thyroid stimulating hormone (1.16 mIU/L, normal 0.40– 4.00). A non-contrast magnetic resonance imaging (MRI) of the brain on Day 2 showed a punctate focus of restricted diffusion within the left hippocampus, visible on T2-weighted and diffusion-weighted sequences – an abnormality known to be associated with transient global amnesia (Fig. 1). Following the seizure, she had a severe hypoactive delirium disproportionate to a post-ictal state such that she required ventilatory support in the intensive care unit. She was treated with intravenous hypertonic saline and at the time of discharge had a normal serum sodium (139 mmol/L), urine sodium of 26 mmol/L and normalisation of her mental state with no further seizures. Of note, water intake was not restricted prior to the seizure and she was encouraged to drink. The presence of transient global amnesia may have masked the recognition of developing confusion. If this had been recognised, severe hyponatraemia may have been diagnosed earlier, prior to the seizure. Although well described as a clinical entity, the pathophysiology of transient global amnesia remains poorly understood. Multiple studies report an association with unilateral hippocampal changes on magnetic resonance diffusion-weighted imaging, with an incidence of 41– 85%. These are typically described as 1–3 mm highsignal foci in the CA1 domain, most prominent 24–48 h after the initial episode, persisting for 7–10 days and resolving on follow-up imaging performed at 1–6 months. Underlying pathological vascular processes have been hypothesised. We are only aware of one prior report of significant hyponatraemia in the context of transient global amnesia: a 2017 case report from Turkey describes a 56-year-