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An exotic cause for confusion in the garden
  1. F Williams,
  2. L Ginsberg,
  3. R Brenner,
  4. A Cohen
  1. Medical Student
    Department of Neurology, Royal Free Hospital, London, UK
  2. Consultant Neurologist
    Department of Neurology, Royal Free Hospital, London, UK
  3. Consultant Neurologist
    Department of Neurology, Royal Free Hospital, London, UK
  4. Specialist Registrar
    Department of Neurology, Royal Free Hospital, London, UK
  1. Dr A Cohen, Department of Neurology, Royal Free Hospital, London NW3 2QG, UK; acohen{at}

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A 70-year-old retired accountant presented with progressive confusion. He was unable to give a clear account of recent events so his wife provided most of the history. She had first noticed four months previously that he had been unable to organise social events for his local Rotary club, and also had lost his ability to manage the household finances. There was then a progressive decline in his memory and organisational skills with increasing confusion about everyday events. In addition he had developed a tremor when holding the newspaper or trying to write. He also complained of muscle cramps in his legs and a band of sensitivity around his abdomen, which were severe enough to wake him at night. He appeared anxious and confused at social occasions, and was sweating and complaining that his head felt hot. The only significant medical history was a raised blood cholesterol for which he was taking simvastatin. There was no relevant family history.

General examination was normal and he was afebrile. On cranial nerve examination he had jerky pursuit eye movements and slow tongue movements. On examination of the limbs he had normal tone, power, reflexes and sensation, but impaired coordination; there was a fine postural tremor in the hands and a bilateral intention tremor, left worse than right. His gait was slow and broad-based. He scored 20/30 on Folstein’s Mini-Mental State Examination (MMSE), and 71% on the Addenbrooke’s cognitive examination (ACE). Detailed neuropsychological testing showed global cognitive impairment suggesting both cortical and subcortical involvement.

Initial blood tests showed a sodium of 127 mmol/l and a raised ESR (37 mm/h). Further evaluation of the hyponatraemia revealed a low plasma osmolality (268 mOsm/kg) (normal 275–295 mOsm/kg), inappropriately high urine osmolality (676 mOsm/kg) and high urine sodium (67 mmol/l) in the absence of hypovolaemia, confirming the diagnosis …

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