Central and extrapontine myelinolysis in a patient in spite of a careful correction of hyponatremia

We report the case of a 54-year-old alcoholic female patient who was hosita lized for neurologic alterations along with a severe hyponatremia (plasma N a+: 97 m-Eq/1). She suffered from potomania and was given, a few days befor e admission, a thiazide diuretic for hypertension. A careful correction of plasma Na+ levels was initiated over a 48-hour period (rate of correction < 10 mEq/l/24h) in order to avoid brain demyelination. After a 2-day period of clinical improvement, her neurologic condition started to deteriorate. B y the 5th day of admission, she became tetraplegic, presented pseudobulbar palsy, ataxia, strabism, extrapyramidal stiffness and clouding of conscious ness. Scintigraphic and MRI investigations demonstrated pontine and extrapo ntine lesions associated with Gayet-Wernicke encephalopathy. After correcti on of ionic disorders (hyponatremia, hypokaliemia) and vitamin B (thiamine) deficiency, the patient almost completely recovered without notable disabi lities. This case illustrates that profound hyponatremia, in a paradigm of slow onset, can be compatible with life. It also demonstrates that demyelin ating lesions, usually considered as a consequence of a too fast correction of hyponatremia, may occur despite the strict observance of recent guideli nes. There is increasing evidence to suggest that pontine swelling and dysf unction may sometimes occur in alcoholic patients even in absence of distur bance in plasma Na+ levels. It is therefore of importance, while managing a hyponatremic alcoholic patient, to identify additional risk factors (hypok aliemia, hypophosphoremia, seizure-induced hypoxemia, malnutrition with vit amin B deficiency) for brain demyelination and to correct them appropriatel y.