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Possible case of peripheral osmotic demyelination syndrome
  1. P J Serrano-Castro1,
  2. G Alonso-Verdegay1,
  3. G López-Martínez2,
  4. A Arjona-Padillo1,
  5. J R Callejón1,
  6. V M Olmedo1,
  7. P Guardado-Santervás1,
  8. A Huete-Hurtado1,
  9. J Olivares-Romero1,
  10. C Naranjo Fernández1
  1. 1
    Unidad de Neurología Clínica y Diagnóstica, Hospital Torrecárdenas, Almería, Spain
  2. 2
    Servicio de Medicina Interna, Hospital Torrecárdenas, Almería, Spain
  1. Pedro J Serrano-Castro, MD, Calle Enrique Granados, 21, Aguadulce-Roquetas de Mar, Almería 04720, Spain; pedro.serrano.c{at}gmail.com or pserrano{at}meditex.es

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Central pontine myelinolysis (CPM) is an uncommon neurological syndrome that is usually related to the rapid restoration of a previous hyponatraemia. Although the most frequent location of CPM injury is the pons, it is now designated osmotic demyelination syndrome (ODS) because, as well as in the brainstem, these injuries can be observed in other parts of the central nervous system (CNS)—for example, the thalamus, subthalamic nucleus, external geniculate body, putamen, globus pallidum, internal capsule, white matter of cerebellum and the deep layers of the brain cortex. However, an exhaustive search of the literature (MEDLINE 1967–2007) has revealed no case report of peripheral nervous system (PNS) demyelination secondary to severe hyponatraemia.

Experimental models of hyponatraemia have shown a marked fall in brain levels of several organic osmolytes during the first few hours after the metabolic insult, followed by a slow restoration over several days.1 The rapid correction of hyponatraemia can lead to low brain concentrations of amino acids and creatine, even after serum sodium correction, producing a net shrinkage of the brain. A high sodium concentration without adequate concentrations of organic osmolytes may predispose the brain to osmotic injury.

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