The perturbation in water balance rather than any change in salt content is the main cause of hyponatremia, the most frequent electrolyte abnormality defined as serum sodium concentration <135 mEq/L. Hyponatremia may be divided as mild (Na>120 mEq/L) or severe (Na<120 mEq/L) hyponatremia, most frequently observed in elderly ICU hospitalized patients. Based on tonicity hyponatremia may be hypotonic (decreased concentration of solute), isotonic, and hypertonic (falsely low sodium). According to the volume of the extracellular fluid (ECF) hyponatremia is further divided as hypovolemic, euvolemic, or hypervolemic hyponatremia. Finally, hyponatremia may develop rapidly as acute (<48 h) with usually severe symptoms, or slowly as chronic hyponatremia, being usually asymptomatic or with mild symptoms. Patient’s medical history and clinical symptoms and signs could point to a certain diagnostic direction. Acute severe hyponatremia is presented with headaches, vomiting, nausea, fatigue, impaired cognition, gait with increased falls symptoms etc., while the severe symptomatology due to hyponatremic encephalopathy is presented as confusion, agitation, seizures, or even coma and death. Nevertheless, an urgent evaluation of the volume and neurological status is essential for prevention of neurological damages. The treatment of hyponatremia should of course be based on the underlying cause, the duration and degree of hyponatremia, the observed symptoms, and volume status of patient.

The term "Osmotic Demyelination Syndrome" (ODS) is synonymous with central pontine myelinolysis (CPM), denoting a condition characterized by brain damage, particularly affecting the white matter tracts of the pontine region. This damage arises due to rapid correction of metabolic imbalances, primarily cases of hyponatremia. Noteworthy triggers encompass severe burns, liver transplantations, anorexia nervosa, hyperemesis gravidarum, and hyperglycaemia, all linked to the development of CPM. Clinical manifestations encompass a spectrum of signs and symptoms, including dysphagia, dysarthria, spastic quadriparesis, pseudobulbar paralysis, ataxia, lethargy, tremors, disorientation, catatonia, and, in severe instances, locked-in syndrome and coma. A recent case involving a 45-year-old woman illustrates these complexities. Upon admission to the Medicine Intensive Care Unit, she presented with symptoms indicative of diminished responsiveness and bilateral weakness in upper and lower limbs. Of significance, the patient had a pre-existing medical history of hyperthyroidism. Extensive diagnostic investigations were undertaken, revealing compelling evidence of profound hyponatremia through blood analyses. Furthermore, magnetic resonance imaging (MRI) was performed, unveiling conspicuous areas of abnormal hyperintensity located in the central pons, intriguingly accompanied by spared peripheral regions. These radiological findings align with the characteristic pattern associated with osmotic demyelination syndrome, illuminating the underlying pathology.

In cancer patients, hyponatremia is detected in about 40% of cases at hospital admission and has been associated to a worse outcome. We have previously observed that cancer cells from differ-ent tissues show a significantly increased proliferation rate and invasion potential, when cul-tured in low extracellular [Na+]. We have recently developed an animal model of hyponatremia using Foxn1nu/nu mice. The aim of the present study was to compare tumor growth and inva-sivity of the neuroblastoma cell line SK-N-AS in hyponatremic vs. normonatremic mice. Ani-mals were subcutaneously implanted with luciferase-expressing SK-N-AS cells. When masses reached about 100 mm3, hyponatremia was induced in a subgroup of animals via desmopressin infusion. Tumor masses were significantly greater in hyponatremic mice, starting from day 14 and until the day of sacrifice (day 28). Immunohistochemical analysis showed a more intense vascularization and higher levels of expression of the proliferating cell nuclear antigen, chro-mogranin A and heme oxigenase-1 gene in hyponatremic mice. Finally, metalloproteases were also more abundantly expressed in hyponatremic animals compared to control ones. To our knowledge, this is the first in vivo demonstration that hyponatremia is associated to increased cancer growth by activating molecular mechanisms that promote proliferation, angiogenesis and invasivity.