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• W2529539420 abstract "Osmotic demyelination syndromes (ODS) include central pontine and extrapontine myelinolysis [ 1 Martin R.J. Central pontine and extrapontine myelinolysis: the osmotic demyelination syndromes. J. Neurol. Neurosurg. Psychiatry. 2004; 75: iii22-iii28 Crossref PubMed Scopus (360) Google Scholar , 2 Huq S. Wong M. Chan H. Crimmins D. Osmotic demyelination syndromes: central and extrapontine myelinolysis. J. Clin. Neurosci. 2007; 14: 684-688 Abstract Full Text Full Text PDF PubMed Scopus (40) Google Scholar , 3 Hurley R.A. Filley C.M. Taber K.H. Central pontine myelinolysis: a metabolic disorder of myelin. J. Neuropsychiatr. Clin. Neurosci. 2011; 23: 369-374 Crossref PubMed Scopus (30) Google Scholar ]. Central pontine myelinolysis was first described by Adams and colleagues as occurring in alcoholic and malnourished patients [ [4] Adams R.D. Victor M. Mancall E.L. Central pontine myelinolysis: a hitherto undescribed disease occurring in alcoholic and malnourished patients. Arch. Neurol. Psychiatr. 1959; 81: 154-172 Crossref PubMed Scopus (674) Google Scholar ]. Both syndromes result from symmetrical myelin sheaths' disruption in areas where white matter becomes exposed to osmotically active substances cleared from edematous grey matter, namely, the crossing pontocerebellar fibers within the pontine nuclei and other grey matter regions containing heavily myelinated fibers, such as cerebellum, lateral geniculate body, external, and extreme capsules, corpus callosum, striatum, thalamus and neocortical grey-white matter junctions [ 1 Martin R.J. Central pontine and extrapontine myelinolysis: the osmotic demyelination syndromes. J. Neurol. Neurosurg. Psychiatry. 2004; 75: iii22-iii28 Crossref PubMed Scopus (360) Google Scholar , 5 Hurley R.A. Flashman L.A. Chow T.W. Taber K.H. The brainstem: anatomy, assessment, and clinical syndromes. J. Neuropsychiatr. Clin. Neurosci. 2010; 22: iv1-iv7 Crossref Scopus (10) Google Scholar , 6 Ismail F.Y. Szollics A. Szolics M. Nagelkerke N. Ljubisavljevic M. Clinical semiology and neuroradiologic correlates of acute hypernatremic osmotic challenge in adults: a literature review. AJNR Am. J. Neuroradiol. 2013; 34: 2225-2232 Crossref PubMed Scopus (19) Google Scholar ]. The theory in place is a reduced adaptive capacity of neuroglia to large shifts in serum osmolality [ [2] Huq S. Wong M. Chan H. Crimmins D. Osmotic demyelination syndromes: central and extrapontine myelinolysis. J. Clin. Neurosci. 2007; 14: 684-688 Abstract Full Text Full Text PDF PubMed Scopus (40) Google Scholar ]. Hereafter, a hyperosmotic environment induces glial dehydration and apoptosis, with subsequent demyelination [ [7] Kumar S. Fowler M. Gonzalez-Toledo E. Jaffe S.L. Central pontine myelinolysis, an update. Neurol. Res. 2006; 28: 360-366 Crossref PubMed Scopus (94) Google Scholar ]. There is a well-established link between these disorders and rapid osmolar shifts, particularly precipitous correction of sodium in hyponatremic patients [ [8] Singh T.D. Fugate J.E. Rabinstein A.A. Central pontine and extrapontine myelinolysis: a systematic review. Eur. J. Neurol. 2014; 21: 1443-1450 Crossref PubMed Scopus (134) Google Scholar ]. However, it has been increasingly recognized its occurrence in the setting of other osmotic challenges, such as hyper and hypoglycemia and hypernatremia [ [6] Ismail F.Y. Szollics A. Szolics M. Nagelkerke N. Ljubisavljevic M. Clinical semiology and neuroradiologic correlates of acute hypernatremic osmotic challenge in adults: a literature review. AJNR Am. J. Neuroradiol. 2013; 34: 2225-2232 Crossref PubMed Scopus (19) Google Scholar ]. Besides alcoholism and malnutrition, other conditions may predispose the occurrence of these imbalances, such as prolonged diuretic use, liver transplant, central and nephrogenic diabetes insipidus [ [6] Ismail F.Y. Szollics A. Szolics M. Nagelkerke N. Ljubisavljevic M. Clinical semiology and neuroradiologic correlates of acute hypernatremic osmotic challenge in adults: a literature review. AJNR Am. J. Neuroradiol. 2013; 34: 2225-2232 Crossref PubMed Scopus (19) Google Scholar ], and psychiatric conditions, namely psychogenic polydipsia and eating disorders [ 1 Martin R.J. Central pontine and extrapontine myelinolysis: the osmotic demyelination syndromes. J. Neurol. Neurosurg. Psychiatry. 2004; 75: iii22-iii28 Crossref PubMed Scopus (360) Google Scholar , 9 Patel A.S. Matthews L. Bruce-Jones W. Central pontine myelinolysis as a complication of refeeding syndrome in a patient with anorexia nervosa. J. Neuropsychiatr. Clin. Neurosci. 2008; 20: 371-373 Crossref PubMed Scopus (29) Google Scholar ]. Patients with these comorbidities may develop ODS at relatively normal sodium levels [ [6] Ismail F.Y. Szollics A. Szolics M. Nagelkerke N. Ljubisavljevic M. Clinical semiology and neuroradiologic correlates of acute hypernatremic osmotic challenge in adults: a literature review. AJNR Am. J. Neuroradiol. 2013; 34: 2225-2232 Crossref PubMed Scopus (19) Google Scholar ]. Clinical manifestations arise mainly from the involvement of central basis pons and consist in quadriplegia with pseudobulbar palsy, sometimes with altered mental status [ [8] Singh T.D. Fugate J.E. Rabinstein A.A. Central pontine and extrapontine myelinolysis: a systematic review. Eur. J. Neurol. 2014; 21: 1443-1450 Crossref PubMed Scopus (134) Google Scholar ], although many others are possible, including movement disorders and psychiatric manifestations, particularly if there is extrapontine spreading [ 1 Martin R.J. Central pontine and extrapontine myelinolysis: the osmotic demyelination syndromes. J. Neurol. Neurosurg. Psychiatry. 2004; 75: iii22-iii28 Crossref PubMed Scopus (360) Google Scholar , 3 Hurley R.A. Filley C.M. Taber K.H. Central pontine myelinolysis: a metabolic disorder of myelin. J. Neuropsychiatr. Clin. Neurosci. 2011; 23: 369-374 Crossref PubMed Scopus (30) Google Scholar ]. There is no correlation between symptoms and initial sodium level, correction rate and comorbidities [ [6] Ismail F.Y. Szollics A. Szolics M. Nagelkerke N. Ljubisavljevic M. Clinical semiology and neuroradiologic correlates of acute hypernatremic osmotic challenge in adults: a literature review. AJNR Am. J. Neuroradiol. 2013; 34: 2225-2232 Crossref PubMed Scopus (19) Google Scholar ]. Given the paucity and low specificity of the clinical manifestations, brain magnetic resonance imaging (MRI) plays a key role in the diagnosis, classically revealing a symmetric pontine “bat-wing” lesion, visualized as hypointense in T1 and hyperintense in T2-weighted images. Less frequently, extrapontine lesions, cerebral volume changes and/or vascular complications can be documented [ 6 Ismail F.Y. Szollics A. Szolics M. Nagelkerke N. Ljubisavljevic M. Clinical semiology and neuroradiologic correlates of acute hypernatremic osmotic challenge in adults: a literature review. AJNR Am. J. Neuroradiol. 2013; 34: 2225-2232 Crossref PubMed Scopus (19) Google Scholar , 10 Zahr N.M. Structural and microstructral imaging of the brain in alcohol use disorders. Handb. Clin. Neurol. 2014; 125: 275-290 Crossref PubMed Scopus (35) Google Scholar ]. There seems to occur a clinical-radiological dissociation [ [6] Ismail F.Y. Szollics A. Szolics M. Nagelkerke N. Ljubisavljevic M. Clinical semiology and neuroradiologic correlates of acute hypernatremic osmotic challenge in adults: a literature review. AJNR Am. J. Neuroradiol. 2013; 34: 2225-2232 Crossref PubMed Scopus (19) Google Scholar ]. In hypernatremic states, extrapontine lesions are seen more often than central pontine ones [ [6] Ismail F.Y. Szollics A. Szolics M. Nagelkerke N. Ljubisavljevic M. Clinical semiology and neuroradiologic correlates of acute hypernatremic osmotic challenge in adults: a literature review. AJNR Am. J. Neuroradiol. 2013; 34: 2225-2232 Crossref PubMed Scopus (19) Google Scholar ]. The mortality rate in ODS is estimated as being as high as 25% [ [8] Singh T.D. Fugate J.E. Rabinstein A.A. Central pontine and extrapontine myelinolysis: a systematic review. Eur. J. Neurol. 2014; 21: 1443-1450 Crossref PubMed Scopus (134) Google Scholar ] and the survivors' outcome is variable, though it seems to be better in the absence of extrapontine demyelination [ [6] Ismail F.Y. Szollics A. Szolics M. Nagelkerke N. Ljubisavljevic M. Clinical semiology and neuroradiologic correlates of acute hypernatremic osmotic challenge in adults: a literature review. AJNR Am. J. Neuroradiol. 2013; 34: 2225-2232 Crossref PubMed Scopus (19) Google Scholar ]." @default.
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