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Table of Contents    
Year : 2018  |  Volume : 66  |  Issue : 2  |  Page : 559-560

Osmotic demyelination syndrome in the setting of hypernatremia

1 Department of Radio Diagnosis, Sanjay Gandhi Postgraduate Institute of Medical Sciences, Lucknow, Uttar Pradesh, India
2 Department of Anaesthesiology, Sanjay Gandhi Postgraduate Institute of Medical Sciences, Lucknow, Uttar Pradesh, India

Date of Web Publication15-Mar-2018

Correspondence Address:
Dr. Neeraj Jain
Department of Radiodiagnosis, Sanjay Gandhi Postgraduate Institute of Medical Sciences, Lucknow - 226 014, Uttar Pradesh
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Source of Support: None, Conflict of Interest: None

DOI: 10.4103/0028-3886.227332

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How to cite this article:
Jain N, Phadke RV, Chauhan G, Ambesh S P. Osmotic demyelination syndrome in the setting of hypernatremia. Neurol India 2018;66:559-60

How to cite this URL:
Jain N, Phadke RV, Chauhan G, Ambesh S P. Osmotic demyelination syndrome in the setting of hypernatremia. Neurol India [serial online] 2018 [cited 2021 Jan 22];66:559-60. Available from:


Osmotic demyelination syndrome is a well-known entity caused by rapid correction of sodium imbalance and is reported mainly in malnourished, severely ill, and chronic alcoholic patients. Majority of case reports and studies have shown its relationship with rapid correction of hyponatremia; however, only a few case reports have revealed its occurrence even in the setting of normonatremia and hypernatremia, such as occurring in postpartum patients and patients with chronic renal failure who are on dialysis. Various theories have been proposed to explain its pathophysiology; however, a majority of them have revealed that it is the result of injury to gray matter rich regions due to the presence of myelino-toxic substances, which are released due to osmotic injury to the endothelium. Central and extrapontine myelinolysis are its two subtypes, which involve pons and basal ganglia regions, respectively. Magnetic resonance imaging (MRI) features are fairly characteristic and include an altered signal intensity and restricted diffusion in the central part of pons with sparing of ventrolateral pons and pontine portion of the corticospinal tracts. We present a case of osmotic demyelination syndrome in a chronic alcoholic patient whose electrolyte analysis revealed hypernatremia at the time of admission.

A 32-year old male patient presented to the critical care department in a delirious state; he had a history of long-term alcohol abuse and recurrent seizures. There was no history of trauma, fever, or convulsions preceding the delirious state. His serum sodium level was elevated (172 mEq/L) at the time of admission, which was corrected over a period of 5 days and brought down to 136 mEq/L. Other electrolytes, blood glucose, and serum creatinine levels were within normal limits. Infective markers for dengue and malaria were also negative. Subsequently, his general condition worsened and he developed decerebrate rigidity. On day 5 of the admission, MRI brain was performed which revealed symmetrical altered signal intensity in bilateral basal ganglia, thalamus, pons, and cerebellar hemisphere, appearing hyperintense on T2-weighted/fluid-attenuated inversion recovery sequence and hypointense on T1-weighted sequence; no evidence of restricted diffusion was noted on diffusion-weighted imaging, and the contrast study showed a subtle patchy enhancement [Figure 1] and [Figure 2]. Magnetic resonance angiography and venography showed no significant abnormality. No evidence of blooming to suggest hemorrhage was noted on susceptibility-weighted imaging (SWI) [Figure 3]. The pattern of brain involvement was suggestive of osmotic demyelination syndrome (ODS).
Figure 1: MRI brain axial sections, T2 (a and b) and FLAIR (c and d) images show a symmetrical hyperintense signal in bilateral basal ganglia, thalamus and pons

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Figure 2: Pre (a and b) and post contrast (c and d) T1W images show a hypointense signal in the thalamus and pons with patchy heterogeneous enhancement

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Figure 3: T2W coronal images (a) show symmetrical hyperintense signals in bilateral thalamus and pons. SWI image (b) shows no evidence of blooming

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ODS is typically caused by rapid correction of hyponatremia; however, irrespective of the presence of a hypernatremic or a hyponatremic state, rapid correction of electrolyte imbalance can result in osmotic demyelination.[1] Although ODS is commonly associated with alcoholism, other common causes include chronic liver disease, malnutrition, prolonged diuretic use, burns, psychogenic polydipsia, and post liver transplant, etc.[2] The usual ways of presentation include lethargy, dysarthria, and altered mental status. The development of pseudobulbar palsy and spastic quadriparesis indicate involvement of the pons and midbrain.[3] The exact mechanism behind selective involvement of the pons, and in some case, of basal ganglia is debatable, but the possible explanation is the release of myelino-toxic substance due to osmotic injury to the endothelium in gray matter rich regions.[4]

Computed tomography scans may show hypodensity in the pons and basal ganglia region. Symmetrical central pons hyperintensity on T2-weighted MRI images is a characteristic finding; ventrolateral pons and pontine portion of the corticospinal tract are typically spared.[5] Caudate nucleus, lentiform nucleus, and thalami are also involved in some cases and referred to as extrapontine myelinolysis. Diffusion-weighted MRI may show restricted diffusion in the involved areas and can help in early diagnosis in some cases.[6]

Differential diagnosis includes brain stem infarct, encephalitis, and neoplastic lesions such as a glioma.

Possibility of ODS should be considered in a patient presenting with sodium and other electrolyte imbalance and the history of alcoholic abuse, chronic liver disease, or malnutrition with characteristic symmetrical involvement of central pons, thalamus, and basal ganglia. Significant hypernatremia at the time of admission was an unusual finding in this case in addition to pontine and extrapontine involvement.

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There are no conflicts of interest.

  References Top

Phajir Vishwanath SR, Sekhar M, Bele K, Chandrashekar RK. Postpartum hypernatremic cerebral encephalopathy with osmotic myelinolysis: Report of two cases and review with emphasis on magnetic resonance imaging findings. Int J Adv Med Health Res 2015;2:112-5.  Back to cited text no. 1
Martin RJ. Central pontine and extra-pontine myelinolysis: The osmotic demyelination syndromes. J Neurol Neurosurg Psychiatry 2004;75.  Back to cited text no. 2
Lauren R, Illowsky BK. Myelinolysis after correction of hyponatraemia. Ann Intern Med 1997;126:57-62.  Back to cited text no. 3
Norenberg MD, Leslie KO, Robertson AS. Association between rise in serum sodium and central pontine myelinolysis. Ann Neurol 1982;11:128-35.  Back to cited text no. 4
Howard SA, Barletta JA, Klufas RA, Saad A, Girolami UD. Osmotic demyelination syndrome. RadioGraphics 2009;29:933-93.  Back to cited text no. 5
Ruzek KA, Campeau NG, Miller GM. Early diagnosis of central pontine myelinolysis with diffusion-weighted imaging. AJNR Am J Neuroradiol 2004;25:210-3.  Back to cited text no. 6


  [Figure 1], [Figure 2], [Figure 3]


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