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NEUROIMAGE
Year : 2021  |  Volume : 69  |  Issue : 3  |  Page : 777-778

“Mercedes Benz Sign: Osmotic Demyelination Syndrome”


Department of Neurology, Post Graduate Institute of Medical Education and Research, Chandigarh, India

Date of Submission25-Jun-2017
Date of Decision25-Jul-2017
Date of Acceptance08-Aug-2019
Date of Web Publication24-Jun-2021

Correspondence Address:
Dr. Sahil Mehta
Department of Neurology, Post Graduate Institute of Medical Education and Research, Chandigarh - 160 012
India
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Source of Support: None, Conflict of Interest: None


DOI: 10.4103/0028-3886.319223

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How to cite this article:
Kumar AS, Naheed D, Balaini N, Mehta S, Lal V. “Mercedes Benz Sign: Osmotic Demyelination Syndrome”. Neurol India 2021;69:777-8

How to cite this URL:
Kumar AS, Naheed D, Balaini N, Mehta S, Lal V. “Mercedes Benz Sign: Osmotic Demyelination Syndrome”. Neurol India [serial online] 2021 [cited 2021 Jul 27];69:777-8. Available from: https://www.neurologyindia.com/text.asp?2021/69/3/777/319223




A 34-year-old man with a history of alcohol abuse was transferred from local hospital with a history of vertigo, unsteadiness, nausea, vomiting, and fatigue followed by subacute onset quadriparesis. He reported to have had 10–20 episodes of large volume watery stools five days prior to the onset of neurological deficits. Neurological examination revealed bilateral coarse gaze evoked nystagmus, bilateral facial hypoesthesia, bilateral peripheral facial paralysis, quadriparesis with extensor plantar reflex on the left side. The deep tendon reflexes were brisk with gait ataxia. His routine investigations including renal function tests and electrolytes were normal with no history of rapid correction of hyponatremia. Cerebrospinal fluid analysis was within normal limits. Cranial MRI performed on day two of hospitalization showed T1 hypointense and T2 hyper intense triangular lesion in the central pons with minimal diffusion restriction and no contrast enhancement simulating “Mercedes Benz Sign” [Figure 1]. He was managed conservatively and showed significant improvement at three months follow up.
Figure 1: Demonstrates (a) T1 hypointense, (b and c) T2 and FLAIR hyperintense triangular lesion in the center of pons with mild diffusion restriction (d and e) simulating “Mercedes Benz Sign” (f) T1W Sagittal section of brain

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Osmotic Demyelination Syndrome (ODS) was first defined and described by Adams and colleagues in 1959.[1] One of the most important risk factors for development of ODS is rapid correction of hyponatremia. But, ODS has been reported in normonatremic and hypernatremic patients also, especially when associated with chronic alcoholism, diabetes mellitus, hypokalemia, liver transplantation, pituitary surgery, hepatocellular dysfunction, hypophosphatemia, lithium toxicity, and chronic kidney disease.[2],[3] Classical radiological picture of central pontine myelinolysis involves central pons with sparing of pontine tegmentum and ventrolateral pons giving the appearance of various signs namely trident sign, piglet sign, and butterfly sign.[4],[5]

Declaration of patient consent

The authors certify that they have obtained all appropriate patient consent forms. In the form, the patient(s) has/have given his/her/their consent for his/her/their images and other clinical information to be reported in the journal. The patients understand that their names and initials will not be published and due efforts will be made to conceal their identity, but anonymity cannot be guaranteed.

Financial support and sponsorship

Nil.

Conflicts of interest

There are no conflicts of interest.



 
  References Top

1.
Adams RD, Victor M, Mancall EL. Central pontine myelinolysis: A hitherto undescribed disease occurring in alcoholic and malnourished patients. AMA Arch Neurol Psychiatry 1959;81:154-72.  Back to cited text no. 1
    
2.
McNamara PH, Williams J, McCabe DJ, Walsh RA. Striking central pontine myelinolysis in a patient with alcohol dependence syndrome without hyponatremia. JAMA Neurol 2016;73;234-5.  Back to cited text no. 2
    
3.
Singh TD, Fugate JE, Rabinstein AA. Central pontine and extrapontine myelinolysis: A systematic review. Eur J Neurol 2014;21:1443-50.  Back to cited text no. 3
    
4.
Biotti D, Durupt D. A trident in the brain, central pontine myelinolysis. Pract Neurol 2009;9:231-2.  Back to cited text no. 4
    
5.
Miller GM, Baker HL Jr, Okazaki H, Whisnant JP. Central pontine myelinolysis and its imitators: MR findings. Radiology 1988;168;795-802.  Back to cited text no. 5
    


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