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Table of Contents    
Year : 2012  |  Volume : 60  |  Issue : 4  |  Page : 426-428

Central pontine and extrapontine myelinolysis: Diffusion weighted imaging and diffusion tensor imaging on follow-up

1 Department of Biomedical Imaging, University Malaya Research Imaging Centre, Kuala Lumpur, Malaysia
2 Department of Medicine, Neurology Unit, Faculty of Medicine, University Malaya, Kuala Lumpur, Malaysia

Date of Web Publication6-Sep-2012

Correspondence Address:
Kartini Rahmat
Department of Biomedical Imaging, University Malaya Research Imaging Centre, Kuala Lumpur
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Source of Support: None, Conflict of Interest: None

DOI: 10.4103/0028-3886.100712

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How to cite this article:
Nair SR, Ramli NM, Rahmat K, Mei-Ling ST. Central pontine and extrapontine myelinolysis: Diffusion weighted imaging and diffusion tensor imaging on follow-up. Neurol India 2012;60:426-8

How to cite this URL:
Nair SR, Ramli NM, Rahmat K, Mei-Ling ST. Central pontine and extrapontine myelinolysis: Diffusion weighted imaging and diffusion tensor imaging on follow-up. Neurol India [serial online] 2012 [cited 2023 Dec 8];60:426-8. Available from:


Central pontine and extrapontine myelinolysis (CPM, EPM) or osmotic demyelination syndrome are commonly a consequence of vigorous sodium correction and exhibits characteristic features on conventional magnetic resonance imaging (MRI). Advanced diffusion weighted (DWI) and diffusion tensor imaging (DTI) have been found to elucidate osmotic disturbances of water molecules and disruption of fiber tracts even before changes of demyelination are seen on conventional MRI. Here we describe the long-term follow-up imaging findings in a patient with osmotic demyelination syndrome.

A 54-year-old woman, an untreated hypertensive patient, presented with a history of acute gastroenteritis of 1 week and high blood pressure of 190/100 mmHg. She was started on diuretic (indapamide). Subsequently, her condition rapidly deteriorated with generalized body weakness and seizures. Blood investigation showed severe hyponatremia (serum sodium: 97 mmol/L). The low sodium level was corrected within 24 h to 124 mmol/L. Initial two brain MRI were apparently normal. After a week, she was referred to our center for further management. Examination revealed Glasgow Coma Scale (GCS) score of 6/15 with reactive pupils and flaccid quadriparesis. Plantar response was extensor bilaterally. Serum sodium was normal (138 mmol/L). MRI done 3 weeks later showed hyperintensity on T2-weighted and fluid attenuation inversion recovery (FLAIR) images in the basis pontis [Figure 1]. Symmetrical hyperintensities were also seen in the basal ganglia and posterior limb of both internal capsules suggestive of CPM and EPM [Figure 1]. Over the next 1.5 years, her general condition was poor. Repeat MRI with DWI and DTI showed gross cerebral and cerebellar atrophy with volume loss in both caudate heads. The pons had undergone gliosis. Hyperintensity on apparent diffusion coefficient (ADC) with corresponding hypointensity on DWI was seen in the pons and the right putamen [Figure 2]. The DTI (TR = 12,000 ms, TE = 82.7 ms, FOV = 24 mm, matrix = 128 × 128, thickness = 3.0 mm, 32 directions and diffusion-weighted factor, b = 700 s/mm 2 ) showed asymmetrical fiber loss in the right corticospinal tract (CST) and the right anterior thalamic radiation (ATR) [Figure 3].
Figure 1: Magnetic resonance images done 3 weeks after the initial presentation. (a) Axial T2-weighted, (b) coronal FLAIR of the brain showing hyperintensities in the basis pontis (white arrows), (c) axial T2-weighted, (d) coronal FLAIR of the brain showing symmetrical hyperintensities in the posterior limbs of internal capsules (white arrowheads), head of both caudate nuclei (black arrowheads) and putamen (black arrows) bilaterally

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Figure 2: Magnetic resonance images on follow-up 1.5 years after initial presentation. (a) Diffusion-weighted imaging (DWI), (b) apparent diffusion coefficient (ADC ) map of the corresponding areas of the brain in axial section showing residual hypointensity on the DWI (white arrow) and hyperintensity on the ADC (block arrow) in the pons, (c) and (d) similar changes are seen in the right putamen (arrowheads) consistent with vasogenic edema

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Figure 3: Magnetic resonance images on follow-up 1.5 years after initial presentation. (a) Regions of interests (ROI) were drawn in the putamen bilaterally for tractography of the anterior thalamic tract (ATT). Tractography of the ATT in the (b) patient showing asymmetrical loss of fibers bilaterally [right (white arrow) > left (white arrowhead)] and (c) healthy control showing preserved volume and symmetry of the tracts bilaterally (white block arrows). (d) ROIs drawn in the cerebellopontine region bilaterally for tractography of the corticospinal tracts (CST). Tractography of the CST in the (e) patient showing asymmetrical loss of fibers bilaterally [right (yellow block arrow) > left (yellow arrowhead)] and (f) healthy control showing preservation of the tracts bilaterally (yellow arrows)

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Ten months later, she succumbed to lung infection.

Characteristic MRI changes of CPM/EPM may not be apparent until the first 2 weeks of illness. [1] Our patient did not have MRI changes until 4 weeks after presentation. Typical changes on standard MRI are hypointensity on T1-weighted with associated hyperintensity on T2-weighted in the affected areas. These areas develop cytotoxic edema causing hyperintensity on FLAIR and restricted diffusion on DWI. [2] Abnormal pontine signal on T2-weighted follow-up imaging usually lags behind clinical improvement. [1] Hyperintensity on T2-weighted images is shown to persist for few years, more likely due to gliosis. [1] However, ADC values in the affected areas have shown to normalize with clinical improvement. [3] The persistence of hyperintensity on DWI, in some cases, is due to shine-through of T2 brightness. [3] In this patient, the DWI scan done 1.5 years later showed gliosis in the putamen and pons.

DTI allows objective assessment of the fiber tracts using tractography in which volume loss, displacement, and asymmetry of the fiber tracts can be obtained. DTI images can be processed to give fractional anisotropy (FA) and mean diffusivity (MD) values. Decreased FA and increased MD values indicate destruction of fiber tracts from demyelination and gliosis. [4] Two regions of interest in the CST and the ATR were drawn by two experienced neuroradiologists blinded to the patients to obtain the FA, MD, and tractography using Functool preinstalled in the workstation. The patient compared with the healthy control showed lower FA in these regions (FA CST: 0.26±0.17 vs 0.35±0.24 and ATR: 0.27±0.09 vs 0.30±0.15). Markedly higher MD was noted in these regions compared with the healthy control (>30% higher) [MD (×10−3 mm 2 /s) CST: 2.72±1.21 vs 1.31±0.74 and ATR: 1.10±0.26 vs 0.82±0.11].

Most times treatment is supportive with poor outcome. [1] However, with medical advancement, latest treatment options have given significant neurologic improvement within a short period of time. [5] Therefore, the emphasis on DWI and DTI are nevertheless important for early diagnosis to initiate treatment and prevent irreversible brain damage. Long-term follow-up using DWI and DTI is also useful.

 » References Top

1.Chan CY, Lam HS, Jinkins JR. Clinics in diagnostic imaging (45). Osmotic myelinolysis (central potine myelinolysis). Singapore Med J 2000;41:45-8.  Back to cited text no. 1
2.Moritani T, Ekholm S, Westesson PL. Diffusion-weighted MR imaging of the brain. 2 nd ed.Germany: Springer; 2009. P.176-79.  Back to cited text no. 2
3.Cramer SC, Stegbauer KC, Schneider A, Mukai J, Maravilla KR. Decreased diffusion in central pontine myelinolysis. AJNR Am J Neuroradiol 2001;22:1476-9.  Back to cited text no. 3
4.Loh KB, Rahmat K, Lim SY, Ramli N. A hot cross bun sign from diffusion tensor imaging and tractography perspective. Neurol India 2011;59:266-9.  Back to cited text no. 4
5.Ludwig KP, Thiesset HF, Gayowski TJ, Schwartz JJ. Plasmapheresis and intravenous immune globulin improve neurologic outcome of central pontine myelinolysis occurring post orthotopic liver transplant Ann Pharmacother 2011;45:e10. Feb 8 (Epub ahead of print).  Back to cited text no. 5


  [Figure 1], [Figure 2], [Figure 3]

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