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CASE REPORT
Year : 2017  |  Volume : 32  |  Issue : 4  |  Page : 333-335  

Localized pontine uptake in Fluorine-18-Fuorodeoxyglucose positron emission tomography/computed tomography in a case of hyponatremia: A case report and review of literature


Department of Nuclear Medicine, Apollo Hospitals, Chennai, Tamil Nadu, India

Date of Web Publication12-Oct-2017

Correspondence Address:
Thangalakshmi Sivathapandi
Department of Nuclear Medicine, Apollo Hospitals, No. 21, Greams Lane, Off. Greams Road, Chennai - 600 006, Tamil Nadu
India
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Source of Support: None, Conflict of Interest: None


DOI: 10.4103/ijnm.IJNM_59_17

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   Abstract 


A rare acquired demyelinating lesion of the pons central pontine myelinolysis (CPM) typically occurs after rapid correction of hyponatremia. There is disruption of blood–brain barrier due to osmotic stress allowing access for inflammatory mediators in extravascular brain tissue, which most likely attracts glial cells of the brain, attracts macrophages, and activates astrocytes. We present a case of female with a known history of inflammatory bowel disease who presented with altered sensorium and hyponatremia. Fluorine-18-fuorodeoxyglucose (F-18-FDG) positron emission tomography/computed tomography (PET/CT) was performed which showed localized FDG uptake in the pons, consistent with the CPM findings observed on magnetic resonance imaging. Pontine uptake in F-18-FDG PET CT in hyponatremic patients who were clinically deteriotating even after correction of hyponatremic status aids for the diagnosis of CPM.

Keywords: Central pontine myelinolysis, demyelination, fluorine-18-fluorodeoxyglucose positron emission tomography/computed tomography


How to cite this article:
Sivathapandi T, Simon S, Elangovan I. Localized pontine uptake in Fluorine-18-Fuorodeoxyglucose positron emission tomography/computed tomography in a case of hyponatremia: A case report and review of literature. Indian J Nucl Med 2017;32:333-5

How to cite this URL:
Sivathapandi T, Simon S, Elangovan I. Localized pontine uptake in Fluorine-18-Fuorodeoxyglucose positron emission tomography/computed tomography in a case of hyponatremia: A case report and review of literature. Indian J Nucl Med [serial online] 2017 [cited 2021 May 11];32:333-5. Available from: https://www.ijnm.in/text.asp?2017/32/4/333/216557




   Introduction Top


Adams et al.[1] in 1959 were the first one to describe central pontine myelinolysis (CPM) a demyelinating lesion of the pons, which may cause neurological symptoms, including weakness, impaired control of the limbs, gait instability, dysarthria, dysphagia, and altered mental status. CPM is subdivided into CPM and extrapontine myelinolysis (EPM).[2]

Although the exact pathogenesis of CPM is not clear, it is believed that rapid correction of sodium in chronic hyponatremia plays a vital role.[1] Case reports and articles have been published on CPM based on clinical, computed tomography (CT), and magnetic resonance imaging (MRI)[3],[4] findings. To our knowledge, only one case report has described the CPM using combined positron emission tomography (PET)/CT [5] so far.


   Case Report Top


A 68-year-old Asian female with a known history of inflammatory bowel disease over 8 years was admitted with a history of constipation and altered sensorium for 5 days. Clinical neurological examination was normal. Glasgow Coma Scale (GCS) score was 15. Electrolyte values showed hyponatremia (97 mmol/L), hypokalemia (2.9 mmol/L), hypochloremia (62 meq/L), and hypomagnesemia (1.2). She was treated with 3% NaCl and other electrolytes were also replaced. Sodium was given intravenously as an isotonic saline solution at a rate of 50 mL/h and a maximum limit of 12 mmol per 24 h.

The following day she developed fever (103 F) and difficult to wake up (GCS: 6, sodium: 107 mmol/L, potassium: 3.3 mmol/L). She was investigated for fever with complete blood count, and blood and urine cultures. She was started on empirical antibiotics pending culture reports. Malignancy was suspected, and hence, fluorine-18-fuorodeoxyglucose (F-18-FDG) PET/CT was ordered. The F-18-FDG PET/CT performed [Figure 1] had findings that could be compatible with CPM in the pons with no corresponding CT abnormality, and an MRI of the brain done a day after.
Figure 1: Fluorine-18-fuorodeoxyglucose positron emission tomography/computed tomography showing localized fuorodeoxyglucose uptake in the pons, with normal and symmetrical activity in the rest of the brain

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PET/CT was consistent with CPM in MRI [Figure 2]. The sodium change was reviewed and it was noted that changing every day was around 8 meq except on 1 day when it was around 11 meq. The patient was given supportive management during hospital stay. At the time of discharge, the patient could eat and drink independently. She was able to walk independently and take care of her day-to-day activities on her own.
Figure 2: Magnetic resonance - scan T2-weighted image showing a hyperintensive region in the central part of pons

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   Discussion Top


CPM is an uncommon demyelinating condition with predilection for the central portion of the basis pontis although extrapontine regions such as putamina, caudate nuclei, thalami, cerebellum, splenium of the corpus callosum, and subcortical white matter may also get involved at times either separately or in concert with the pontine lesion.[6],[7] Conditions which can lead to CPM are chronic alcoholism, malnutrition, hyponatremia, liver disease, liver transplants, systemic hypotension, and infections.[8] Kleinschmidt-DeMasters and Norenberg were the first to describe the increased risk of CPM with rapid correction of hypernatremia.[9]

The exact underlying pathogenesis of CPM is still under debate; however, studies suggest that any fluctuation in osmotic forces and ion shifts can lead to changes in cell volume and cell membrane function which in turn causes cellular stress and myelinolysis. Other clinical studies have shown that during correction of hyponatremia, myelinolysis occurs due to the brain's overshoot of sodium or compression of myelin by edematous cellular element.[8],[10]

The lesions in CPM are usually symmetrical [4] and contain sheets of lipid-laden macrophages and a large number of reactive astrocytes during active disease.[11] The increased metabolism of these accumulated cells is probably responsible for the localized uptake of FDG seen on the PET scanning.

One other case report [5] has described hypermetabolism in the pons in the form of localized focal uptake of F-18-FDG in an alcoholic patient with CPM. The F-18-FDG-PET CT scanning was done 10 days after the onset of decreased sensorium. The authors suggested that the metabolism in these activated cells could be the mechanism responsible for the localized FDG-uptake seen on PET/CT during active CPM.

In the present case report scenario, F-18-FDG PET/CT was performed 5 days after the onset of decreased sensorium. F-18-FDG-PET showed normal and symmetrical F-18-FDG uptakes in both hemispheres, but with a focus of abnormally increased F-18-FDG uptake in the central pons [Figure 1]. Standard uptake values of this region of interest had a maximum of 13.8. The scan was done using a Philips Gemini PET/CT TF 64 (with time-of-flight capability), with a CT exposure of 107 mAs, PET time per bed position (frame duration) 120 s, and an injected dose of 299 MBq F-18-FDG.


   Conclusion Top


Pontine uptake in F-18-FDG PET CT in hyponatremic patients who were clinically deteriotating even after correction of hyponatremic status aids for the diagnosis of CPM.

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 Psychiatry1959;81:154-72.  Back to cited text no. 1
    
2.
Alleman AM. Osmotic demyelination syndrome: Central pontine myelinolysis and extrapontine myelinolysis. Semin Ultrasound CT MR 2014;35:153-9.  Back to cited text no. 2
    
3.
Yoon B, Shim YS, Chung SW. Central pontine and extrapontine myelinolysis after alcohol withdrawal. Alcohol Alcohol 2008;43:647-9.  Back to cited text no. 3
    
4.
Shah SO, Wang A, Mudambi L, Ghuznavi N, Fekete R. Asymptomatic central pontine myelinolysis: A case report. Case Rep Neurol 2012;4:167-72.  Back to cited text no. 4
    
5.
Rønne F, Tfelt-Hansen PC, Rørdam L. Central pontine myelinolysis and localized uorodeoxyglucose uptake seen on 18F-FDG PET/CT. World J Nucl Med 2017;6:56-8.  Back to cited text no. 5
    
6.
Bourgouin PM, Chalk C, Richardson J, Duang H, Vezina JL. Subcortical white matter lesions in osmotic demyelination syndrome. AJNR Am J Neuroradiol 1995;16:1495-7.  Back to cited text no. 6
    
7.
Hurley RA, Filley CM, Taber KH. Central pontine myelinolysis: A metabolic disorder of myelin. J Neuropsychiatry Clin Neurosci 2011;23:369-74.  Back to cited text no. 7
    
8.
Lupato A, Fazio P, Fainardi E, Cesnik E, Casetta I, Granieri E. A case of asymptomatic pontine myelinolysis. Neurol Sci 2010;31:361-4.  Back to cited text no. 8
    
9.
Kleinschmidt-DeMasters BK, Norenberg MD. Rapid correction of hyponatremia causes demyelination: Relation to central pontine myelinolysis. Science 1981;211:1068-70.  Back to cited text no. 9
    
10.
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. 10
    
11.
Love S. Demyelinating diseases. J Clin Pathol 2006;59:1151-9.  Back to cited text no. 11
    


    Figures

  [Figure 1], [Figure 2]



 

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