Localized Pontine Uptake in Fluorine-18-Fuorodeoxyglucose Positron Emission Tomography/Computed Tomography in a Case of Hyponatremia: A Case Report and Review of Literature

Introduction

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)[34] findings. To our knowledge, only one case report has described the CPM using combined positron emission tomography (PET)/CT[5] so far.

Case Report

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.

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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.

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Figure 2 Magnetic resonance - scan T2-weighted image showing a hyperintensive region in the central part of pons

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Discussion

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.[67] 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.[810]

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

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.