PMC5368399_01
CT scan of the head on admission. Imaging shows no gross acute intracranial abnormality, except for mild bifrontal cerebellar atrophy and a 0.5 x 0.3 cm focal hypodense signal in the right pons (arrow), defined as beam hardening artifact.
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Computed tomography (CT) of the head without contrast showed no acute intracranial abnormality except for a small hypodense area seen at the right portion of the pons, attributed to a beam hardening artifact (Figure 1).
Serum sodium levels (in mMol/L) during hospitalization.
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Within 24 hours of admission, the patient's serum sodium was corrected from 106 mMol/L to 121 mMol/L, a 15-point increase (Figure 2).
MRI obtained on hospital day 5. T2-weighted images (a), FLAIR (b), and DWI (c) showed no evidence of intracranial pathology.
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On day 5, brain MRI was obtained (Figure 3) and lumbar puncture (LP) was performed to evaluate for structural, infectious, inflammatory, demyelinating, vasculitis, and/or autoimmune etiology.
Head PET scan with F-fluorodeoxyglucose tracer on hospital day 14. Scans display focally intense hypermetabolic activity at the pons.
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While skeleton, neck, chest, abdomen, and pelvis scans showed no abnormal uptake of the tracer (data not shown), PET scan revealed abnormal hypermetabolic activity in the pons, suggestive of possible central pontine myelinolysis (Figure 4).
MRI with and without contrast on hospital day 15. T2-weighted MRI shows mild diffuse hyperintense signal changes in the pons (a); DWI sequence shows restricted diffusion (b) with corresponding ADC hypointensity (c) in central pons. These findings were not present when compared to MRI on hospital day 5 (Figure 3) and are consistent with central pontine myelinolysis.
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Follow-up brain MRI with contrast was then obtained on day 15, which showed restricted diffusion in the central pons confirming the diagnosis of CPM (Figure 5).