Female, 21 years old, with brainstem lesion. Patchy but symmetric FLAIR hyperintensity is redemonstrated affecting the central pons in the vicinity of the transverse pontine fibers. Just posterior to this, there are thin linear foci of hyperintensity bilaterally which may correspond to the medial lemnisci. No significant interval change is seen when compared to recent prior examinations. On review of multiple prior examinations, abnormal signal in the pons is noted to have first become apparent on the 12/31/13 scan and has progressed over the intervening time. No other areas of focal signal abnormality are seen, and in particular, the other deep gray nuclei are unaffected.The region of abnormal signal in the pons was interrogated with single voxel spectroscopy (TE 35 ms). As a comparison, the nearest normal-appearing tissue was also interrogated more inferiorly in the pons. The lesional spectrum demonstrates reduction in the major metabolic peaks relative to normal appearing tissue. No evidence of lipid or lactate is seen. No atypical peaks are detected.
Signal abnormality in the pons is redemonstrated showing no significant change from the recent prior examinations. This abnormality first became detectable in late 2013 and has progressed from that point.Spectroscopic assessment of the lesional tissue demonstrates a pattern consistent with chronic tissue injury. No lactate is seen to suggest active failure of aerobic metabolism. No lipid is detected to indicate ongoing membrane degradation. Although the differential remains broad for this abnormality, the pattern and morphology of the lesion are suggestive of prior osmotic demyelination. An inborn error of metabolism is not excluded, though patient age and imaging features make this less likely. Active inflammation and neoplasia are considered unlikely.