The correlation of dystonia severity and serum transaminases in a child with a brain injury.

BACKGROUND Severe anoxic brain injury can lead to prolonged episodes of status dystonicus. Sustained dystonia can result in skeletal muscle breakdown and elevation of serum transaminases, which can initially be confused with polypharmacy-related hepatotoxicity or an underlying metabolic condition. PATIENT We present a 19-month-old boy who sustained a severe anoxic brain injury in the setting of a viral upper respiratory tract infection. Within 2 weeks after injury, he developed prolonged periods of severe dystonia. RESULTS Serum creatine kinase peaked at 4504 U/L, alanine transaminase at 183 U/L, and aspartate transaminase at 198 U/L. CONCLUSIONS This child demonstrated a clear correlation between severity of dystonia after brain injury and changes in serum alanine transaminase, aspartate transaminase, and creatine kinase. In the literature, aspartate transaminase and alanine transaminase elevations have been reported in seizures, myopathies, and extreme exercise. This is the first report of serum transaminase elevation secondary to dystonia. Early identification of skeletal muscle causes of increased alanine transaminase and aspartate transaminase may prevent unnecessary investigations and can reduce concern about medication-related hepatotoxicity.