Citation

Mrkobrada S, Gnanakumar V. Pediatr. Neurol. 2014; 51(4): 573-575.

Affiliation

Department of Clinical Neurosciences, Foothills Medical Centre, Alberta Children's Hospital, University of Calgary, Alberta, Canada.

Copyright

(Copyright © 2014, Elsevier Publishing)

DOI

10.1016/j.pediatrneurol.2014.06.012

PMID

25266623

Abstract

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.

Language: en