Abstract
Rasmussen encephalitis (RE) is a rare but devastating unihemispheric brain disorder that often affects children. The clinical picture is characterized by intractable focal epilepsy and progressive decline of functions associated with the affected hemisphere.2 Despite its known inflammatory background and T-cell involvement, immunotherapy appears to slow rather than halt disease progression, and hemispherotomy appears to be the only solution for intractable epilepsy.
A potential early therapeutic window has been suggested, and new therapeutic agents have become available.1 A monoclonal antibody targeting CD52 that leads to long-term depletion of lymphocytes (alemtuzumab) has previously been considered as a possible treatment option for RE, but clinical data are limited.