Related Experiment Video
Updated: Jul 15, 2026

Induction and Clinical Scoring of Chronic-Relapsing Experimental Autoimmune Encephalomyelitis
Published on: July 4, 2007
Long term response to steroid therapy in Rasmussen encephalitis
N Bahi-Buisson1, V Villanueva, C Bulteau
1Hôpital Necker Enfants Malades Service de Neurologie et maladies métaboliques-Paris APHP Universite Rene Descartes, Paris V, Paris, 75005 France. nadia.habi-buisson@nck.ap-hop-paris.fr
High-dose steroids can help Rasmussen encephalitis (RE) early on, but long-term seizure control is not guaranteed. Some patients experience relapses requiring further treatment like hemispherotomy.
Area of Science:
- Neurology
- Pediatric Neurology
- Epileptology
Background:
- Rasmussen encephalitis (RE) is a severe, progressive focal epilepsy.
- It leads to significant motor and cognitive decline.
- Previous studies suggested early steroid therapy benefits RE.
Purpose of the Study:
- To evaluate the long-term efficacy of high-dose steroid therapy for Rasmussen encephalitis.
- To assess outcomes in patients with RE treated with steroids.
Main Methods:
- Retrospective review of 11 patients diagnosed with RE.
- Patients were followed for an average of 9 years.
- Outcomes assessed included seizure frequency, motor function, and need for hemispherotomy.
Main Results:
- Six patients showed no benefit from steroids and required hemispherotomy.
- Five patients experienced seizure reduction and improved motor function with steroids.
- Two responders died suddenly; two others relapsed and needed hemispherotomy.
- One patient had sustained seizure control, though with moderate recurrence.
Conclusions:
- Early high-dose steroid treatment can be beneficial for Rasmussen encephalitis.
- Long-term relapses can occur even in initial responders.
- Delayed hemispherotomy may still be necessary for seizure control in RE.
Related Concept Videos
Rocky Mountain Spotted Fever
Encephalitis ll: Pathophysiology
Encephalitis l: Introduction
Arboviral Encephalitis
Cryptococcal Meningitis
Bacterial Meningitis II: Pathophysiology