Email updates

Keep up to date with the latest news and content from BMC Neurology and BioMed Central.

Open Access Highly Accessed Case report

Treatment of refractory epilepsy with natalizumab in a patient with multiple sclerosis. Case report

Stefano Sotgiu1*, Maria R Murrighile1 and Gabriela Constantin2

Author Affiliations

1 Department of Neuroscience, Section of Neurology, University of Sassari, Viale San Pietro 10, 07100 Sassari, Italy

2 Department of Pathology and Diagnostics, Section of General Pathology, University of Verona, Strada le Grazie 8, 37134 Verona, Italy

For all author emails, please log on.

BMC Neurology 2010, 10:84  doi:10.1186/1471-2377-10-84

Published: 23 September 2010



Multiple sclerosis (MS) is considered an autoimmune disease of the central nervous system and therapeutic inhibition of leukocyte migration with natalizumab, an anti-alpha4 integrin antibody, is highly effective in patients with MS. Recent studies performed in experimental animal models with relevance to human disease suggested a key role for blood-brain barrier damage and leukocyte trafficking mechanisms also in the pathogenesis of epilepsy. In addition, vascular alterations and increased leukocyte accumulation into the brain were recently documented in patients with refractory epilepsy independently on the disease etiology.

Case report

Here we describe the clinical course of a 24-year-old patient with MS in whom abrupt tonic-clonic generalized seizures manifested at disease onset. Although MS had a more favorable course, treatment with glatiramer acetate and antiepileptic drugs for 7 years had no control on seizure generation and the patient developed severe refractory epilepsy. Interestingly, generalized seizures preceded new MS relapses suggesting that seizure activity may contribute to MS worsening creating a positive feedback loop between the two disease conditions. Notably, treatment with natalizumab for 12 months improved MS condition and led to a dramatic reduction of seizures.


Our case report suggests that inhibition of leukocyte adhesion may represent a new potential therapeutic approach in epilepsy and complement the traditional therapy with anti-epileptic drugs.