Cavitary Lesions in a Series of 20 Multiple Sclerosis Patients (P06.129)

OBJECTIVE: To analyse clinical and radiological characteristics in MS patients with large cavitary lesions. BACKGROUND: Large cavitary lesions are not typical for multiple sclerosis (MS). Cavitary white matter changes may be seen in megalencephalic leukoencephalopathy with subcortical cysts, Alexander disease, mitochondrial leukoencephalopathies, vanishing white matter disease, leukoencephalopathy with calcifications and cysts, cytomegalovirus infection, and cerebral autosomal dominant arteriopathy with subcortical infarcts and leukoencephalopathy. DESIGN/METHODS: We studied MS patients with large cavitary brain lesions. Patient characteristics, disease onset/duration/subtype, expanded disability status scale (EDSS), Mini Mental State (MMS), corpus callosum lesions, history of segmental myelitis, CSF oligoclonal bands (OCB), visual evoked potentials (VEP), vanishing white matter disease genetic analysis, and characteristics of the cavitary lesions were analyzed. RESULTS: Twenty patients were analyzed, 6 man and 14 women. Mean age of disease onset was 37.6 (range: 17-58). Mean disease duration was 9 years. 7 / 20 patients presented MS symptoms since less 5 years. 10/20 patients had initial relapsing-remitting MS and 10/20 patients had primary-progressive MS. All of the patients turned in a progressive form. Mean EDSS was 5.5. Mean MMS was 20/30. Segmental myelitis was present in 12 cases. OCB were found in 12 patients. VEP was performed in 6 patients, and pathological in all but one. Vanishing white matter disease genetic analysis was performed and negative in 7 patients. Inferior corpus callosum lesions were seen in all patients with available sagittal FLAIR sequences. Cavitary lesions were strictly supratentorial, and located inside the diffuse leukoencephalopathy, with often a posterior predominance. CONCLUSIONS: MS patients with large cavitary lesions seem to represent a MS subgroup, predominantly women, with relatively late disease onset, predominantly primary-progressive type, relatively high EDSS scores, and severe cognitive dysfunction. Disclosure: Dr. Corlobe has nothing to disclose. Dr. Renard has nothing to disclose. Dr. Brochet has received personal compensation from BayerHealthcare, Novartis Pharma, Merck-Serono and Biogen-Idec. Dr. Brochet received personal compensation for serving as associate editor for a journal published by LEN (publisher). This journal is supported by Biogen-Idec. ....Dr. Brochet has received research support from Merck-Serono, Biogen-Idec and Bayer Healthcare. Dr. Vukusic has nothing to disclose. Dr. Edan has received personal compensation for activities with Biogen Idec, Teva Neuroscience, BENEFIT, and LFB. Dr. Edan has received research support from Bayer and Serono, Inc. Dr. Deburghgraeve has nothing to disclose. Dr. Goizet has nothing to disclose. Dr. Dupuy has nothing to disclose. Dr. Touzet has nothing to disclose. Dr. Deschamps has nothing to disclose. Dr. Zephir has received personal compensation for activities with Biogen Idec, Bayer Pharmaceuticals Corporation, Merck Serono, Teva Neuroscience, Sanofi-Aventis Pharmaceuticals, Inc. and Novartis as a consultant. Dr. Creange has nothing to disclose. Dr. Castelnovo has nothing to disclose. Dr. Boesplfug Tanguy has nothing to disclose. Dr. Labauge has nothing to disclose.