Restricted Diffusion Preceding Gadolinium Enhancement in Acute Multiple Sclerosis Lesions (P03.052)

Abstract

Objective: Describe clinical and magnetic resonance imaging (MRI) characteristics of acute multiple sclerosis (MS) lesions with restricted diffusion preceding gadolinium (Gd) enhancement. Background Apparent diffusion coefficient (ADC) signal reduction in acute MS lesions has been reported, but the temporal pattern of gadolinium (Gd) enhancement relative to ADC changes has not been well described. Previous case reports either do not comment on Gd enhanced imaging or describe simultaneous Gd enhancement of lesions at the time of ADC reduction. We present three examples of acute MS lesions with decreased ADC followed by Gd enhancement. Design/Methods: Three patients (2 female, 1 male), ages 26-42, all with brain MRI studies within 48 hours of onset of acute neurological symptoms, were evaluated at our MS center within the past year. All underwent screening bloodwork and spine MRI, and 2 had cerebrospinal fluid (CSF) studies. Follow-up imaging was conducted approximately 1 month after initial MRIs. Results: Initial brain MRI revealed lesions in a location accounting for the new neurologic manifestations, >1 cm in diameter, and with prominent restricted diffusion but no Gd enhancement. The MS diagnoses were supported on the basis of CSF findings, laboratory exclusion of alternative diagnoses, lesion evolution, and additional lesions characteristic of MS on brain and/or spine MRI. All patients received IV methylprednisolone, 1000 mg daily for at least 3 days. Follow-up imaging at 1 month demonstrated patchy Gd enhancement throughout the lesions with resolving restricted diffusion. Two of 3 patients had additional follow-up imaging more than 1 month later which demonstrated total resolution of Gd enhancement. Conclusions: Although restricted diffusion without coincident Gd enhancement is most commonly associated with cerebral ischemia, acute MS lesions may demonstrate this pattern. The mechanism is uncertain but may reflect early demyelination prior to inflammation-associated blood-brain barrier disruption. Disclosure: Dr. Hyland has nothing to disclose. Dr. Bermel has received personal compensation for activities with Astellas, Biogen Idec, Novartis, and Teva Neuroscience as a consultant and/or speaker. Dr. Cohen has received personal compensation for activities with Biogen Idec, Eli Lilly & Company, Novartis, and Vaccinex. Dr. Cohen has received research support for activities with Biogen Idec, BioMS, Genzyme Corporation, Novartis, Synthon, and Teva Neuroscience.