Functional magnetic resonance imaging and multiple sclerosis

There is increasing evidence that the severity of the clinical manifestations of multiple sclerosis (MS) does not result simply from the extent of tissue destruction, rather it represents a complex balance between tissue damage, tissue repair and cortical reorganization. Functional magnetic resonance imaging provides information regarding the extent and nature of brain plasticity following MS-related structural injury, with the potential to limit the clinical manifestations of the disease. An altered recruitment of regions devoted normally to the performance of a given task and/or the recruitment of additional areas that are not typically activated by healthy people for performing that given task have been described in patients with MS, independent of their clinical phenotype, when investigating visual, cognitive and motor systems. These functional changes have been related not only to the extent and severity of brain damage within and outside T2-visible lesions and to the involvement of specific brain structures, but also to the degree of spinal cord and optic nerve involvement. It has also been suggested that an altered recruitment of specific brain regions might be associated with the appearance of clinical symptoms in MS, such as fatigue. Brain functional changes have been shown to be dynamic over time, not only after an acute relapse, but also in clinically stable patients. More recently, in patients at the earliest clinical stage of the disease, it has been shown that such changes might contribute to predicting the evolution to definite MS, and it has been postulated that dynamic changes of brain cortical activations might occur with the progression of the disease. An increased recruitment of the cerebral networks might represent the first step of cortical reorganization with the potential to maintain a normal level of function in the course of MS. The progressive failure of these mechanisms might, on the one hand, result in the activation of previously silent second-order compensatory areas, and on the other, contribute to the accumulation of irreversible disability.