Journal of neuroimaging : official journal of the American Society of Neuroimaging · 2007
Functional MRI in multiple sclerosis.
СтатьяОбзорНазвание и аннотация: Перевод пока не подготовлен
Обработка статьи · этапы, ошибки и управление
Загрузка состояния…
Ошибки и ограничения
История · было → стало
Состояние обновляется каждые 5 секунд, пока блок открыт. Процент показывается только там, где известен объём работы. Пауза останавливает продолжение этапа; текущий запрос к источнику может завершиться.
Rocca Maria A, Filippi Massimo
Аннотация
There is increasing evidence that the severity of the clinical manifestations of multiple sclerosis (MS) does not simply depend on the extent of tissue destruction, but rather represents a complex balance among tissue damage, tissue repair, and cortical reorganization. Functional magnetic resonance imaging (fMRI) provides information about the extent and nature of brain plasticity, which follows MS structural injury and might have the potential to limit the clinical manifestations of the disease. An altered recruitment of regions normally devoted to the performance of a given task and/or the recruitment of additional areas, which 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 the visual, cognitive, and motor systems. These functional changes have been related to the extent and severity of brain damage within and outside T2-visible lesions and to the involvement of specific central nervous system (CNS) structures, including the spinal cord and the optic nerve. Brain functional changes have been shown to be dynamic over time, not only after an acute relapse, but also in clinically stable patients. An increased recruitment of the cerebral networks might represent a 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 clinical manifestations of the disease.