An update on opsoclonus

被引:100
作者
Wong, Agnes
机构
[1] Hosp Sick Children, Dept Ophthalmol & Vis Sci, Toronto, ON M5G 1X8, Canada
[2] Univ Toronto, Dept Ophthalmol & Vis Sci, Toronto, ON, Canada
关键词
antineuronal antibodies; autoimmunity; fastigial nucleus; neuroblastoma; opsoclonus; paraneoplastic syndrome;
D O I
10.1097/WCO.0b013e3280126b51
中图分类号
R74 [神经病学与精神病学];
学科分类号
摘要
Purpose of review The aim of this article is to review opsoclonus with particular emphasis on its immunopathogenesis and pathophysiology. Recent findings Infections (West Nile virus, Lyme disease), neoplasms (non-Hodgkin's lymphoma, renal adenocarcinoma), celiac disease, and allogeneic hematopoietic stem cell transplantation can cause opsoclonus. Newly identified autoantibodies include antineuroleukin, antigliadin, antiendomsial, and anti-CV2. Evidence suggest that the autoantigens of opsoclonus reside in postsynaptic density, or on the cell surface of neurons or neuroblastoma cells (where they exert antiproliferative and proapoptotic effects). Most patients, however, are seronegative for antibodies. Cell-mediated immunity may also play a role, with B and T cell recruitment in the cerebrospinal fluid linked to neurological signs. Rituximab, an anti-CD20 monoclonal antibody seems efficacious as an adjunctive therapy. Although changes in synaptic weighting of saccadic burst neuron circuits in the brainstem have been implicated disinhibition of the fastigial nucleus in the cerebellum, or damage to afferent projections to the fastigial nucleus, is a more plausible pathophysiologic mechanism which is supported by functional magnetic resonance imaging findings in patients. Summary There is increasing recognition that both humoral and cell mediated immune mechanisms are involved in the pathogenesis of opsoclonus. Further studies are needed to further elucidate its immunopathogenesis and pathophysiology in order to develop novel efficacious therapy.
引用
收藏
页码:25 / 31
页数:7
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