Massive astrocyte destruction in neuromyelitis optica despite natalizumab therapy

被引：82

作者：

Barnett, M. H. ^{[1
,2
]}

Prineas, J. W. ^{[1
,2
]}

Buckland, M. E. ^{[3
,4
]}

Parratt, J. D. E. ^{[2
]}

Pollard, J. D. ^{[1
]}

机构：

[1] Univ Sydney, Brain & Mind Res Inst, Sydney, NSW 2006, Australia

[2] Univ Sydney, Inst Clin Neurosci, Sydney, NSW 2006, Australia

[3] Royal Prince Alfred Hosp, Dept Neuropathol, Sydney, NSW, Australia

[4] Univ Sydney, Discipline Pathol, Sydney, NSW 2006, Australia

来源：

MULTIPLE SCLEROSIS JOURNAL | 2012年 / 18卷 / 01期

关键词：

demyelination; immunology; relapsing-remitting; Tysabri; B-CELLS; DISTINCTION; AQUAPORIN-4; LESIONS;

D O I：

10.1177/1352458511421185

中图分类号：

R74 [神经病学与精神病学];

学科分类号：

100204 [神经病学];

摘要：

Auto-antibody mediated astrocyte injury is implicated as a primary event in neuromyelitis optica (NMO) by biomarker, post-mortem and experimental studies that differentiate the condition from multiple sclerosis. We describe the clinical, radiological and neuropathological features of a severe cerebral attack in a natalizumab-treated patient with relapsing myelitis and serum aquaporin-4 antibodies. Our findings support autopsy evidence that abrupt astrocyte destruction precedes demyelination in NMO, and emphasize the importance of serological testing in patients with limited disease. Adherence to current NMO diagnostic criteria may delay treatment, or lead to inappropriate therapy with beta-interferon or natalizumab.

引用

页码：108 / 112

页数：5

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