Ogawa M, Ishimaru K, Shiroto T, Baba M, Matsunaga M
Third Department of Medicine, Hirosaki University School of Medicine.
Rinsho Shinkeigaku. 1994 Jun;34(6):577-81.
We describe a 35-year-old woman with benign intracranial hypertension (BIH) secondary to systemic lupus erythematosus (SLE). She had low grade fever and skin eruptions, but neurological examination revealed no abnormal findings. Antinuclear and anti ds-DNA antibodies were positive, and complements were decreased. MRI demonstrated diffuse hyperintense white matter lesions on T2-weighted imaging. Mild bilateral papilledemas developed in the fundi, when her headache was exacerbated. The cerebrospinal fluid (CSF) pressure was 550 mmH2O. Cerebral angiography showed no cerebral sinus thrombosis. She was diagnosed as BIH secondary to SLE. Since RI cisternography revealed remarkably delayed absorption of the CSF, it was speculated that the CSF absorption by arachnoid villi would be probably disturbed in association with some autoimmune mechanisms by SLE. The subsequent rise of intraventricular pressure may result in retrograde transependymal flow of the CSF and the diffuse hyperintense white matter lesions on MRI.
我们描述了一名35岁患有继发于系统性红斑狼疮（SLE）的良性颅内高压（BIH）的女性。她有低热和皮疹，但神经系统检查未发现异常。抗核抗体和抗双链DNA抗体呈阳性，补体降低。MRI在T2加权成像上显示弥漫性高信号白质病变。当她头痛加剧时，眼底出现轻度双侧视乳头水肿。脑脊液（CSF）压力为550 mmH2O。脑血管造影显示无脑窦血栓形成。她被诊断为继发于SLE的BIH。由于放射性脑池造影显示脑脊液吸收明显延迟，推测蛛网膜绒毛对脑脊液的吸收可能因SLE的某些自身免疫机制而受到干扰。随后脑室压力升高可能导致脑脊液逆行经室管膜流动以及MRI上弥漫性高信号白质病变。
