Postcontrast MRI of Cranial Meninges: Leptomeningitis Versus Pachymeningitis
Postcontrast MRI of Cranial Meninges: Leptomeningitis Versus Pachymeningitis
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DOI：
10.1097/00004728-199509000-00005
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发表时间：
1995-09
影响因子：
1.3
通讯作者：
F. Kioumehr;M. Dadsetan;N. Feldman;Glenn Mathison;H. Moosavi;S. Rooholamini;R. Verma
中科院分区：
文献类型：
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作者：
F. Kioumehr;M. Dadsetan;N. Feldman;Glenn Mathison;H. Moosavi;S. Rooholamini;R. Verma
目的探讨脑膜增强MRI的特点及其与临床疾病的关系。材料与方法回顾性分析83例头颅MRI增强后脑膜强化患者的MRI表现、临床资料及实验室检查结果。脑膜不同层次的强化模式可分为两种类型：软脑膜强化（软脑膜和蛛网膜），当脑膜增强沿脑回回旋和/或累及基底池周围的脑膜时;硬脑膜（硬脑膜），当强化沿着颅骨，大脑镰，或小脑幕没有延伸到皮质回或基底池受累。基底池周围的增强被认为是软脑膜的，因为硬脑膜-蛛网膜在该区域与软脑膜-蛛网膜分离很远。此外，脑膜增强被分为五个病因亚组，即，癌性的、感染性的、炎性的、反应性的和化学的。病史、临床表现和脑脊液分析结果用于区分感染性脑膜炎和癌性脑膜炎。由于手术、分流术或创伤引起的脑膜增强被认为是反应性的，而破裂的囊肿（皮样囊肿或囊尾蚴样囊肿）或鞘内化疗被归类为化学性脑膜炎。继发于胶原血管病或结节病的脑膜炎被认为是炎性的。结果83例脑膜炎患者中，肿瘤性脑膜炎30例，感染性脑膜炎28例，反应性脑膜炎14例，化学性脑膜炎8例，炎性脑膜炎3例。25例（83%）癌性脑膜炎、14例（100%）反应性脑膜炎、3例（100%）炎性脑膜炎和1例（12%）化学性脑膜炎表现为硬脑膜强化，而28例（100%）感染性脑膜炎和7例（78%）化学性脑膜炎表现为软脑膜强化。只有5例（17%）癌性脑膜炎亚组显示软脑膜强化。这5例中有4例是由于脑实质内肿瘤直接扩散或通过神经周围延伸，而不是血行受累。仅1例癌性脑膜炎患者表现为软脑膜强化，但无明显脑实质内病变。结论对脑膜强化的不同类型（软脑膜炎与硬脑膜炎）的识别有助于鉴别感染性脑膜炎与癌性脑膜炎。本研究显示感染性脑膜炎多以软脑膜炎表现，而癌性脑膜炎则以硬脑膜炎表现。
Objective Our goal was to characterize the patterns of meningeal enhancement in postcontrast MR images and correlate these patterns with the clinical disorders. Materials and Methods The MR scans, medical records, and laboratory findings of 83 patients, whose postcontrast MR studies of the head demonstrated meningeal enhancement, were reviewed retrospectively. The patterns of enhancement of the different layers of the meninges were divided into two types: leptomeningeal (pia and arachnoid), when enhancement of the meninges followed the convolutions of the gyri and/or involved the meninges around the basal cisterns; and pachymeningeal (dura), when the enhancement was thick and linear or nodular along the inner surface of the calvarium, falx, or tentorium without extension into the cortical gyri or basal cistern involvement. Enhancement around the basal cistern was considered leptomeningeal, since the dura-arachnoid is widely separated from the pia-arachnoid in this region. Further, the meningeal enhancement was divided into five etiologic subgroups, i.e., carcinomatous, infectious, inflammatory, reactive, and chemical. The medical history, clinical presentation, and findings on CSF analysis were used to distinguish infectious from carcinomatous meningitis. Meningeal enhancement due to surgery, shunt, or trauma was considered reactive, while ruptured cysts (dermoid or cysticercoid) or intrathecal chemotherapy were classified as chemical meningitis. Meningitis secondary to involvement by collagen vascular disease or sarcoidosis was considered to be inflammatory. Results Thirty of the 83 subjects had carcinomatous, 28 infectious, 14 reactive, 8 chemical, and 3 inflammatory etiology for meningitis. Twenty-five cases (83%) of the carcinomatous, 14 (100%) of the reactive, 3 (100%) of the inflammatory, and 1 (12%) of the chemical meningitis subgroups demonstrated pachymeningeal enhancement, while 28 cases (100%) of the infectious meningitis and 7 (78%) of the chemical meningitis subgroups had leptomeningeal enhancement. Only five cases (17%) of the carcinomatous meningitis subgroup showed leptomeningeal enhancement. Four of these five cases were as a result of direct spread of intraparenchymal tumors or through perineural extension, rather than hematogenous involvement. Only one patient with carcinomatous meningitis demonstrated leptomeningeal enhancement without clear intraparenchymal lesion. Conclusion The recognition of various patterns of meningeal enhancement (leptomeningitis versus pachymeningitis) may help in differentiating between infectious and carcinomatous meningitis. This study demonstrated that infectious meningitis presents mostly as leptomeningitis, while carcinomatous meningitis presents as pachymeningitis.