Kioumehr F, Dadsetan M R, Feldman N, Mathison G, Moosavi H, Rooholamini S A, Verma R C
Department of Radiological Sciences, Olive View-UCLA Medical Center, Sylmar 91342, USA.
J Comput Assist Tomogr. 1995 Sep-Oct;19(5):713-20. doi: 10.1097/00004728-199509000-00005.
Our goal was to characterize the patterns of meningeal enhancement in postcontrast MR images and correlate these patterns with the clinical disorders.
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.
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.
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.
我们的目标是描述增强后磁共振成像(MR)中脑膜强化的模式,并将这些模式与临床疾病相关联。
回顾性分析83例患者的MR扫描、病历及实验室检查结果,这些患者头部增强MR检查显示有脑膜强化。脑膜不同层的强化模式分为两种类型:软脑膜(蛛网膜和软膜)强化,即脑膜强化沿着脑回的脑沟走行和/或累及脑基底池周围的脑膜;硬脑膜强化,即强化沿着颅骨内表面、大脑镰或小脑幕呈厚的线性或结节状,不延伸至皮质脑回或不累及脑基底池。脑基底池周围的强化被认为是软脑膜强化,因为在该区域硬脑膜-蛛网膜与软膜-蛛网膜广泛分离。此外,脑膜强化分为五个病因亚组,即癌性、感染性、炎症性、反应性和化学性。利用病史、临床表现及脑脊液分析结果区分感染性脑膜炎和癌性脑膜炎。手术、分流或创伤导致的脑膜强化被认为是反应性的,而破裂囊肿(皮样囊肿或囊尾蚴样囊肿)或鞘内化疗所致的脑膜强化被归类为化学性脑膜炎。胶原血管病或结节病累及继发的脑膜炎被认为是炎症性的。
83例患者中,30例脑膜炎病因是癌性,28例是感染性,14例是反应性,8例是化学性,3例是炎症性。癌性脑膜炎亚组25例(83%)、反应性脑膜炎亚组14例(100%)、炎症性脑膜炎亚组3例(100%)及化学性脑膜炎亚组1例(12%)表现为硬脑膜强化,而感染性脑膜炎亚组28例(100%)及化学性脑膜炎亚组7例(之8%)表现为软脑膜强化。癌性脑膜炎亚组仅5例(17%)表现为软脑膜强化。这5例中有4例是由于脑实质内肿瘤直接蔓延或经神经周围蔓延所致,而非血行播散。仅有1例癌性脑膜炎患者表现为软脑膜强化而无明确的脑实质内病变。
认识脑膜强化的各种模式(软脑膜炎与硬脑膜炎)可能有助于区分感染性脑膜炎和癌性脑膜炎。本研究表明,感染性脑膜炎大多表现为软脑膜炎,而癌性脑膜炎表现为硬脑膜炎。