PubMedDate not supplied
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.