POSTCONTRAST MRI OF CRANIAL MENINGES - LEPTOMENINGITIS VERSUS PACHYMENINGITIS

Objective: Our goal was to characterize the patterns of meningeal enha ncement in postcontrast MR images and correlate these patterns with th e clinical disorders. Materials and Methods: The MR scans, medical rec ords, and laboratory findings of 83 patients, whose postcontrast MR st udies of the head demonstrated meningeal enhancement, were reviewed re trospectively. The patterns of enhancement of the different layers of the meninges were divided into two types: leptomeningeal (pia and arac hnoid), when enhancement of the meninges followed the convolutions of the gyri and/or involved the meninges around the basal cisterns; and p achymeningeal (dura), when the enhancement was thick and linear or nod ular along the inner surface of the calvarium, fair, or tentorium with out extension into the cortical gyri or basal cistern involvement. Enh ancement 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 etio logic subgroups, i.e., carcinomatous, infectious, inflammatory, reacti ve, and chemical. The medical history, clinical presentation, and find ings on CSF analysis were used to distinguish infectious from carcinom atous meningitis. Meningeal enhancement due to surgery, shunt, or trau ma was considered reactive, while ruptured cysts (dermoid or cysticerc oid) or intrathecal chemotherapy were classified as chemical meningiti s. 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 infla mmatory, and 1 (12%) of the chemical meningitis subgroups demonstrated pachymeningeal enhancement, while 28 cases (100%) of the infectious m eningitis and 7 (78%) of the chemical meningitis subgroups had leptome ningeal enhancement. Only five cases (17%) of the carcinomatous mening itis subgroup showed leptomeningeal enhancement. Four of these five ca ses were as a result of direct spread of intraparenchymal tumors or th rough perineural extension, rather than hematogenous involvement. Only one patient with carcinomatous meningitis demonstrated leptomeningeal enhancement without clear intraparenchymal lesion. Conclusion: The re cognition of various patterns of meningeal enhancement (leptomeningiti s versus pachymeningitis) may help in differentiating between infectio us and carcinomatous meningitis. This study demonstrated that infectio us meningitis presents mostly as leptomeningitis, while carcinomatous meningitis presents as pachymeningitis.