Meningeal Inflammation Research Articles

Meningeal inflammation and cortical demyelination in acute multiple sclerosis.

Cortical gray matter (GM) pathology, involving demyelination and neurodegeneration, associated with meningeal inflammation, could be important in determining disability progression in multiple sclerosis (MS). However, we need to know more about how cortical demyelination, neurodegeneration, and meningeal inflammation contribute to pathology at early stages of MS to better predict long-term outcome. Tissue blocks from short disease duration MS (n = 12, median disease duration = 2 years), progressive MS (n = 21, disease duration = 25 years), non-diseased controls (n = 11), and other neurological inflammatory disease controls (n = 6) were quantitatively analyzed by immunohistochemistry, immunofluorescence, and in situ hybridization. Cortical GM demyelination was extensive in some cases of acute MS (range = 1-48% of total cortical GM), and subpial lesions were the most common type (62%). The numbers of activated (CD68+ ) microglia/macrophages were increased in cases with subpial lesions, and the density of neurons was significantly reduced in acute MS normal appearing and lesion GM, compared to controls (p < 0.005). Significant meningeal inflammation and lymphoid-like structures were seen in 4 of 12 acute MS cases. The extent of meningeal inflammation correlated with microglial/macrophage activation (p < 0.05), but not the area of cortical demyelination, reflecting the finding that lymphoid-like structures were seen adjacent to GM lesions as well as areas of partially demyelinated/remyelinated, cortical GM. Our findings demonstrate that cortical demyelination, neuronal loss, and meningeal inflammation are notable pathological hallmarks of acute MS and support the need to identify early biomarkers of this pathology to better predict outcome. Ann Neurol 2018;84:829-842.

Cytokine profiles in cerebrospinal fluid of patients with meningitis at a tertiary general hospital in China.

There has been a great deal of evidence indicating that cytokines participate in meningeal inflammation. Different cytokine profiles may be presented in central nervous system (CNS) infection due to different pathogens. We have attempted to investigate cytokine profiles in cerebrospinal fluid (CSF) of patients with CNS infection. Forty-three patients with CNS infection including tuberculous meningitis, purulent meningitis and cryptococcal meningitis were enrolled and 11 patients with normal CSF were enrolled as control group. The concentrations of Th1-, Th2- and Th17-type cytokines in CSF were detected using multiplex cytokine assay. Furthermore, the correlation between CSF cytokines and CSF parameters in CNS infection was analyzed. The CSF levels of IL-1β, IL-4, IL-6, IL-10, IL-17, IL-23, IL-33, IFN-γ, TNF-α and sCD40L among the patients with CNS infection were all higher than control group (all P<0.05). A remarkable elevation of CSF IL-6 in the patients with CNS infection was observed with the least overlap of the CSF concentrations compared to controls. Moreover, CSF IL-6 levels were strongly negatively correlated with CSF glucose and the CSF/blood glucose ratio (r=-0.4375, P=0.0042; r=-0.4991, P=0.0009). The excessive activation of immune response characterized by elevated levels of CSF Th1-, Th2- and Th17-type cytokines has been observed during CNS infection. Furthermore, we observed negative correlations between CSF IL-6 levels and CSF glucose and CSF/blood glucose ratio in CNS infection. And we suggested that combined CSF IL-6 levels with CSF glucose may serve as a novel biomarker pool for the differential of CNS infection.

Longitudinal Persistence of Meningeal Enhancement on Postcontrast 7T 3D-FLAIR MRI in Multiple Sclerosis.

Preliminary research has demonstrated that postgadolinium 3D-FLAIR MR imaging at 7T may be a valuable tool for detecting abnormal meningeal enhancement and inflammation in MS; however, researchers have not systematically investigated its longitudinal persistence. We hypothesized that persistence of meningeal enhancement in MS varies on the basis of pattern of enhancement as well as demographic and clinical factors such as treatment status, disease phenotype, and disability score. Thirty-one subjects with MS were prospectively scanned before and after intravenous contrast administration at 2 time points, approximately 1 year apart. Fifteen subjects in the cohort were scanned at another time approximately 1 year later. Foci of enhancement were categorized into 4 subtypes: subarachnoid spread/fill, subarachnoid nodular, vessel wall, and dural foci. We reviewed follow-up scans to determine whether foci changed between time points and then compared persistence with demographic and clinical variables. Persistence ranged from 71% to 100% at 1 year and 73% to 100% at 2 years, depending on the enhancement pattern. Subarachnoid spread/fill and subarachnoid nodular subtypes persisted less often than vessel wall and dural foci. Persistence was not significantly different between those on/off treatment and those with progressive/nonprogressive disease phenotypes. The number of persisting foci was significantly different in subjects with/without increasing Expanded Disability Status Scale scores (median, 12 versus 7.5, P = .04). Longitudinal persistence of meningeal enhancement on 3D-FLAIR at 7T in MS varies by pattern of enhancement and correlates with worsening disability; however, it is not significantly different in those on/off treatment or in those with progressive/nonprogressive disease phenotypes.

Imaging of meningeal inflammation should become part of the routine MRI protocol – Commentary

Imaging of meningeal inflammation should become part of the routine MRI protocol – Commentary

Imaging of meningeal inflammation should become part of the routine MRI protocol – No

Imaging of meningeal inflammation should become part of the routine MRI protocol – No

Imaging of meningeal inflammation should become part of the routine MRI protocol – Yes

Imaging of meningeal inflammation should become part of the routine MRI protocol – Yes

Cortical and meningeal pathology in progressive multiple sclerosis: a new therapeutic target?

Multiple sclerosis (MS) is an inflammatory and neurodegenerative disease that involves an intricate interaction between the central nervous system and the immune system. Nevertheless, its etiology is still unknown. MS exhibits different clinical courses: recurrent episodes with remission periods ('relapsing-remitting') that can evolve to a 'secondary progressive' form or persistent progression from the onset of the disease ('primary progressive'). The discovery of an effective treatment and cure has been hampered due to the pathological and clinical heterogeneity of the disease. Historically, MS has been considered as a disease exclusively of white matter. However, patients with progressive forms of MS present with cortical lesions associated with meningeal inflammation along with physical and cognitive disabilities. The pathogenesis of the cortical lesions has not yet been fully described. Animal models that represent both the cortical and meningeal pathologies will be critical in addressing MS pathogenesis as well as the design of specific treatments. In this review, we will address the state-of-the-art diagnostic and therapeutic alternatives and the development of strategies to discover new therapeutic approaches, especially for the progressive forms.

The prognostic factors of HIV-negative adult cryptococcal meningitis with a focus on cranial MRI-based neuroimaging findings

The prognostic significance of clinical characteristics and neuroimaging features, especially cranial magnetic resonance imaging (MRI)-based neuroimaging features, in patients with human immunodeficiency virus (HIV)-negative cryptococcal meningitis (CM) has rarely been examined in the literature. We analyzed the clinical characteristics and MRI findings of 65 HIV-negative patients (43 men, 22 women, age 19–86 years) collected during a study period of 15 years (January 2001–December 2015). Their underlying conditions included diabetes mellitus, liver cirrhosis, hematologic disorders, autoimmune disorders, malignancy, chronic obstructive pulmonary disease, adrenal insufficiency and organ transplantation, and their clinical presentations included headache, altered consciousness, fever, seizure, visual disturbance and hearing impairment. The main cranial MRI findings were basal meningeal enhancement (44.6%, 29/65), dilated Virchow-Robin space/pseudocyst (43.1%, 28/65), “dirty” cerebrospinal fluid sign (38.5%, 25/65), hydrocephalus (36.9%, 21/65), acute/subacute cerebral infarct (ASCI, 21.5%, 14/65), cryptococcoma (9.2%, 6/65), and hazy brain base (1.5%, 1/65). The therapeutic results of the 65 patients were evaluated using the Glasgow Outcome Scale (GOS). A comparison of the good outcome group (GOS score = 4–5, n = 37) and poor outcome group (GOS score = 1–3, n = 28) revealed that both the presence of seizures and ASCI were significantly associated with the prognosis. A comparison of the groups with ASCI (n = 14) and without ASCI (n = 51) revealed that the presence of basal meningeal enhancement was a significant factor for the development of ASCI, and that this correlation may be associated with intense basal meningeal inflammation in adjacent small vessels.

Current understanding of meningeal and cerebral vascular function underlying migraine headache.

The exact mechanisms underlying the onset of a migraine attack are not completely understood. It is, however, now well accepted that the onset of the excruciating throbbing headache of migraine is mediated by the activation and increased mechanosensitivity (i.e. sensitization) of trigeminal nociceptive afferents that innervate the cranial meninges and their related large blood vessels. To provide a critical summary of current understanding of the role that the cranial meninges, their associated vasculature, and immune cells play in meningeal nociception and the ensuing migraine headache. We discuss the anatomy of the cranial meninges, their associated vasculature, innervation and immune cell population. We then debate the meningeal neurogenic inflammation hypothesis of migraine and its putative contribution to migraine pain. Finally, we provide insights into potential sources of meningeal inflammation and nociception beyond neurogenic inflammation, and their potential contribution to migraine headache.

Prodromal headache in anti-NMDAR encephalitis: An epiphenomenon of NMDAR autoimmunity.

ObjectiveTo investigate the nature of prodromal headache in anti‐NMDA receptor (NMDAR) encephalitis.MethodsRetrospective review of the clinical information of 39 patients with anti‐NMDAR encephalitis admitted between January 1999 and September 2017. Five patients with an atypical presentation were excluded. Thus, in 34 patients (median 27 years [range, 12–47 years]; 28 [82%] female), the clinical features were compared between patients who initially reported headache and those who did not report.ResultsTwenty‐two patients (65%) reported headache either transiently (n = 5) or continuously (n = 17). Encephalitic symptoms (psychobehavioral memory alterations, seizure, dyskinesias, or altered level of consciousness) developed in 20 patients with median 5.5 days (range, 1‐29 days) after headache onset. In one patient, NMDAR antibodies were detected in CSF 3 days after headache onset. Patients with headache had more frequently fever (14/22 [64%] vs. 2/12 [17%] p = 0.013) and higher CSF pleocytosis (median white blood cells 79/μl [range, 6‐311/μl] vs. 30/μl [range, 2‐69/μl], p = 0.035) than those without headache, but there was no difference in gender, age at onset, seizure, migraine, CSF oligoclonal band detection, elevated IgG index, tumor association, or brain MRI abnormalities between them.ConclusionsHeadache often developed with fever and pleocytosis, but it was rapidly replaced by psychiatric symptoms. Based on current knowledge on the antibody‐mediated mechanisms that cause a decrease of synaptic NMDAR through crosslinking and internalization leading to a state mimicking “dissociative anesthesia,” we speculated that prodromal headache is not likely caused by direct effect of the autoantibodies but rather meningeal inflammation (noninfectious aseptic meningitis) that occurs in parallel to intrathecal antibody synthesis as an epiphenomenon of NMDAR autoimmunity. Psychobehavioral alterations following headache is an important clue to the diagnosis.

Monocyte-derived IL-1 and IL-6 are differentially required for cytokine-release syndrome and neurotoxicity due to CAR T cells.

In the clinic, chimeric antigen receptor-modified T (CAR T) cell therapy is frequently associated with life-threatening cytokine-release syndrome (CRS) and neurotoxicity. Understanding the nature of these pathologies and developing treatments for them are hampered by the lack of appropriate animal models. Herein, we describe a mouse model recapitulating key features of CRS and neurotoxicity. In humanized mice with high leukemia burden, CAR T cell-mediated clearance of cancer triggered high fever and elevated IL-6 levels, which are hallmarks of CRS. Human monocytes were the major source of IL-1 and IL-6 during CRS. Accordingly, the syndrome was prevented by monocyte depletion or by blocking IL-6 receptor with tocilizumab. Nonetheless, tocilizumab failed to protect mice from delayed lethal neurotoxicity, characterized by meningeal inflammation. Instead, the IL-1 receptor antagonist anakinra abolished both CRS and neurotoxicity, resulting in substantially extended leukemia-free survival. These findings offer a therapeutic strategy to tackle neurotoxicity and open new avenues to safer CAR T cell therapies.

Ontogeny of white matter, toll-like receptor expression, and motor skills in the neonatal ferret

Inflammation caused by perinatal infection, superimposed with hypoxia and/or hyperoxia, appears to be important in the pathogenesis of preterm neonatal encephalopathy, with white matter particularly vulnerable during the third trimester. The associated inflammatory response is at least partly mediated through Toll-like receptor (TLR)-dependent mechanisms. Immunohistochemistry, gene expression, and behavioral studies were used to characterize white matter development and determine TLR3 and TLR4 expression and accumulation in the neonatal ferret brain. Expression of markers of white matter development increased significantly between postnatal day (P)1 and P10 (NG2, PDGFRα) or P15 (Olig2), and either remained elevated (NG2), or decreased again at P40 (PDGFRα, Olig2). Olig2 immunostaining within the internal capsule was also greatest at P15. Myelin basic protein (MBP) immunostaining and mRNA expression increased markedly from P15 to P40 and into adulthood, which correlated with increasing performance on behavioral tests (negative geotaxis, cliff aversion, righting reflex, and catwalk gait analysis). TLR4 and TLR3 positive staining was low at all ages, but TLR3 and TLR4 mRNA expression both increased significantly from P1 to P40. Following lipopolysaccharide (LPS) and hypoxia/hyperoxia exposure at P10, meningeal and parenchymal inflammation was seen, including an increase in TLR4 positive cells. These data suggest that the neuroinflammation associated with prematurity could be modeled in the newborn ferret.

Rheumatoid meningitis developed in patient with stable rheumatoid arthritis and myasthenia gravis\u2014detailed analysis of intracranial inflammation using flow cytometry

BackgroundRheumatoid meningitis (RM) is a rare disorder that often develops during a remission phase of rheumatoid arthritis (RA). This is the first study to demonstrate differences in regard to immunological disturbance between blood and cerebrospinal fluid (CSF) samples obtained from a patient with RM using flow cytometry.Case presentationA 36-year-old woman with RA and generalized myasthenia gravis (MG) developed RM during a remission phase. Although both RA and MG were stable and well controlled, she noticed fever, headache, and transient sensory disturbance. Blood and CSF examination findings suggested aseptic meningitis, while brain magnetic resonance imaging revealed restricted portions of meningitis and associated cortical lesions, compatible with a diagnosis of RM. The dose of oral prednisolone was increased, which ameliorated the symptoms within 1 week along with improvement in CSF findings. This patient exhibited features of RM that were manifested in a manner independent of the activity of RA. An investigation of cellular immunity using CSF specimens with flow cytometry showed differences in regard to the pathogenesis of inflammation in the CSF as compared to outside of the central nervous system. In contrast to results obtained with paired blood samples, CSF cells at the peak stage of RM showed a marked increase in CCR3+ Th2 cells and marked decrease in CD8+ cells, suggesting an immunoregulatory disturbance in the CSF. Those findings indicated a CSF-specific activation of humoral immunity, resulting in augmentation of meningeal inflammation, as shown by excess synthesis of intrathecal IgG and markedly elevated interleukin-6 level. Results of the present detailed investigation of lymphocyte subsets revealed a discrepancy regarding the process of inflammation in this RM patient between CSF and blood samples.ConclusionsRM is not a simple reflection of the immune status of RA, as the pathogenesis seems related to, at least in part, CSF-specific immunological dysregulation.

Meningeal inflammation drives long-term engraftment by monocytes that impair CNS immunity

Abstract Tissue-resident macrophages have an embryonic origin and can be replenished by blood monocytes in some tissues during adulthood. Under steady-state conditions, infiltrating monocytes can share phenotypic and genotypic features with their embryonically-derived counterparts. However, little is known about the properties of monocytes/macrophages that establish tissue residency after an inflammatory challenge. The meninges of the central nervous system (CNS) are populated by a dense network of specialized macrophages that serve as immune sentinels. Following infection by lymphocytic choriomeningitis virus (LCMV), these resident macrophages become activated by innate inflammatory cytokines, acquire viral antigens, and are targeted by infiltrating cytotoxic T lymphocytes (CTL), which leads to their depletion. Innate cytokines and chemokines released by CTL also promote a massive recruitment of inflammatory monocytes from the periphery. Surprisingly, these infiltrating monocytes engraft the meningeal niche and remain in situ several months after viral clearance. This leads to significant phenotypic and functional changes in meningeal immunity – a defect that can be partially restored by blocking IFNγ signaling. Importantly, macrophages that establish residency in the meninges after an inflammatory event are deficient in bacterial and immunoregulatory sensors, which impedes their ability to detect pathogens and dampen subsequent meningeal immune responses. Collectively, these data indicate that monocytes can engraft the meninges after an inflammatory challenge and contribute to long-term alterations in CNS immunity.

Endoscopic endonasal double flap technique for reconstruction of large anterior skull base defects: technical note

IntroductionOne of the main concerns in endoscopic endonasal approaches to the skull base has been the high incidence and morbidity associated with cerebrospinal fluid leaks. The introduction and routine use of vascularized flaps allowed a marked decrease in this complication followed by a great expansion in the indications and techniques used in endoscopic endonasal approaches, extending to defects from huge tumours and previously inaccessible areas of the skull base. ObjectiveDescribe the technique of performing endoscopic double flap multi-layered reconstruction of the anterior skull base without craniotomy. MethodsStep by step description of the endoscopic double flap technique (nasoseptal and pericranial vascularized flaps and fascia lata free graft) as used and illustrated in two patients with an olfactory groove meningioma who underwent an endoscopic approach. ResultsBoth patients achieved a gross total resection: subsequent reconstruction of the anterior skull base was performed with the nasoseptal and pericranial flaps onlay and a fascia lata free graft inlay. Both patients showed an excellent recovery, no signs of cerebrospinal fluid leak, meningitis, flap necrosis, chronic meningeal or sinonasal inflammation or cerebral herniation having developed. ConclusionThis endoscopic double flap technique we have described is a viable, versatile and safe option for anterior skull base reconstructions, decreasing the incidence of complications in endoscopic endonasal approaches.

Inflammatory intrathecal profiles and cortical damage in multiple sclerosis.

Gray matter (GM) damage and meningeal inflammation have been associated with early disease onset and a more aggressive disease course in multiple sclerosis (MS), but can these changes be identified in the patient early in the disease course? To identify possible biomarkers linking meningeal inflammation, GM damage, and disease severity, gene and protein expression were analyzed in meninges and cerebrospinal fluid (CSF) from 27 postmortem secondary progressive MS and 14 control cases. Combined cytokine/chemokine CSF profiling and 3T magnetic resonance imaging (MRI) were performed at diagnosis in 2 independent cohorts of MS patients (35 and 38 subjects) and in 26 non-MS patients. Increased expression of proinflammatory cytokines (IFNγ, TNF, IL2, and IL22) and molecules related to sustained B-cell activity and lymphoid-neogenesis (CXCL13, CXCL10, LTα, IL6, and IL10) was detected in the meninges and CSF of postmortem MS cases with high levels of meningeal inflammation and GM demyelination. Similar proinflammatory patterns, including increased levels of CXCL13, TNF, IFNγ, CXCL12, IL6, IL8, and IL10, together with high levels of BAFF, APRIL, LIGHT, TWEAK, sTNFR1, sCD163, MMP2, and pentraxin III, were detected in the CSF of MS patients with higher levels of GM damage at diagnosis. A common pattern of intrathecal (meninges and CSF) inflammatory profile strongly correlates with increased cortical pathology, both at the time of diagnosis and at death. These results suggest a role for detailed CSF analysis combined with MRI as a prognostic marker for more aggressive MS. Ann Neurol 2018 Ann Neurol 2018;83:739-755.

Novel and preclinical treatment strategies in pneumococcal meningitis.

Pneumococcal meningitis is the most frequent form of bacterial meningitis in Europe and the United States. Although early antimicrobial and adjuvant therapy with dexamethasone have helped to improve disease outcome in adults, mortality and morbidity rates remain unsatisfactorily high, emphasizing the need for additional treatment options. Promising targets for adjuvant therapy have been identified recently and will be the focus of this review. Brain disease in pneumococcal meningitis is caused by direct bacterial toxicity and excessive meningeal inflammation. Accordingly, promising targets for adjuvant therapy comprise limiting the release of toxic bacterial products and suppressing inflammation in a way that maximally protects against tissue injury without hampering pathogen eradication by antibiotics. Among the agents tested so far in experimental models, complement inhibitors, matrix-metalloproteinase inhibitors, and nonbacteriolytic antibiotics or a combination of the above have the potential to more efficiently protect the brain either alone (e.g., in children and outside the high-income settings) or in addition to adjuvant dexamethasone. Additionally, new protein-based pneumococcal vaccines are being developed that promise to improve disease prevention, namely by addressing the increasing problem of serotype replacement seen with pneumococcal conjugate vaccines. Pneumococcal meningitis remains a life-threatening disease requiring early antibiotic and targeted anti-inflammatory therapy. New adjuvant therapies showed promising results in animal models but need systematic clinical testing.

A new focal model resembling features of cortical pathology of the progressive forms of multiple sclerosis: Influence of innate immunity

Multiple sclerosis (MS) is an inflammatory and demyelinating disease of unknown aetiology that causes neurological disabilities in young adults. MS displays different clinical patterns, including recurrent episodes with remission periods (“relapsing-remitting MS” (RRMS)), which can progress over several years to a secondary progressive form (SPMS). However, 10% of patients display persistent progression at the onset of disease (“primary progressive MS” (PPMS)). Currently, no specific therapeutic agents are available for the progressive forms, mainly because the underlying pathogenic mechanisms are not clear and because no animal models have been specifically developed for these forms. The development of MS animal models is required to clarify the pathological mechanisms and to test novel therapeutic agents.In the present work, we overexpressed interleukin 1 beta (IL-1β) in the cortex to develop an animal model reflecting the main pathological hallmarks of MS. The treated animals presented with neuroinflammation, demyelination, glial activation, and neurodegeneration along with cognitive symptoms and MRI images consistent with MS pathology. We also demonstrated the presence of meningeal inflammation close to cortical lesions, with characteristics similar to those described in MS patients. Systemic pro-inflammatory stimulation caused a flare-up of the cortical lesions and behavioural symptoms, including impairment of working memory and the appearance of anxiety-like symptoms.Our work demonstrated induced cortical lesions, reflecting the main histopathological hallmarks and cognitive impairments characterizing the cortical pathology described in MS patients with progressive forms of the disease.

Diagnostic Value of CRP, Procalcitonin, and Ferritin Levels in Cerebrospinal Fluid of Children with Meningitis.

Bacterial meningitis is a serious disease with high rate of mortality and morbidity in children. Invasion of pathogens causes brain and meningeal inflammation, which leads to the release of biomarkers into cerebrospinal fluid (CSF). Identification of these biomarkers can help the physicians to differentiate between bacterial and aseptic meningitis. In the current study, some of these biomarkers such as Procalcitonin, C reactive protein (CRP), and Ferritin, were compared in cerebrospinal fluid (CSF) of patients with bacterial and aseptic meningitis. In a prospective cross sectional study in a referral children hospital in Tehran during 2011- 2013, the CSF levels of Procalcitonin, Ferritin, and CRP were measured in 57 children with clinically suspected meningitis. The Mann-Whitney u test and the chi-square test were used to compare two groups, children with bacterial and aseptic meningitis. The cut-offs of biomarker levels for differentiation between the 2 groups were constructed by receiver-operating - characteristic curve (ROC). 57 subjects (30 bacterial and 27 aseptic meningitis), were enrolled in this survey. In comparing the two groups, the CSF levels of Ferritin, CRP, and procalcitonin in bacterial meningitis were significantly higher than in aseptic meningitis (P values=˂0.001, 0.001, ˂0.001respectively), with sensitivity/ specificity being 92.9% / 68%, 92.9% / 84%, and 96.4% / 80%, respectively. Positive Predictive Values (PPV) were, correspondingly, 96.4%, 92.8%, and 92.8% for procalcitonin, Ferritin, and CRP. Corresponding Negative Predictive Values (NPV) were, respectively equal to 95.4%, 70%, and 88%. CSF of children with bacterial meningitis contains higher levels of inflammatory mediators including Procalcitonin, Ferritin, and CRP, compared to aseptic meningitis The biomarkers provided high sensitivity (especially PCT) and specificity (especially CRP). Using these complementary biomarkers would be useful for early diagnosis of bacterial meningitis and selection of appropriate treatment.

Contrast-enhanced fluid-attenuated inversion recovery magnetic resonance imaging was useful in detecting inflammation of the meninges in neuropsychiatric systemic lupus erythematosus: a case report

A 49-year-old woman was admitted to our hospital with recurrent episodes of paresthesia attacks evolving in 5 to 15 minutes from the left hand to the left leg through the left trunk. Neurological examination revealed cortical sensory disturbance in her left hand. Although contrast-enhanced T1-weighted MRI findings were unremarkable, contrast-enhanced fluid-attenuated inversion recovery (FLAIR) MRI revealed abnormal leptomeningeal enhancement over the sulcus of the parietal lobe, including the sulcus around the postcentral gyrus. Because we assumed the cause of the recurrent sensory attack to be meningeal inflammation around the primary somatosensory cortex, we treated this patient by increasing the dose of prednisolone. The increase in prednisolone dose completely resolved the symptom, as well as the abnormal leptomeningeal enhancement on contrast-enhanced FLAIR MRI. In patients with suspected meningeal inflammation, contrast-enhanced FLAIR MRI, which is reported to be more sensitive than contrast-enhanced T1-weighted MRI in detecting subtle abnormal leptomeningeal enhancement, should be the modality of choice.