Leptomeningeal Enhancement on 3D‐FLAIR MRI in Multiple Sclerosis: Systematic Observations in Clinical Practice

Titelbaum, David S.; Engisch, Renate; Schwartz, Eric D.; Napoli, Salvatore; Samaan, Soleil; Katz, Jordan; Lathi, Ellen

doi:10.1111/jon.12774

Cited by 15 publications

(35 citation statements)

References 35 publications

(137 reference statements)

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“…Beside the heterogeneity in immune cellular composition, which is more complex within dural layers, meningeal membranes are characterized by the presence of the arachnoid barrier (AB) cells at the interface with the dura and the blood-meningeal barrier (Figure 1A,B). While the AB is considered an insurmountable hurdle for the inward passage to the CSF of molecules released from leaky dural capillaries, and, in addition, no evidence exists for the involvement of the dura mater in MS, the MRI detection of dural nodular enhancement, close to veins and sinuses [14], remains to be elucidated. cord meningeal inflammation, white and grey demyelination, and axon loss in motor and sensory tracts [25].…”

Section: Meningeal Inflammationmentioning

confidence: 99%

Intrathecal Inflammation in Progressive Multiple Sclerosis

Monaco

Nicholas

Reynolds

et al. 2020

IJMS

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Progressive forms of multiple sclerosis (MS) are associated with chronic demyelination, axonal loss, neurodegeneration, cortical and deep gray matter damage, and atrophy. These changes are strictly associated with compartmentalized sustained inflammation within the brain parenchyma, the leptomeninges, and the cerebrospinal fluid. In progressive MS, molecular mechanisms underlying active demyelination differ from processes that drive neurodegeneration at cortical and subcortical locations. The widespread pattern of neurodegeneration is consistent with mechanisms associated with the inflammatory molecular load of the cerebrospinal fluid. This is at variance with gray matter demyelination that typically occurs at focal subpial sites, in the proximity of ectopic meningeal lymphoid follicles. Accordingly, it is possible that variations in the extent and location of neurodegeneration may be accounted for by individual differences in CSF flow, and by the composition of soluble inflammatory factors and their clearance. In addition, “double hit” damage may occur at sites allowing a bidirectional exchange between interstitial fluid and CSF, such as the Virchow–Robin spaces and the periventricular ependymal barrier. An important aspect of CSF inflammation and deep gray matter damage in MS involves dysfunction of the blood–cerebrospinal fluid barrier and inflammation in the choroid plexus. Here, we provide a comprehensive review on the role of intrathecal inflammation compartmentalized to CNS and non-neural tissues in progressive MS.

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Section: Meningeal Inflammationmentioning

confidence: 99%

Intrathecal Inflammation in Progressive Multiple Sclerosis

Monaco

Nicholas

Reynolds

et al. 2020

IJMS

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“…(29) The acquisition of the 3D T2w-FLAIR sequence was mostly 10 minutes after Gd-injection, with two studies reporting either earlier (3 minutes)(20) or later acquisition (up to 54 minutes). (15) It is noteworthy that latter study suggested that individual LME foci might have different enhancement kinetics and thus different peak enhancement time points, and that differences in LME detection between scanner types could be due to differences in 3D T2w-FLAIR sequences.…”

Section: Resultsmentioning

confidence: 81%

“…(32) In contrast to these studies with relatively small sample size and consequently lower statistical power, one study including 241 MS patients observed resolution of LME in 2 patients after high-dose steroid treatment within 6 months follow-up. (15)…”

Section: Resultsmentioning

confidence: 99%

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Leptomeningeal Enhancement in Multiple Sclerosis and Other Neurological Diseases: A Systematic Review and Meta-Analysis

Ineichen

Tsagkas

Absinta

et al. 2021

Preprint

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BackgroundThe lack of systematic evidence on leptomeningeal enhancement (LME) on MRI in neurological diseases, including multiple sclerosis (MS), hampers its interpretation in clinical routine and research settings.PurposeTo perform a systematic review and meta-analysis of MRI LME in MS and other neurological diseases.Materials and MethodsIn a comprehensive literature search in Medline, Scopus, and Embase, out of 2292 publications, 459 records assessing LME in neurological diseases were eligible for qualitative synthesis. Of these, 135 were included in a random-effects model meta-analysis with subgroup analyses for MS.ResultsOf eligible publications, 161 investigated LME in neoplastic neurological (n=2392), 91 in neuroinfectious (n=1890), and 75 in primary neuroinflammatory diseases (n=4038). The LME-proportions for these disease classes were 0.47 [95%-CI: 0.37–0.57], 0.59 [95%-CI: 0.47–0.69], and 0.26 [95%-CI: 0.20–0.35], respectively. In a subgroup analysis comprising 1605 MS cases, LME proportion was 0.30 [95%-CI 0.21–0.42] with lower proportions in relapsing-remitting (0.19 [95%-CI 0.13–0.27]) compared to progressive MS (0.39 [95%-CI 0.30–0.49], p=0.002) and higher proportions in studies imaging at 7T (0.79 [95%-CI 0.64–0.89]) compared to lower field strengths (0.21 [95%-CI 0.15–0.29], p<0.001). LME in MS was associated with longer disease duration (mean difference 2.2 years [95%-CI 0.2–4.2], p=0.03), higher Expanded Disability Status Scale (mean difference 0.6 points [95%-CI 0.2–1.0], p=0.006), higher T1 (mean difference 1.6ml [95%-CI 0.1–3.0], p=0.04) and T2 lesion load (mean difference 5.9ml [95%-CI 3.2–8.6], p<0.001), and lower cortical volume (mean difference −21.3ml [95%-CI −34.7–-7.9], p=0.002).ConclusionsOur study provides high-grade evidence for the substantial presence of LME in MS and a comprehensive panel of other neurological diseases. Our data could facilitate differential diagnosis of LME in clinical settings. Additionally, our meta-analysis corroborates that LME is associated with key clinical and imaging features of MS.PROSPERO No: CRD42021235026.Summary statementOur systematic review and meta-analysis synthesize leptomeningeal enhancement proportions across a comprehensive panel of neurological diseases, including multiple sclerosis, and assesses its prognostic value in multiple sclerosis.Summary dataLeptomeningeal enhancement (LME) is a nonspecific imaging feature present across many neurological disorders, including neoplasm, infection, and primary neuroinflammation.The presence of LME is associated with worse clinical and imaging outcomes in multiple sclerosis, justifying its ascertainment in clinical practice.Neuroinflammatory animal models can be used to further investigate the pathophysiology of LME, including its pathological tissue signature and/or its association with cortical pathology.

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“…Additional clinical scenarios likely warrant the use of contrast agents, such as suspicion of progressive multifocal leukoencephalopathy (PML), or other secondary cause of new symptoms, such as malignancy. There is also emerging literature regarding the detection of leptomeningeal inflammation in MS, which currently requires gadolinium for detection 19–23 …”

Section: Discussionmentioning

confidence: 99%

Limited Utility of Gadolinium Contrast Administration in Routine Multiple Sclerosis Surveillance

Johnston

Johnson

Solomon

et al. 2020

Journal of Neuroimaging

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BACKGROUND AND PURPOSE Assess the incidence of enhancing lesions on follow‐up MRIs in patients with multiple sclerosis (MS) to determine the utility of intravenous, gadolinium‐based contrast agent (IV‐GBCA) use in routine follow‐up imaging. METHODS We retrospectively identified head MRIs associated with an MS diagnosis acquired between January 1, 2015and January 10, 2018. Final reports were reviewed to determine the presence of (1) a new or larger lesion, (2) at least one enhancing lesion, and (3) if at least one enhancing lesion was new or larger on Fluid‐Attenuation Inversion Recovery (FLAIR). For MRIs with at least one enhancing lesion, but no new or larger enhancing lesions, reports and images of the preceding MRI were reviewed. RESULTS A total of 1,805 MRIs performed on 920 patients were included. 354/1,805 (20%) MRIs reported new or enlarging lesions. 138/1,805 (8%) MRIs reported at least one enhancing lesion. Of these, 117/138 (85%) reported at least one enhancing lesion that was new or larger. In the remaining 21 MRIs which contained an enhancing lesion but none of the enhancing lesions were reported as new or enlarging, at least one enhancing lesion was present on preceding MRI. CONCLUSIONS Enhancing lesions are uncommon on follow‐up MRIs in MS patients. Our data suggest that new enhancing lesions are not present on a follow‐up MRI when two conditions are met: (1) preceding MRI does not demonstrate any enhancing lesions and (2) there is no interval change of the lesions on the current 3D‐T2‐FLAIR sequence compared to the preceding 3D‐T2‐FLAIR sequence. IV‐GBCA should be reserved for instances when temporal knowledge of lesion formation is needed.

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Leptomeningeal Enhancement on 3D‐FLAIR MRI in Multiple Sclerosis: Systematic Observations in Clinical Practice

Cited by 15 publications

References 35 publications

Intrathecal Inflammation in Progressive Multiple Sclerosis

Intrathecal Inflammation in Progressive Multiple Sclerosis

Leptomeningeal Enhancement in Multiple Sclerosis and Other Neurological Diseases: A Systematic Review and Meta-Analysis

Limited Utility of Gadolinium Contrast Administration in Routine Multiple Sclerosis Surveillance

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