1. Introduction
Dural-based lymphomas are rare but clinically relevant, ranging from (i) indolent primary dural lymphoma (PDL) —most commonly extranodal marginal zone lymphoma (EMZL)/mucosa-associated lymphoid tissue (MALT) lymphoma—to (ii) aggressive disease that may be primary dural (less often) or reflect dural involvement within secondary CNS lymphoma (SCNSL). These entities frequently share a “meningioma-like” radiological phenotype and therefore carry a non-negligible risk of delayed diagnosis and anchoring bias [ 1 , 2 , 3 ]. Quantitatively, a multi-institutional cohort of dural marginal zone lymphoma reported upfront tumor resection in 65% (17/26) of patients because the preoperative impression was meningioma [ 4 ]. Similarly, histopathology-confirmed cohorts confirm that dural MZL commonly presents as a dura-based enhancing mass with a meningioma-like phenotype [ 5 ], supporting the clinical relevance of a biopsy-first/biology-first strategy to reduce anchoring bias and unnecessary resections.
This distinction is not merely nosological but carries immediate management implications. When clinical and radiological red flags raise suspicion for a “meningioma-mimicking lesion” consistent with lymphoma, anchoring bias should be actively avoided and the diagnostic work-up promptly redirected towards histopathologic confirmation and appropriate staging.
Accurate classification (PDL EMZL/MALT, PDL non-EMZL/MALT including dural DLBCL, and secondary dural involvement/SCNSL) has direct consequences for the diagnostic work-up (extent of systemic staging and CSF assessment according to context), radiotherapy and surgical decision-making (biopsy vs. resection), the need for CNS-directed chemotherapy (particularly high-dose methotrexate [HD-MTX]-based regimens in aggressive cases), and follow-up strategies [ 6 , 7 ].
The 5th edition of the WHO classifications for CNS tumors and hematolymphoid neoplasms, together with international EHA–ESMO guidance for primary and secondary central nervous system lymphoma (PCNSL/SCNSL), provides the conceptual framework within which dural lymphomas should be positioned across the spectrum of CNS lymphoma and SCNSL [ 6 , 8 , 9 , 10 ]. However, these documents devote limited space to the specificities of pachymeningeal disease. Consequently, diagnostic and therapeutic strategies for dural lesions are often extrapolated from the far more abundant evidence on parenchymal presentations. At present, there are no dedicated guidelines for the management of dural lymphomatous lesions.
The primary aim of this narrative review, intended for a multidisciplinary neuro-oncological audience, is to summarize available evidence on epidemiology, imaging patterns (conventional and advanced MRI; 18F-FDG PET and, in selected settings, somatostatin receptor [SSTR] tracers), histopathological correlates, and management strategies for dural lymphomas, with particular emphasis on PDL. We further propose a pragmatic, hypothesis-generating, multidisciplinary operational framework comprising four clinico-biological clusters, along with a diagnostic pathway that integrates MRI and PET findings with hematologic staging, aimed at minimizing anchoring bias and avoiding unnecessary surgical resections.
2. Materials and Methods
2.1. Study Design and Objectives
Owing to the rarity of dural lymphomas and the heterogeneity of reported data—frequently nested within PCNSL or SCNSL series—we conducted a structured narrative review and critical synthesis with the following objectives: (1) define an operational nosological framework distinguishing PDL from secondary dural involvement/SCNSL; and (2) propose an integrated decision pathway—including hematologic staging—supporting differential diagnosis, therapeutic stratification, and treatment planning [ 1 , 3 , 8 ]. Within this framework, we emphasize multimodal imaging analysis, leveraging morphological and metabolic patterns to guide pre-biopsy diagnostic orientation in “meningioma-like” presentations and to support differential diagnosis against major extra-axial mimics.
2.2. Data Sources and Search Strategy
We searched PubMed/MEDLINE, Embase, and Scopus from database inception to November 2025, using combinations of free-text terms and, for PubMed, MeSH terms and keyword equivalents. Boolean operators (AND, OR, NOT) and truncation (*) were used to refine results. Search strings included, among others: dural lymphoma, primary dural lymphoma, dural marginal zone, MALT lymphoma dura, pachymeningeal lymphoma, secondary CNS lymphoma, meningioma mimics, diffusion, perfusion, FDG PET, and somatostatin receptor PET. The search was designed to map the evidence base and identify recurring themes (imaging and early management) rather than to produce quantitative estimates or pooled effect sizes. An example PubMed/MEDLINE search string is provided in the Supplement (Table S1) .
2.3. Study Selection and Inclusion/Exclusion Criteria
We included: (1) observational studies (single-center or multicenter case series) reporting histotype, imaging, treatment, and outcomes; (2) reviews, position papers, and guidelines relevant to PCNSL/SCNSL and diagnostic–therapeutic frameworks; and (3) neuroradiological studies focused on imaging patterns and differential diagnosis of dural masses and/or CNS lymphoma. We excluded studies in which the lymphoma was predominantly intra-axial (parenchymal) and lacked a primary or dominant dural component; conference abstracts without full data; isolated case reports without additional management or radiological value; and non-English papers (except highly clinically relevant exceptions, documented).
2.4. Screening and Data Extraction
Two authors independently screened titles and abstracts and assessed full-text articles; disagreements were resolved by consensus. Extracted variables included: setting/denominator (PCNSL/SCNSL/systemic lymphoma cohorts), criteria for “dural-based disease,” histotype (EMZL/MALT vs. DLBCL vs. others), location (convexity/falx/skull base/spinal), MRI patterns (DWI/ADC; perfusion when available), PET (FDG ± SSTR), treatment (surgery/radiotherapy/chemotherapy), and outcomes (response, local/systemic relapse, and overall or progression-free survival when reported).
2.5. Methodological Quality Appraisal
To improve methodological transparency, we performed a structured methodological quality appraisal of the major included clinical studies, tailored to the predominant study designs (retrospective cohorts and case series). Because this work is a narrative review and not a meta-analysis, the appraisal was not used as a strict exclusion criterion. Instead, it was used to inform interpretive weighting of evidence, particularly for imaging-pattern descriptions, management inferences, and algorithm-supporting considerations.
For retrospective cohort studies, we assessed key risk-of-bias and reporting domains applicable to observational designs (e.g., clarity of cohort definition and denominator, ascertainment of dural involvement and histopathologic diagnosis, completeness of baseline imaging and staging description, treatment reporting, follow-up completeness, and outcome definition/reporting). For case series, we applied an analogous structured appraisal focusing on case selection, diagnostic ascertainment, consecutive inclusion (when stated), completeness of clinical/imaging characterization, intervention description, and outcome/follow-up reporting. Given the rarity of dural lymphoma and the limited literature base, studies were retained even when some domains were incompletely reported, but these limitations were considered in the narrative synthesis and in the weighting of conclusions.
Key appraisal domains across the major studies included in Table 1 are summarized in Supplementary Table S2 .
2.6. Synthesis and Reporting
We organized the synthesis according to a biology-stratified framework: primary dural lymphoma (PDL; EMZL/MALT vs. non-EMZL/MALT) versus secondary dural involvement/SCNSL (aggressive vs. disseminated indolent lymphoma), focusing on practical consequences for diagnosis, staging, and treatment selection. Because the proposed algorithm is intended for front-end triage of “meningioma-like” dural-based lesions and prevention of anchoring bias at first presentation, we applied an explicit biology-stratified weighting of evidence when deriving imaging phenotype descriptions and initial decision nodes. Specifically, we prioritized PDL series (particularly cohorts in which dural mimicry and preoperative misclassification as meningioma were central clinical issues) to inform imaging phenotype characterization and biopsy-first decision logic. Evidence from cohorts with secondary dural involvement/SCNSL was not primarily used to infer meningioma-like dural mimic patterns. Instead, it chiefly informed (i) clinical red-flag triggers, (ii) systemic work-up and staging logic, and (iii) management principles after tissue diagnosis. Outcomes were summarized descriptively within operational clusters and were not pooled across PDL and secondary dural involvement/SCNSL populations. A summary table of key clinical series is provided in Table 1 . Given heterogeneous designs and denominators (PDL series vs. cohorts derived from PCNSL/SCNSL), and the predominance of retrospective evidence, formal quantitative synthesis was not attempted. Instead, a structured methodological quality appraisal ( Supplementary Table S2 ) was used to support interpretive weighting of evidence across studies, with particular attention to denominator clarity, diagnostic/staging ascertainment, completeness of imaging protocol reporting, and follow-up/outcome reporting.
3. Operational Definition and Classification
Dural involvement in CNS lymphoma lies between primary CNS lymphoma and the SCNSL spectrum, yet its rarity and exclusion from prospective studies often lead to its integration within broader categories (PCNSL sensu stricto or generic SCNSL), with potential for improper treatment. A clear operational definition of PDL versus secondary dural involvement is therefore critical for any diagnostic–therapeutic algorithm [ 3 , 6 , 8 , 9 ].
We use “primary dural lymphoma (PDL)” to denote a lymphomatous neoplasm arising from the pachymeninges in the absence of detectable systemic disease on standard hematologic staging (e.g., whole-body PET/CT and/or CT chest–abdomen–pelvis; ± bone marrow biopsy depending on context). Available series suggest that the most frequently reported histotype is dural EMZL/MALT, biologically akin to MALT lymphomas at other sites, typically “meningioma-like” on imaging, and generally associated with favorable outcomes with locoregional approaches [ 1 , 2 , 4 , 5 , 11 ].
In neuro-oncological cohorts drawn from PCNSL denominators, the histologic distribution may include a comparatively higher proportion of dural DLBCL, plausibly reflecting selection effects and referral bias [ 1 ].
Less commonly, PDL presents with non-EMZL/MALT histotypes, most notably intracranial or spinal dural DLBCL (PD-DLBCL) or follicular lymphoma and other variants. In these cases, although the lesion is dural-based, clinical behavior and treatment intensity resemble more closely aggressive CNS lymphoma [ 1 , 4 ].
Variations in terminology and case composition reflect differences in WHO classification frameworks. In brief, WHO CNS5 includes “MALT lymphoma of the dura” among primary CNS lymphomas and promotes an integrated, layered diagnostic approach based on morphology, immunophenotype, molecular/genetic data, and clinico-radiological context [ 8 ]. Conversely, WHO-HAEM5 considers dural EMZL/MALT a site-associated variant of MALT lymphomas, emphasizing its biological affinity with extra-CNS extranodal MALT [ 9 ]. Practically, these perspectives support a cautious, integrative approach combining neuro-oncology and hematology: (1) complete systemic staging per hematology standards, not only to exclude secondary CNS involvement, but also to identify synchronous or occult extranodal sites; and (2) prolonged follow-up, given the possibility—albeit uncommon—of late extracranial relapse [ 11 ].
“Secondary dural involvement” refers to pachymeningeal disease occurring in the context of known or concurrently diagnosed systemic lymphoma, i.e., within SCNSL. Here, the dura is one possible compartment of disease alongside brain parenchyma, leptomeninges, cranial nerves, and/or spinal roots; by definition, an extra-CNS component is detectable on systemic staging [ 3 , 7 ]. Most commonly, it reflects systemic DLBCL with CNS involvement at presentation or relapse, although scenarios in indolent and other aggressive lymphomas have been reported [ 3 ]. Clinical management follows SCNSL principles and is associated with an overall poorer prognosis compared with most PDLs [ 3 , 6 , 7 ].
In the remainder of this review, we use “dural lymphoma” as an umbrella term encompassing primary and secondary dural disease, structured into four operational subgroups: (1A) PDL, EMZL/MALT (“classic” indolent form); (1B) PDL, non-EMZL/MALT (predominantly PD-DLBCL; less often follicular lymphoma or other variants); (2A) dural involvement in SCNSL from aggressive lymphomas (predominantly DLBCL); and (2B) dural involvement in disseminated indolent lymphomas. These clusters are intended as biology- and management-oriented operational paradigms, not as an averaged representation of behavior across heterogeneous cohorts. In practice, the framework supports early differential diagnosis and staging decisions while keeping separate the evidence used to define meningioma-mimic imaging patterns (mainly PDL-based data) from the evidence guiding red-flag assessment, systemic staging, and post-diagnosis management intensity (primarily SCNSL/secondary involvement data).
Although simplified, this grid provides a shared multidisciplinary language and facilitates integrated interpretation of presentation, imaging, and therapeutic choices [ 1 , 3 , 4 ]. To facilitate an operational, bias-resistant interpretation of “meningioma-like” pachymeningeal lesions, Table 2 summarizes the typical clinico-radiological profiles of the four dural lymphoma clusters, highlighting key discriminators, early diagnostic priorities (biopsy and hematologic staging), and initial management implications. The schema reflects distinct clinico-biological and therapeutic paradigms and should not be interpreted as pooled or averaged behavior across heterogeneous PDL and SCNSL-derived cohorts.
4. Clinical Presentation, Epidemiology, and Therapeutic Overview
Although dural involvement is uncommon within the broader spectrum of CNS lymphomas, it carries significant clinical relevance due to the high risk of misclassification as a “meningioma-like” lesion and its resulting therapeutic implications. Misattribution to a benign extra-axial pathology may delay correct diagnosis and prompt inappropriate treatment strategies, in a setting where management differs substantially between indolent, predominantly locoregional disease and aggressive forms, whether primary or secondary.
Epidemiologic estimates are heterogeneous and strongly dependent on the denominator and referral patterns. One review suggested that PDL accounts for <1% of all CNS lymphomas; conversely, in PCNSL-based cohorts the proportion may appear higher, reaching 6.3% in a bi-institutional series (20/316 PCNSL) [ 1 , 2 ].
4.1. A. PDL, EMZL/MALT
Historical series identify dural EMZL/MALT as the prototypical PDL presentation. In the series by Venkataraman et al. (32 cases), there was a female predominance (27F/5M) and a median age of approximately 50 years [ 5 ]. Patients most commonly present with mass-effect symptoms from an extra-axial tumor (headache, seizures, focal deficits), with lesions on the convexity/falx/tentorium or skull base frequently interpreted preoperatively as meningiomas [ 4 , 11 ]
In terms of natural history, disease is often confined to the dura at diagnosis, with excellent responses after locoregional treatment (surgery and/or focal radiotherapy) [ 4 , 11 ]. Nonetheless, late extracranial relapse after complete local response has been described; this may reflect occult disease not detected at baseline and/or subsequent dissemination rather than “metastasis” in a strict sense [ 11 ].
Histologic confirmation is crucial because it directly informs prognosis and management: dural EMZL/MALT, typically indolent and frequently localized, is associated with more favorable outcomes than high-grade primary CNS lymphomas. Dural EMZL/MALT typically shows positivity for B-cell markers and BCL2, negativity for CD10 and BCL6, usually lacking MUM1 expression, with low Ki-67 expression [ 5 ]. A potentially helpful feature is the presence of clonal IgG4-positive plasma cells, documented by light-chain restriction (predominant κ or λ), a pattern described in marginal zone lymphoma involving the CNS. Importantly, IgG4 positivity per se does not equate to IgG4-related disease (IgG4-RD); some EMZL/MALT lymphomas may arise in an IgG4-RD background, and an etiopathogenetic relationship has been hypothesized [ 22 ].
In patients with EMZL/MALT lymphoma associated with hepatitis C virus (HCV) infection, initial antiviral therapy is recommended and may improve outcomes and, in select cases, induce lymphoma regression. Screening includes anti-HCV antibodies and, if positive, HCV-RNA PCR to confirm active infection and quantify viral load [ 23 ]. Direct-acting antivirals (DAAs) have transformed HCV treatment, achieving very high rates of sustained virologic response across most genotypes [ 24 ].
Beyond radiotherapy, systemic approaches—including HD-MTX–based and non–HD-MTX regimens—have been reported [ 25 ]. However, combined chemo-radiotherapy carries a substantial risk of neurotoxicity and is therefore generally unnecessary and not routinely recommended in this indolent, often localized setting [ 26 ].
4.2. B. PDL, Non-EMZL/MALT (DLBCL and Other Histotypes)
Non-EMZL/MALT PDL is uncommon in traditional dural pathology series, yet it may be relatively overrepresented in cohorts from tertiary neuro-oncology centers. In the series by Karschnia et al., DLBCL comprised 10 of 20 PDL cases, whereas MZL accounted for 6 of 20 [ 1 ]. Taken together, these data suggest that “MZL predominance” can coexist with a clinically meaningful DLBCL subset—an apparent discrepancy likely driven by differing denominators, referral bias, and center-specific case mix.
In immunocompetent patients, the immunophenotype typical of PCNSL-DLBCL reflects mature B-cell origin with post-germinal-center activation and a predominantly non-GCB (activated B-cell-like) profile: CD20+, CD79a+, PAX5+, usually CD10−, variably BCL6+, strong MUM1/IRF4+, high Ki-67 (>80–90%), and typically negative for CD5/CD138 in classic immunocompetent cases; an ABC/non-GCB phenotype is prevalent [ 27 ].
Clinically, PD-DLBCL shares a dural-based extra-axial localization and “meningioma-like” appearance with EMZL but tends to exhibit faster growth and neurological deterioration over weeks. Skull-base/cavernous sinus involvement with cranial neuropathies and spinal dural/epidural masses causing compressive myelopathy or radiculopathy have been reported [ 2 , 22 ].
Biologically and clinically, these forms often require systemic CNS-directed therapy analogous to aggressive PCNSL [ 1 , 6 , 10 ]. Combinations of HD-MTX with other cytotoxic agents capable of crossing the blood–brain barrier are recommended (ideally evaluated in prospective trials). Regimens cited include MATRix, R-MBVP, rituximab–HD-MTX–carmustine–etoposide–prednisone, R-MPV, and R-MT. High-dose chemotherapy followed by autologous hematopoietic stem cell transplantation (HDC-ASCT) is recommended as consolidation in eligible patients with responsive or stable disease after adequate induction therapy [ 6 ].
Beyond DLBCL, other PDL histotypes have been described (e.g., dural follicular lymphoma, mantle cell lymphoma with dural infiltration, and very rare dural presentations of other lymphoproliferative neoplasms), largely as case reports or small series. For these variants, treatment is necessarily extrapolated from experience with dural EMZL, PCNSL, and systemic lymphomas of the corresponding histotype [ 28 , 29 , 30 , 31 , 32 ]. Overall, compared with dural EMZL/MALT, these variants tend to exhibit more aggressive biology and less favorable outcomes.
4.3. A. Dural Involvement in SCNSL from Aggressive Lymphomas
Within SCNSL, dural disease typically occurs as part of a multicompartment pattern involving brain parenchyma, leptomeninges, and/or neuroaxial structures such as cranial nerves and spinal roots; isolated dural disease is uncommon. In unselected cohorts of systemic DLBCL, CNS involvement is overall infrequent and limited to a minority of patients; however, risk is heterogeneous and increases substantially in the presence of unfavorable clinical and/or biological features, including high-risk extranodal sites, high disease burden, and aggressive molecular profiles (e.g., lymphomas arising in immune-privileged sites, the MCD molecular class per LymphGen, and double-hit/double-expressor phenotypes), reaching approximately 10–15% in high risk patients [ 3 , 33 , 34 ].
SCNSL events typically arise early in the disease course—often within the first year—suggesting that a subset of patients may already harbor subclinical CNS involvement at baseline. These events are associated with a poor prognosis despite intensive treatment strategies [ 3 , 14 ]. Evidence informing prognostication, contemporary intensive strategies (including transplant-based regimens), neuroradiological MRI phenotypes, and extranodal marginal zone lymphoma cohorts with CNS/dural involvement is derived from retrospective series, prospective trials, and real-world datasets [ 12 , 13 , 15 , 16 , 17 , 18 , 19 , 20 , 35 ].
4.4. B. Dural Involvement in Disseminated Indolent Lymphomas
CNS involvement in indolent lymphomas is rare. In a large cohort the reported frequency was 2.8% (33/1163) [ 36 ]. In series focusing on indolent lymphomas with CNS involvement, the dural compartment may be under-represented or not consistently separated radiologically. Therefore, practical classification often relies on integrating neuroimaging with systemic staging [ 21 ]. Imaging may show solitary or multiple dural “meningioma-like” masses or diffuse pachymeningeal thickening, noting that mixed patterns with leptomeningeal/parenchymal components are not uncommon [ 21 ].
Treatment is guided by histology and systemic disease burden. Published cases of indolent B-cell lymphomas with dural/CNS involvement report rituximab-based systemic approaches, including bendamustine–rituximab (BR) and R-CHOP [ 37 , 38 ]. BTK inhibitors (e.g., ibrutinib) have also been used in selected scenarios [ 39 ].
5. Imaging
Imaging is central to the diagnostic–therapeutic pathway in CNS neoplasms, enabling non-invasive characterization and longitudinal monitoring through morphological, functional, and metabolic parameters. In dural lymphomas—where appearances can be nonspecific and mimic meningioma, pachymeningitis, or dural metastases—integrating CT, multiparametric MRI, and PET/CT is pivotal to strengthen suspicion, guide targeted biopsy, and help distinguish primary from secondary disease within staging workflows [ 40 , 41 ]. Management implications of imaging–staging integration and criteria prompting tissue sampling are addressed in “Future directions” ( Box 1 and Box 2 ; Figure 1 ).
Evidence on CNS lymphoma imaging supports a shift toward multiparametric assessment beyond conventional sequences, incorporating diffusion, perfusion, spectroscopy, and PET (including hybrid PET/CT or PET/MRI). This aligns with WHO integrated diagnostics and major international recommendations [ 41 , 42 ]. However, most quantitative DWI/ADC and perfusion data derive from parenchymal PCNSL; applying these metrics to dural-based lesions is partly conceptual and requires caution, given overlap with atypical/anaplastic meningiomas and other “meningioma mimics.” Advanced parameters should therefore be interpreted alongside morphology, bone changes, growth pattern, and clinical context, rather than as stand-alone criteria [ 43 , 44 ].
A systematic approach is not merely technical quality control but a methodological requirement: reproducible MRI and PET/CT protocols share terminology among neuroradiology, neurosurgery, hematology, and oncology. A stable conceptual framework (here, the four clinico-biological clusters) is a prerequisite for using imaging as a stratification tool rather than a static depiction of the lesion. Figure 1 The algorithm applies to a “meningioma-like” extra-axial pachymeningeal lesion and proceeds through five main steps. Clinical context assessment and acquisition of core imaging: CT (density and, crucially, bone changes: hyperostosis vs. erosion/osteolysis) plus contrast-enhanced MRI (pre-/post-contrast T1, T2, FLAIR, DWI/ADC, SWI/T2*; perfusion if feasible; ± spectroscopy/high-resolution 3D). PET/CT integration and Biopsy-First Score: FDG PET/CT to assess extra-CNS disease and support staging; SSTR PET in the meningioma setting with explicit attention to “discordant SSTR-PET” (SSTR uptake with red-flag CT/MRI and/or clinical features, such as osteolysis/erosion rather than hyperostosis, infiltrative/diffuse or multifocal pachymeningeal spread, marked diffusion restriction, disproportionate edema, rapid interval growth, or hematologic history/immunosuppression). Biopsy-First Score ( Box 1 ) and initial branching: assign 2 points to Major criteria and 1 point to Minor criteria; apply pragmatic thresholds—0–1 low suspicion (standard pathway), 2–3 intermediate suspicion (biopsy-first favored if no decompressive indication), ≥4 high suspicion (biopsy-first plus early systemic staging). Pattern-based triage: if the overall profile is meningioma-typical (i.e., a coherent pattern across CT/MRI/PET suggesting a benign meningothelial lesion), follow the standard dural mass management pathway. Otherwise, triage major pachymeningeal mimics according to the dominant combined imaging/clinical pattern: - Inflammatory: diffuse/multifocal thickening with intense enhancement; possible systemic inflammatory lesions; biopsy is often decisive. - Metastatic: nodular/en plaque/”carpet-like” disease; bone lysis; possible parenchymal metastases; PET/CT may suggest an extracranial primary. - Lymphomatous: meningioma-like dural mass with a supportive multiparametric profile (e.g., diffusion restriction and infiltrative interfaces, disproportionate edema, bone erosion/osteolysis, and/or discordant SSTR-PET), prompting tissue confirmation. Lymphomatous pattern: perform hematologic staging (whole-body PET/CT and/or CT chest–abdomen–pelvis; ±bone marrow biopsy; CSF assessment per clinical context) + define surgical strategy. In the absence of a primary decompressive indication (critical mass effect or medically refractory seizures), prioritize minimally invasive tissue diagnosis, reserve debulking for selected emergencies. After tissue diagnosis, integrate it with clinical history and systemic staging to assign the operational cluster (1A/1B/2A/2B) and corresponding therapy.
This figure is intended as a hypothesis-generating triage framework for multidisciplinary decision support and not as a validated clinical decision rule.
5.1. Diagnostic Modalities: CT, MRI, and PET/CT
In suspected dural lymphoma, the imaging work-up is often sequential: initial cranial CT, followed by contrast-enhanced MRI and, when indicated, PET/CT (or PET/MRI) to define systemic extent.
CT remains essential as a first-line choice of imaging. In CNS lymphomas, including dural forms, lesions may appear iso- to relatively hyperdense and show intense, relatively homogeneous enhancement after iodinated contrast [ 40 ]. For dural masses, CT is particularly valuable for bone assessment: lymphoma more often shows a normal calvarium or erosive/osteolytic changes, whereas frank hyperostosis is less typical than in meningioma. Bone lysis should broaden the differential diagnosis to include lymphoma and metastasis [ 44 , 45 ].
Contrast-enhanced MRI remains the modality of choice for dural evaluation. A standardized protocol should include at a minimum, pre- and post-contrast T1, T2, FLAIR, DWI with ADC maps, SWI/T2*, and, when feasible, perfusion spectroscopy and high-resolution 3D acquisitions may be added [ 41 ]. MRI enables: (1) confirmation of extra-axial origin and mapping of dural extent; (2) assessment of relationships with parenchyma, leptomeninges, venous sinuses, and bone; (3) functional characterization via diffusion and perfusion [ 40 , 42 ].
18F-FDG PET/CT is particularly useful in hematology to identify extra-CNS sites and distinguish truly confined PDL from secondary disease with systemic involvement; it may also support targeted biopsy and response monitoring [ 41 , 46 ]. A separate consideration is SSTR PET (e.g., 68Ga-DOTATATE/DOTATOC), widely used in meningioma. When adjacent calvarial involvement is present, bone tracer uptake on SSTR PET may support the diagnosis of transosseous meningioma and help differentiate it from lymphoma-related osteolysis [ 47 ]. However, SSTR uptake should not be interpreted as a rule-in test for meningioma when discordant features are present [ 48 ]. We define “discordant SSTR-PET” as SSTR uptake compatible with meningioma but accompanied by a red-flag profile on MRI/CT and/or clinical assessment (e.g., erosion/osteolysis rather than hyperostosis, marked diffusion restriction, infiltrative or diffuse/multifocal pachymeningeal spread, disproportionate edema, multifocality or rapid progression, hematologic history or clinically significant immunosuppression) [ 49 , 50 ]. In these situations, the pathway favors a biopsy-first approach rather than proceeding directly to extensive resection [ 51 ].
5.2. MRI Sequences: Key Features and Practical Interpretation
Moving from modalities to sequences, MRI interpretation of dural lymphoma relies on combinations of findings rather than isolated signs.
Post-gadolinium T1 sequences define enhancement patterns: dural lymphomas frequently show intense, relatively homogeneous enhancement of a dural-based extra-axial mass, often with a “dural tail,” a nonspecific feature that contributes to confusion with meningioma. Some series report relatively extensive vasogenic edema, a less sharp cortical interface, and possible erosive bone changes [ 44 , 45 ].
T2 and FLAIR sequences, while less specific, help characterize edema and possible leptomeningeal involvement. Dural lymphomas are often iso- to moderately hyperintense on T2; cortico-subcortical edema may be more evident in biologically aggressive or secondary forms, and FLAIR facilitates detection of leptomeningeal extension beyond contiguity effects [ 40 , 41 ].
Diffusion (DWI) and ADC maps are among the most useful parameters to raise suspicion for lymphoma, but they are not pathognomonic in dural masses. Hypercellularity and a high nuclear-to-cytoplasmic ratio often produce diffusion restriction and low ADC values; however, restriction can also be seen in atypical/malignant meningiomas and other highly cellular dural tumors. Diffusion should therefore be interpreted alongside perfusion and morphology [ 40 , 43 , 44 ].
Only a limited number of studies have specifically investigated diffusion-weighted imaging in the assessment of dural lymphoma, and no validated ADC cut-off values are currently available to reliably differentiate dural lymphoma from its mimickers. Published case reports and small case series suggest that diffusion restriction is often homogeneous and may be more pronounced than in adjacent brain parenchyma; moreover, restriction appears more marked in DLBCL/SCNSL compared with EMZL/MALT [ 52 , 53 , 54 , 55 , 56 ]. A systematic evaluation of diffusion restriction patterns and quantitative ADC metrics in dural lymphoma represents, therefore, a promising area for future research.
MRI perfusion (DSC/DCE) may provide additional information. Typical meningiomas often show higher perfusion than many mimics, including some lymphomas, but exceptions exist and universally validated cut-offs are lacking. rCBV and related parameters should therefore be considered supportive markers within a multiparametric approach (morphology, bone involvement, DWI/ADC, and clinical context). Reported perfusion metrics vary across studies because of heterogeneity in acquisition and post-processing [ 44 , 57 , 58 ].
SWI/T2* can aid differential diagnosis: dural lymphomas typically show little or no intralesional susceptibility, consistent with limited hemorrhagic or calcified components, whereas susceptibility foci are more frequent in some dural metastases and in calcified meningiomas [ 42 , 44 ].
MR spectroscopy (MRS) contributes metabolic characterization, typically showing elevated choline with reduced N-acetylaspartate and possible lipid/lactate components in highly cellular lesions, including lymphomas. In meningiomas, an alanine peak is often described and may add supportive value [ 40 ]. Magnetic resonance spectroscopy of dural-based lesions remains technically challenging: susceptibility-related field inhomogeneities near bone and air-containing cavities can result in suboptimal shimming, and lipid signals from adjacent scalp and diploic marrow may contaminate spectra, limiting reliability and reproducibility [ 59 ].
Although diffusion restriction/low ADC, low-perfusion patterns, MR spectroscopy features, and PET findings may each increase suspicion for lymphoma in the appropriate context, substantial overlap exists between dural lymphoma, meningioma (including atypical/aggressive variants), metastases, and inflammatory pachymeningeal disorders. Therefore, no single imaging biomarker should be used in isolation as a rule-in criterion for dural lymphoma or meningioma. Imaging biomarkers should instead be interpreted as probabilistic, context-dependent features within a multiparametric and multidisciplinary diagnostic workflow.
5.3. Cluster-Based Analysis: Radiological Correlations
The practical value of these techniques emerges when applied to the four clinico-biological clusters. The goal is not to assign histology from imaging alone, but to use radiological information to strengthen or weaken the likelihood of each cluster in an individual patient.
In cluster 1A (PDL, EMZL/MALT), the typical scenario is an immunocompetent middle-aged woman with one or more “meningioma-like” extra-axial masses. MRI often shows iso- to hypointense T1 and iso- to moderately hyperintense T2 signal, homogeneous enhancement with a dural tail, and usually normal or minimally altered adjacent bone. Diffusion restriction may be present but not necessarily marked; perfusion and spectroscopy, when available, may support a less aggressive profile than dural DLBCL while remaining within the lymphomatous spectrum. FDG PET/CT is negative outside the dural lesion, and negative systemic staging supports an indolent PDL classification.
In cluster 1B (PDL, non-EMZL/MALT; especially PD-DLBCL), the initial appearance may be similar but with stronger aggressiveness signals: faster growth, more extensive vasogenic edema, a less sharp parenchymal interface, and more marked diffusion restriction with low ADC values. Bone erosion/osteolysis or more invasive involvement of the cortical plane may occur compared with typical meningioma [ 44 , 45 ]. FDG uptake may be high at the dural lesion while systemic staging remains negative; this combination favors cluster 1B.
Cluster 2A (dural involvement in SCNSL from aggressive lymphoma) is suggested primarily by the fact that the dura is rarely the sole compartment involved. Imaging may show a multicompartment pattern (parenchymal lesions, leptomeningeal involvement, diffuse or nodular dural thickening), and PET/CT may reveal systemic sites. Here, MRI characterizes CNS compartments, whereas integrated staging—often via PET/CT—defines systemic extent and biology [ 41 ].
Finally, cluster 2B (dural involvement in disseminated indolent lymphoma) can be radiologically similar to PDL MALT, with solitary or multiple “meningioma-like” dural masses, sometimes en plaque. In this setting, the discriminator is typically systemic context and staging: brain imaging alone may not reliably distinguish 1A from 2B, and classification depends largely on evidence of systemic disease [ 21 , 41 ].
5.4. Radiological Differential Diagnosis and Reasoning Schemes
In routine neuroradiological practice, many dural-based lesions are initially interpreted as meningiomas. However, a subset of “meningioma-like” masses represent mimics (metastatic, inflammatory, or lymphomatous) with substantially different management implications. To reduce anchoring bias, we propose a set of red flags ( Box 1 ) and a decision pathway that prompts early tissue diagnosis and staging when appropriate.
Radiological differential diagnosis requires a multiparametric approach integrating extra-axial features, bone changes, enhancement patterns, and functional sequences (DWI/ADC and perfusion), acknowledging that no single sign is definitive and that advanced parameters are typically supportive within dural lesion assessment [ 43 , 44 , 60 ]. In selected contexts, a peripheral rim-like enhancement pattern may provide supportive value in distinguishing meningiomas from malignant dural tumors [ 61 ].
Usability improves when imaging findings are interpreted as combined patterns rather than as isolated signs. Accordingly, we frame the differential around dominant clinico-radiological patterns (meningioma-typical, inflammatory, metastatic, and lymphomatous) and align these patterns with the branch points of Figure 1 to mirror real-world neuroradiology and multidisciplinary board reasoning.
Dural metastases are an important source of diagnostic confusion: they can appear as solitary or multiple nodules, en plaque thickening, or diffuse “carpet-like” enhancement. Bone lysis (more than hyperostosis), coexisting parenchymal metastases, and PET/CT findings suggesting an extracranial primary would support this diagnosis; perfusion may help, but overlaps exist and vary by histotype [ 44 , 57 , 58 ].
Immune-mediated pachymeningitis (including IgG4-related forms) and neurosarcoidosis represent major inflammatory considerations in the differential diagnosis. MRI often shows diffuse or multifocal dural thickening with intense enhancement, sometimes symmetric; marked diffusion restriction is less typical, and perfusion tends not to show profiles strongly suggestive of a hypercellular neoplasm. Clinical context remains central: association with systemic manifestations (orbit, paranasal sinuses, salivary glands, lung parenchyma) and steroid responsiveness can be informative; nevertheless, targeted biopsy is often decisive [ 62 ]. In IgG4-related forms, serum IgG4 and inflammatory markers may support suspicion; on tissue, distinguishing a polyclonal from clonal plasma cell infiltrate through κ/λ light-chain restriction is critical and may indicate an underlying lymphoproliferative process (e.g., IgG4 + MZL).
5.5. Future Directions and a Pragmatic Management Proposal in the Absence of Dedicated Guidelines
In a field lacking specific recommendations, particularly for PDL, developing and validating shared approaches to the initial management of “meningioma-like” dural-based lesions is a priority. The goal is twofold: to reduce anchoring bias and standardizing clinically decisive choices (tissue diagnosis, timing and extent of staging, extent of surgery, and peri-diagnostic corticosteroid use). In practice, phenotypic overlap between meningioma and mimics (metastatic, inflammatory, or lymphomatous) and the inherently probabilistic nature of advanced imaging markers contribute to meaningful inter-operator variability, potentially affecting time to diagnosis, staging appropriateness, and selection of the initial surgical procedure. Figure 1 shows a reproducible decision pathway integrating key clinico-radiological nodes and corresponding actions (targeted biopsy, systemic staging, role of surgery, corticosteroid management) into a pragmatic sequence shared across disciplines. The pathway shown in Figure 1 (integrating Box 1 and Box 2 ) is intended as a pragmatic, hypothesis-generating triage framework to structure multidisciplinary discussion and reduce anchoring bias in the initial assessment of “meningioma-like” dural lesions. It is not a validated clinical decision rule, guideline, or stand-alone tool for treatment selection. As a future adjunct, CSF-based liquid biopsy may complement this pathway—particularly when tissue sampling is high-risk—by enabling detection of lymphoma-associated alterations in CSF ctDNA/cfDNA (e.g., MYD88 L265P and CD79B Y196), with CSF generally offering higher sensitivity than plasma in CNS settings [ 63 ]. Exploratory CSF biomarker approaches (including microRNA/exosome and cytokine/chemokine profiles) remain investigational and are not yet standardized for routine practice, requiring interpretation within the full clinical and radiological context [ 64 , 65 ].
Radiomics-based pipelines, coupled with machine-learning classifiers, may enable a more objective differentiation of dural lymphoma from meningioma and other dural mimickers by leveraging high-dimensional shape and texture features extracted from routine MRI (and, where available, functional sequences such as DWI/perfusion) and/or FDG PET. In primary CNS lymphoma, preliminary radiomics/ML studies have shown encouraging performance for non-invasive diagnostic classification, but translation to the dural compartment will require harmonized acquisition/segmentation workflows and rigorous external validation, ideally aligned with standardized feature definitions (e.g., IBSI) [ 66 , 67 , 68 ].
Within this framework, a structured set of clinico-radiological red flags operationalized as a Biopsy-First Score ( Box 1 ) and early management principles ( Box 2 ) are needed to ensure pathway reproducibility across neuroradiology, neurosurgery, and hemato-oncology. Box 1 translates “clinical context” into explicit, point-based criteria (Major = 2 points; Minor = 1 point) with pragmatic triage thresholds (0–1 low suspicion, 2–3 intermediate, ≥4 high). Box 2 translates this suspicion into operational decisions, clarifying when to prefer a low-morbidity “tissue-first” approach, when to reserve surgery for selected indications (decompression/debulking), and how to optimize the biopsy–staging–therapy sequence (including pragmatic considerations on corticosteroid timing). Figure 1 integrates Box 1 and Box 2 into an explicit decision pathway that makes clear when to deviate from conventional dural mass management and how to prioritize diagnostic and staging steps. Before proceeding to the initial branching of the diagnostic pathway, clinicians are encouraged to calculate the Biopsy-First Score ( Box 1 ). This tool is intended as pragmatic decision support and does not replace clinical judgment; urgent decompression may take precedence (e.g., critical mass effect, medically refractory seizures, or neurological deterioration).
Evidence strength across the main decision nodes is heterogeneous and should be interpreted accordingly. Components supported by relatively stronger evidence include: (i) recognition of recurrent “meningioma-mimic” presentations in primary dural lymphoma series; (ii) prioritization of tissue diagnosis and comprehensive hematologic staging when lymphoma is a credible differential diagnosis; and (iii) post-biopsy staging/management principles aligned with established PCNSL/SCNSL recommendations (although not prospectively validated in a dural-lymphoma–specific algorithm). Components supported by more limited evidence include proposed score weighting and pragmatic thresholds in Box 1 , quantitative imaging thresholds in dural-based lesions, and selected PET pitfalls (particularly in rarer or discordant scenarios), which are derived from smaller retrospective series, case reports, and expert synthesis and therefore require prospective multicenter validation. Box 1 Biopsy-First Score for “meningioma-like” dural lesions. Major criteria are assigned 2 points and minor criteria 1 point; proposed pragmatic thresholds (0–1 low suspicion; 2–3 intermediate suspicion; ≥4 high suspicion) guide triage toward standard management versus a biopsy-first pathway with expedited systemic staging when indicated. Note: This is a pragmatic triage tool synthesized from dural-lymphoma and dural-mimic imaging literature (not a formal guideline; not prospectively validated) Box 1. Biopsy-First Score for meningioma-like dural lesions: when to suspect a lymphomatous mimic and prioritize minimally invasive tissue diagnosis. A. Clinical red flags (context and time) Major: rapid symptom progression (days-weeks) or neurological deterioration atypical for meningioma. Major: hematologic history (known/recent lymphoma) and/or clinically significant immunosuppression. Major: skull-base phenotype (multiple cranial neuropathies) or suspicion of multicompartment disease. Minor: clinicoradiologic incongruence or disproportionate symptoms. B. Morphologic/structural red flags (CT/MRI, including bone) Major: atypical bone pattern: erosion/osteolysis or permeative change (rather than frank hyperostosis). Major: infiltrative behavior: blurred cortical interface or diffuse/multifocal pachymeningeal extension not fitting classic meningioma. Minor: disproportionate vasogenic edema relative to lesion size/implantation. Minor: en plaque or multifocal appearance that does not integrate with the clinical-radiologic context. C. Functional/metabolic red flags (multiparametric MRI and PET) Major: marked diffusion restriction (DWI/ADC) suggestive of hypercellularity in a non-convincing meningioma setting. Major: positive systemic staging (FDG-PET/CT or equivalent) suggesting secondary involvement/SCNSL. Major: receptor-imaging pitfall: SSTR-PET uptake compatible with meningioma but discordant with MRI and/or clinical context. Minor: perfusion/MRS parameters not aligned with typical meningioma (supportive, not decisive). Practical decision rule Biopsy-First Score: assign 2 points to Major criteria and 1 point to Minor criteria, and interpret the total score using the proposed pragmatic thresholds: 0–1 = low suspicion (standard pathway), 2–3 = intermediate suspicion (biopsy-first approach favored if no decompressive indication is present), and ≥4 = high suspicion (biopsy-first approach with early systemic staging). This framework is intended to support early diagnostic stratification and multidisciplinary decision-making. Caveat: in case of critical mass effect, medically refractory seizures, or neurological deterioration, surgical debulking may precede full staging. Supporting sources (all cited in the main text): Karschnia et al., 2020 [ 1 ]; Lyndon et al. [ 44 ], 2019; Maireche et al., 2023 [ 45 ]; Juntikka et al., 2021 [ 51 ]. Box 2 Pragmatic early management principles for suspected dural lymphoma, prioritizing timely biopsy and comprehensive hematologic staging before defining surgical strategy. Interpretation: Dedicated international guidelines for PDL are limited. The following principles are derived from PCNSL/SCNSL recommendations and apply when lymphoma is a credible differential diagnosis. Box 2. Guideline-consistent early management when CNS lymphoma is suspected: applied to meningioma-like dural lesions 1. Prioritize tissue diagnosis (“biopsy-first”) Obtain targeted tissue sampling (stereotactic biopsy; alternatively, diagnostic mini-craniotomy when stereotaxy is impractical). CSF studies can be supportive when positive but have limited sensitivity and should not replace tissue diagnosis when an accessible lesion exists. 2. Reserve resection/debulking for selected emergencies Routine gross-total resection is not a standard initial strategy for suspected CNS lymphoma. Consider decompression/debulking only when required for life-threatening mass effect/intracranial hypertension or when needed to obtain safe diagnostic tissue in a critical anatomical setting. 3. If SCNSL is suspected, stage systemically and choose the safest biopsy site Perform prompt systemic staging (FDG-PET/CT or equivalent total-body imaging) plus standard hematologic work-up. With concurrent systemic disease, diagnosis may be established from a systemic-site biopsy when CNS imaging is consistent after expert review; for isolated CNS relapse or atypical imaging, CNS biopsy is often required. 4. Corticosteroids: avoid pre-biopsy if clinically feasible When suspicion is high and the patient is stable, avoid or defer corticosteroids before biopsy due to potential reduction in diagnostic yield. If steroids are required (edema/intracranial hypertension/neurological deterioration), do not delay biopsy and document dose and duration. Practical one-line rule (for meningioma-like dural lesions) When red flags suggest a lymphomatous mimic and there is no primary decompressive indication, proceed with rapid minimally invasive tissue diagnosis and complete staging before planning extensive “meningioma-like” resection. Key sources (canonical publication years): Bobillo et al., 2023 [ 3 ]; Cwynarski et al., 2023 [ 7 ]; Hoang-Xuan et al., 2023 [ 10 ]; Ferreri et al., 2021 [ 19 ].
Beyond immediate clinical value, explicit criteria ( Box 1 and Box 2 ) and algorithmic implementation ( Figure 1 ) enable more robust evidence generation by harmonizing definitions and thresholds, building more comparable multicenter cohorts, and measuring practice-relevant endpoints: time to tissue diagnosis, rate of unnecessary extensive resections, completeness and appropriateness of staging, impact of pre-treatment steroids on diagnostic yield, and pathway safety. Without such minimum standards, the literature—dominated by retrospective series and reviews—remains intrinsically heterogeneous and difficult to translate into operational recommendations.
A priority research agenda should address three linked domains. First, the proposed framework ( Box 1 and Box 2 ; Figure 1 ) requires prospective multicenter validation using pre-specified, practice-relevant endpoints, including time-to-diagnosis, rate of unnecessary extensive resections, staging appropriateness/completeness, treatment delay, and pathway-related safety outcomes. Second, imaging protocol harmonization is needed to improve reproducibility and comparability across centers, particularly for DWI/ADC acquisition and reporting, perfusion technique/metrics and post-processing, and PET acquisition/interpretive criteria (including management of discordant SSTR-PET scenarios). Third, standardized reporting templates for dural-based lesions should be developed to ensure consistent description of morphology, bone changes, diffusion/perfusion findings, PET patterns, and clinical red flags, thereby enabling more robust multicenter datasets and future consensus-building.
A realistic and methodologically coherent next step would be to develop multidisciplinary consensus recommendations (ideally via structured Delphi/expert panel processes with scientific society endorsement) formalizing: (i) Biopsy-First Score criteria and thresholds ( Box 1 ), (ii) early management principles ( Box 2 ), (iii) harmonized imaging acquisition and reporting requirements (including DWI/ADC, perfusion, and PET interpretive criteria) and standardized reporting templates for dural-based lesions, including predefined red-flag descriptors and bone-pattern terminology (iv) pathway quality indicators. These recommendations would provide a shared basis for multicenter validation of the proposed algorithm ( Figure 1 ) and prospective studies, thereby laying the groundwork for future dedicated guidelines.
6. Limitations
This narrative review has methodological limitations. First, because it was not designed as a formal systematic review, it remains susceptible to selection bias despite a database search strategy and independent screening by two authors. In addition, language and publication biases may persist because we did not include grey literature, non-English studies, or contributions available only as abstracts.
The evidence base on dural and CNS lymphomas consists predominantly of retrospective studies, often with small cohorts and heterogeneous populations (PDL series versus cohorts derived from PCNSL/SCNSL), limiting comparability and generalizability—particularly for imaging findings and clinical outcomes. This limitation is particularly relevant for imaging biomarkers, because heterogeneity in acquisition protocols, post-processing methods, region-of-interest strategies, and reporting terminology further reduces cross-study comparability and may exaggerate the apparent specificity of isolated imaging features.
Importantly, the proposed algorithm and Biopsy-First Score are pragmatic, hypothesis-generating triage frameworks rather than validated decision rules or guidelines, and they should not be used as stand-alone tools. In addition, the level of evidence is not uniform across algorithm components: some points (e.g., biopsy/staging prioritization when lymphoma is suspected) are supported by recurrent patterns across retrospective series and by guideline-consistent principles extrapolated from PCNSL/SCNSL, whereas other components (e.g., selected PET pitfalls, quantitative imaging or biomarker thresholds in rarer scenarios) are supported by smaller series or case reports and remain exploratory.
To improve transparency, we performed a structured methodological quality appraisal of the major included studies ( Supplementary Table S2 ). However, this appraisal was used to contextualize and interpret the evidence rather than as an exclusion framework, because the available literature is sparse and largely retrospective. Accordingly, residual risks of selection bias, ascertainment bias, inconsistent imaging/staging reporting, and incomplete outcome follow-up remain important constraints on the strength and generalizability of the proposed framework.
Eventually, the Biopsy-First Score represents a pragmatic, hypothesis-generating triage framework rather than a validated clinical decision rule or practice guideline. Its inter-rater reproducibility and performance require formal evaluation across centers and imaging workflows to determine generalizability and robustness.
7. Conclusions
Extra-axial dural lesions are frequently evaluated with insufficient radiological rigor, creating a risk of premature diagnostic impact that may inappropriately shape clinical management and expose patients to incorrect treatments. In cases with diagnostic uncertainty—particularly in the absence of significant mass effect or medically refractory seizures—direct referral to craniotomy rather than a biopsy procedure may entail substantially greater procedural risk than a minimally invasive diagnostic approach.
This issue is especially relevant when imaging raises suspicion for dural lymphoma: in such contexts, a biopsy-first pathway may prevent unnecessary resections and facilitate timely initiation of disease-directed therapy. Despite increasing recognition of pachymeningeal lymphomatous involvement, dedicated guidelines for dural lymphoma management are still lacking, and current practice often relies on evidence extrapolated from parenchymal primary CNS lymphoma.
Against this backdrop, the present narrative review aims to provide above all, a critical and as comprehensive as possible, synthesis of the radiological characteristics of extra-axial dural lesions, with particular attention to entities with overlapping phenotypes. The overarching goal is to support a more accurate and efficient diagnostic pathway and better-informed treatment decisions through a structured methodological approach and a practical neuroradiological guide.
Acknowledgments
The Authors thank the Department of Innovation, Research, University and Museum of the Autonomous Province of Bolzano/Bozen for covering the Open Access publication costs.
Disclaimer/Publisher’s Note: The statements, opinions and data contained in all publications are solely those of the individual author(s) and contributor(s) and not of MDPI and/or the editor(s). MDPI and/or the editor(s) disclaim responsibility for any injury to people or property resulting from any ideas, methods, instructions or products referred to in the content.
Supplementary Materials
The following supporting information can be downloaded at: https://www.mdpi.com/article/10.3390/cancers18152369/s1 , Table S1: Example of PubMed/MEDLINE search string; Table S2: Simplified structured methodological quality appraisal of the major clinical studies included in the narrative synthesis.
Author Contributions
Conceptualization, L.Z. and P.P.B.; methodology, L.Z. and P.P.B.; validation, V.B., M.K., A.B., C.V., M.F., A.S. (Alessandro Spimpolo), M.B., A.S. (Andreas Schwarz), P.C.C., L.Z. and P.P.B.; investigation, V.B., L.Z. and P.P.B.; data curation, D.C., L.Z. and P.P.B.; writing—original draft preparation, V.B., L.Z. and P.P.B.; writing—review and editing, V.B., D.C. and L.Z.; visualization, L.Z.; supervision, C.V., P.C.C., A.B., M.K., A.S. (Andreas Schwarz) and P.P.B. All authors have read and agreed to the published version of the manuscript.
Institutional Review Board Statement
Not applicable. This article is a narrative review based exclusively on published literature and did not involve human participants, animals, or the collection of primary data.
Informed Consent Statement
Not applicable.
Data Availability Statement
No new data were created or analyzed in this study. Data sharing is not applicable to this article.
Conflicts of Interest
The authors declare no conflicts of interest.
Abbreviations
The following abbreviations are used in this manuscript: 18F-FDG fluorine-18 fluorodeoxyglucose 3D three-dimensional 68Ga-DOTATATE/DOTATOC gallium-68 somatostatin receptor tracers ABC activated B-cell-like ADC apparent diffusion coefficient Ara-C cytarabine ASCT autologous stem cell transplantation BCL6 B-cell lymphoma 6 BR bendamustine–rituximab BTK Bruton tyrosine kinase CD cluster of differentiation CI confidence interval CNS central nervous system CR complete response CSF cerebrospinal fluid ctDNA circulating tumor DNA cfDNA cell-free DNA CT computed tomography DAAs direct-acting antivirals DCE dynamic contrast-enhanced (MRI) DLBCL diffuse large B-cell lymphoma DSC dynamic susceptibility contrast (MRI) DWI diffusion-weighted imaging EFS event-free survival EHA-ESMO European Hematology Association–European Society for Medical Oncology EMZL extranodal marginal zone lymphoma FDG fluorodeoxyglucose FDG-PET/CT fluorodeoxyglucose positron emission tomography/computed tomography FLAIR fluid-attenuated inversion recovery GCB germinal center B-cell-like HDC high-dose chemotherapy HDC-ASCT high-dose chemotherapy followed by autologous stem cell transplantation HD-MTX high-dose methotrexate HDS high-dose sequential chemoimmunotherapy HDT high-dose therapy HDT-ASCT high-dose therapy with autologous stem cell transplantation HCV hepatitis C virus HCV-RNA hepatitis C virus ribonucleic acid HR hazard ratio IBSI Image Biomarker Standardisation Initiative IgG4 immunoglobulin G4 IgG4-RD IgG4-related disease IRF4 interferon regulatory factor 4 IT intrathecal Ki-67 Ki-67 proliferation index LDH lactate dehydrogenase MALT mucosa-associated lymphoid tissue MARIETTA MATRix-RICE and autologous stem cell transplantation trial acronym MATRix rituximab, methotrexate, cytarabine, thiotepa (regimen) MCD molecular class MCD (LymphGen) MeSH Medical Subject Headings ML machine learning MRI magnetic resonance imaging MRS magnetic resonance spectroscopy MSKCC Memorial Sloan Kettering Cancer Center MUM1 multiple myeloma oncogene 1 MYD88 myeloid differentiation primary response 88 MZL marginal zone lymphoma NHL non-Hodgkin lymphoma non-GCB non–germinal center B-cell-like ORR objective response rate OS overall survival PAX5 paired box 5 PCR polymerase chain reaction PCNSL primary central nervous system lymphoma PD-DLBCL primary dural diffuse large B-cell lymphoma PDL primary dural lymphoma PET positron emission tomography PET/CT positron emission tomography/computed tomography PET/MRI positron emission tomography/magnetic resonance imaging PFS progression-free survival PR partial response rCBV relative cerebral blood volume R-CHOP rituximab, cyclophosphamide, doxorubicin, vincristine, prednisone R-HDS rituximab plus high-dose sequential chemoimmunotherapy RICE rituximab, ifosfamide, carboplatin, etoposide R-MBVP rituximab, methotrexate, carmustine, etoposide, prednisone R-MPV rituximab, methotrexate, procarbazine, vincristine R-MT rituximab–methotrexate RT radiotherapy SCNSL secondary central nervous system lymphoma SCNSL-R Secondary CNS Lymphoma Registry SSTR somatostatin receptor SSTR-PET somatostatin receptor positron emission tomography SWI susceptibility-weighted imaging T1 T1-weighted (MRI) T2 T2-weighted (MRI) T2* T2*-weighted (MRI) WHO World Health Organization WHO CNS5 WHO Classification of Tumors of the Central Nervous System, 5th edition WHO-HAEM5 WHO Classification of Hematolymphoid Tumors, 5th edition
References
1. Karschnia P. Batchelor T.T. Jordan J.T. Shaw B. Winter S.F. Barbiero F.J. Kaulen L.D. Thon N. Tonn J.C. Huttner A.J. Primary dural lymphomas: Clinical presentation, management, and outcome Cancer 2020 126 2811 2820 10.1002/cncr.32834 32176324
2. Fattahi A. Sadeghipour A. Shayanfar N. Najafi M. Ravansalar M. Shahhoseini A. Koohestani H. Javadnia P. Primary dural lymphoma: A comprehensive literature review and report of a case Oncol. Clin. Pract. 2022 18 335 348 10.5603/OCP.2022.0029
3. Bobillo S. Khwaja J. Ferreri A.J. Cwynarski K. Prevention and management of secondary central nervous system lymphoma Haematologica 2023 108 673 689 10.3324/haematol.2022.281457 36384246 PMC9973486
4. de la Fuente M.I. Haggiagi A. Moul A. Young R.J. Sidani C. Markoe A. Vega F. DeAngelis L.M. Lossos I.S. Marginal zone dural lymphoma: The Memorial Sloan Kettering Cancer Center and University of Miami experiences Leuk. Lymphoma 2017 58 882 888 10.1080/10428194.2016.1218006 27649904 PMC5576515
5. Venkataraman G. Rizzo K.A. Chavez J.J. Streubel B. Raffeld M. Jaffe E.S. Pittaluga S. Marginal zone lymphomas involving meningeal dura: Possible link to IgG4-related diseases Mod. Pathol. 2011 24 355 366 10.1038/modpathol.2010.206 21102421 PMC7425666
6. Ferreri A.J.M. Illerhaus G. Doorduijn J.K. Auer D.P. Bromberg J.E.C. Calimeri T. Cwynarski K. Fox C.P. Hoang-Xuan K. Malaise D. Primary central nervous system lymphomas: EHA-ESMO Clinical Practice Guideline for diagnosis, treatment and follow-up Ann. Oncol. 2024 35 491 507 10.1016/j.annonc.2023.11.010 38839484
7. Cwynarski K. Cummin T. Osborne W. Lewis J. Chaganti S. Smith J. Linton K. Greaves P. McKay P. Fox C.P. Management of secondary central nervous system lymphoma Br. J. Haematol. 2023 200 160 169 10.1111/bjh.18539 36408800
8. Louis D.N. Perry A. Wesseling P. Brat D.J. Cree I.A. Figarella-Branger D. Hawkins C. Ng H.K. Pfister S.M. Reifenberger G. The 2021 WHO Classification of Tumors of the Central Nervous System: A summary Neuro Oncol. 2021 23 1231 1251 10.1093/neuonc/noab106 34185076 PMC8328013
9. Alaggio R. Amador C. Anagnostopoulos I. Attygalle A.D. Araujo I.B.O. Berti E. Bhagat G. Borges A.M. Boyer D. Calaminici M. The 5th edition of the World Health Organization Classification of Haematolymphoid Tumours: Lymphoid Neoplasms Leukemia 2022 36 1720 1748 10.1038/s41375-022-01620-2 35732829 PMC9214472
10. Hoang-Xuan K. Deckert M. Ferreri A.J.M. Furtner J. Gallego Perez-Larraya J. Henriksson R. Hottinger A.F. Kasenda B. Lefranc F. Lossos A. European Association of Neuro-Oncology (EANO) guidelines for treatment of primary central nervous system lymphoma (PCNSL) Neuro Oncol. 2023 25 37 53 10.1093/neuonc/noac196 35953526 PMC9825335
11. Iwamoto F.M. DeAngelis L.M. Abrey L.E. Primary dural lymphomas: A clinicopathologic study of treatment and outcome in eight patients Neurology 2006 66 1763 1765 10.1212/01.wnl.0000218284.23872.eb 16769960
12. Tu P.H. Giannini C. Judkins A.R. Schwalb J.M. Burack R. O’Neill B.P. Yachnis A.T. Burger P.C. Scheithauer B.W. Perry A. Clinicopathologic and genetic profile of intracranial marginal zone lymphoma: A primary low-grade CNS lymphoma that mimics meningioma J. Clin. Oncol. 2005 23 5718 5727 10.1200/JCO.2005.17.624 16009945
13. Sunderland A.J. Steiner R.E. Al Zahrani M. Pinnix C.C. Dabaja B.S. Gunther J.R. Nastoupil L.J. Jerkeman M. Joske D. Cull G. An international multicenter retrospective analysis of patients with extranodal marginal zone lymphoma and histologically confirmed central nervous system and dural involvement Cancer Med. 2020 9 663 670 10.1002/cam4.2732 31808316 PMC6970027
14. El-Galaly T.C. Cheah C.Y. Bendtsen M.D. Nowakowski G.S. Kansara R. Savage K.J. Connors J.M. Sehn L.H. Goldschmidt N. Shaulov A. Treatment strategies, outcomes and prognostic factors in 291 patients with secondary CNS involvement by diffuse large B-cell lymphoma Eur. J. Cancer 2018 93 57 68 10.1016/j.ejca.2018.01.073 29477102 PMC5869165
15. Hollender A. Kvaloy S. Lote K. Nome O. Holte H. Prognostic factors in 140 adult patients with non-Hodgkin’s lymphoma with systemic central nervous system involvement Eur. J. Cancer 2000 36 1762 1768 10.1016/S0959-8049(00)00171-4 10974623
16. Jahnke K. Thiel E. Martus P. Schwartz S. Korfel A. Retrospective study of prognostic factors in non-Hodgkin lymphoma patients with secondary central nervous system involvement Ann. Hematol. 2006 85 45 50 10.1007/s00277-005-1096-3 16132909
17. Ferreri A.J. Donadoni G. Cabras M.G. Patti C. Mian M. Zambello R. Tarella C. Di Nicola M. D’Arco A.M. Doa G. High doses of antimetabolites followed by high-dose sequential chemoimmunotherapy and autologous stem-cell transplantation in patients with systemic B-cell lymphoma and secondary CNS involvement: Final results of a multicenter phase II trial J. Clin. Oncol. 2015 33 3903 3910 10.1200/JCO.2015.61.1236 26282634
18. Malikova H. Burghardtova M. Koubska E. Mandys V. Kozak T. Weichet J. Secondary central nervous system lymphoma: Spectrum of morphological MRI appearances Neuropsychiatr. Dis. Treat. 2018 14 733 740 10.2147/NDT.S157959 29559780 PMC5856045
19. Ferreri A.J.M. Doorduijn J.K. Re A. Cabras M.G. Smith J. Ilariucci F. Luppi M. Calimeri T. Cattaneo C. Khwaja J. Chemoimmunotherapy with MATRix-RICE and autologous haematopoietic stem-cell transplantation in diffuse large B-cell lymphoma with secondary CNS involvement (MARIETTA): An international, single-arm, phase 2 trial Lancet Haematol. 2021 8 e110 e121 10.1016/S2352-3026(20)30366-5 33513372 PMC7844712
20. Habringer S. Demel U.M. Fietz A.K. Lammer F. Schroers R. Hofer S. Bairey O. Braess J. Meier-Stiegen A.S. Stuhlmann R. A prospective observational study of real-world treatment and outcome in secondary CNS lymphoma Eur. J. Cancer 2024 196 113436 10.1016/j.ejca.2023.113436 38008033
21. Spectre G. Gural A. Amir G. Lossos A. Siegal T. Paltiel O. Central nervous system involvement in indolent lymphomas Ann. Oncol. 2005 16 450 454 10.1093/annonc/mdi076 15642707
22. Bledsoe J.R. Della-Torre E. Rovati L. Deshpande V. IgG4-related disease: Review of the histopathologic features, differential diagnosis, and therapeutic approach APMIS 2018 126 459 476 10.1111/apm.12845 29924455
23. Walewska R. Eyre T.A. Barrington S. Brady J. Fields P. Iyengar S. Joshi A. Menne T. Parry-Jones N. Walter H. Guideline for the diagnosis and management of marginal zone lymphomas: A British Society of Haematology Guideline Br. J. Haematol. 2024 204 86 107 10.1111/bjh.19064 37957111
24. Merli M. Carli G. Arcaini L. Visco C. Antiviral therapy of hepatitis C as curative treatment of indolent B-cell lymphoma World J. Gastroenterol. 2016 22 8447 8458 10.3748/wjg.v22.i38.8447 27784957 PMC5064026
25. Desjardins C. Larrieu-Ciron D. Choquet S. Mokhtari K. Charlotte F. Nichelli L. Mathon B. Ahle G. Le Garff-Tavernier M. Morales-Martinez A. Chemotherapy is an efficient treatment in primary CNS MALT lymphoma J. Neurooncol. 2022 159 151 161 10.1007/s11060-022-04052-1 35725885
26. Grommes C. Rubenstein J.L. DeAngelis L.M. Ferreri A.J.M. Batchelor T.T. Comprehensive approach to diagnosis and treatment of newly diagnosed primary CNS lymphoma Neuro Oncol. 2019 21 296 305 10.1093/neuonc/noy192 30418592 PMC6380418
27. Quinn Z.L. Zakharia K. Schmid J.L. Schmieg J.J. Safah H. Saba N.S. Primary Dural Diffuse Large B-cell Lymphoma: A Comprehensive Review of Survival and Treatment Outcomes Clin. Lymphoma Myeloma Leuk. 2020 20 e105 e112 10.1016/j.clml.2019.09.600 31902733
28. Beriwal S. Hou J.S. Miyamoto C. Garcia-Young J.A. Primary dural low grade BCL-2 negative follicular lymphoma: A case report J. Neurooncol. 2003 61 23 25 10.1023/A:1021244228163 12587792
29. Tandon R. Mukherjee U. Abrari A. Patir R. Tandon A. Bansal B. Primary dural follicular lymphoma masquerading as meningioma: A case report Br. J. Neurosurg. 2012 26 905 906 10.3109/02688697.2012.685783 22616798
30. Altshuler E. Richhart R. Iqbal U. Chaffin J. Dural Follicular Lymphoma: Case Report and Literature Review J. Investig. Med. High Impact Case Rep. 2021 9 23247096211056768 10.1177/23247096211056768 PMC8641106 34844481
31. Ishiyama K. Okada M. Anzai N. Tashima M. Mantle cell lymphoma manifesting neurological symptoms similar to those of hypertrophic cranial pachymeningitis Rinsho Ketsueki 2011 52 1788 1793 22185803
32. Garg S. Gude G. Chatterjee D. Tewari M.K. Singla R. Ahuja C. Primary Dural Acute Lymphoblastic Leukaemia/Lymphoma Masquerading Meningioma: Report of a Case and Review of Literature Neurol. India 2023 71 987 990 10.4103/0028-3886.388108 37929440
33. Steffanoni S. Doorduijin J.K. Narrative review: Secondary central nervous system lymphoma Ann. Lymphoma 2021 5 5 10.21037/aol-20-39
34. Wright G.W. Huang D.W. Phelan J.D. Coulibaly Z.A. Roulland S. Young R.M. Wang J.Q. Schmitz R. Morin R.D. Tang J. A Probabilistic Classification Tool for Genetic Subtypes of Diffuse Large B Cell Lymphoma with Therapeutic Implications Cancer Cell 2020 37 551 568.e14 10.1016/j.ccell.2020.03.015 32289277 PMC8459709
35. Schmitz N. Zeynalova S. Nickelsen M. Kansara R. Villa D. Sehn L.H. Glass B. Scott D.W. Gascoyne R.D. Connors J.M. CNS International Prognostic Index: A Risk Model for CNS Relapse in Patients with Diffuse Large B-Cell Lymphoma Treated with R-CHOP J. Clin. Oncol. 2016 34 3150 3156 10.1200/JCO.2015.65.6520 27382100
36. Hollender A. Kvaloy S. Nome O. Skovlund E. Lote K. Holte H. Central nervous system involvement following diagnosis of non-Hodgkin’s lymphoma: A risk model Ann. Oncol. 2002 13 1099 1107 10.1093/annonc/mdf175 12176790
37. Tsutsumi Y. Ito S. Nagai J. Tateno T. Teshima T. Patients with marginal zone dural lymphoma successfully treated with rituximab and bendamustine: A report of two cases Mol. Clin. Oncol. 2021 15 208 10.3892/mco.2021.2371 34466224 PMC8375014
38. Okimoto R.A. Perry A. Rubenstein J.L. 77-year-old woman with a dural-based mass. Marginal zone B-cell lymphoma (MZBCL) Brain Pathol. 2015 25 111 112 10.1111/bpa.12233 25521182 PMC4942276
39. Lionakis M.S. Dunleavy K. Roschewski M. Widemann B.C. Butman J.A. Schmitz R. Yang Y. Cole D.E. Melani C. Higham C.S. Inhibition of B Cell Receptor Signaling by Ibrutinib in Primary CNS Lymphoma Cancer Cell 2017 31 833 843.e5 10.1016/j.ccell.2017.04.012 28552327 PMC5571650
40. Haldorsen I.S. Espeland A. Larsson E.M. Central nervous system lymphoma: Characteristic findings on traditional and advanced imaging AJNR Am. J. Neuroradiol. 2011 32 984 992 10.3174/ajnr.A2171 20616176 PMC8013157
41. Pons-Escoda A. Naval-Baudin P. Velasco R. Vidal N. Majós C. Imaging of Lymphomas Involving the CNS: An Update-Review of the Full Spectrum of Disease with an Emphasis on the World Health Organization Classifications of CNS Tumors 2021 and Hematolymphoid Tumors 2022 AJNR Am. J. Neuroradiol. 2023 44 358 366 10.3174/ajnr.A7795 36822829 PMC10084903
42. Bathla G. Hegde A. Lymphomatous involvement of the central nervous system Clin. Oncol. 2016 71 602 609 10.1016/j.crad.2016.02.006 27038652
43. Starr C.J. Cha S. Meningioma mimics: Five key imaging features to differentiate them from meningiomas Clin. Radiol. 2017 72 722 728 10.1016/j.crad.2017.05.002 28554578
44. Lyndon D. Lansley J.A. Evanson J. Krishnan A.S. Dural masses: Meningiomas and their mimics Insights Imaging 2019 10 11 10.1186/s13244-019-0697-7 30725238 PMC6365311
45. Maireche A. Bendjama O. Slimani D. Gatel I. Arab A. Lebcir A. Seddiki K. Imaging features of primary dural lymphoma: A report of 3 cases Radiol. Case Rep. 2023 19 802 811 10.1016/j.radcr.2023.11.029 38111553 PMC10726341
46. Boellaard R. Delgado-Bolton R. Oyen W.J. Giammarile F. Tatsch K. Eschner W. Verzijlbergen F.J. Barrington S.F. Pike L.C. Weber W.A. FDG PET/CT: EANM procedure guidelines for tumour imaging: Version 2.0 Eur. J. Nucl. Med. Mol. Imaging 2015 42 328 354 10.1007/s00259-014-2961-x 25452219 PMC4315529
47. Kunz W.G. Jungblut L.M. Kazmierczak P.M. Vettermann F.J. Bollenbacher A. Tonn J.C. Schichor C. Rominger A. Albert N.L. Bartenstein P. Improved Detection of Transosseous Meningiomas Using 68Ga-DOTATATE PET/CT Compared with Contrast-Enhanced MRI J. Nucl. Med. 2017 58 1580 1587 10.2967/jnumed.117.191932 28450556
48. Bashir A. Broholm H. Clasen-Linde E. Vestergaard M.B. Law I. Pearls and Pitfalls in Interpretation of 68Ga-Dotatoc PET Imaging Clin. Nucl. Med. 2020 45 e279 e280 10.1097/RLU.0000000000003012 32332303
49. Lapa C. Löhr M. Bluemel C. Monoranu C.M. Herrmann K. Primary Central Nervous System Lymphoma and Meningioma in DOTATATE PET/CT Clin. Nucl. Med. 2013 38 994 995 10.1097/RLU.0000000000000244 24152642
50. Hartmann K. Gillman J.A. Lazor J.W. Ware J.B. Weeks J.K. Nasrallah I.M. Farwell M.D. Pantel A.R. 68 Ga-Dotatate PET to Characterize Lesions in the Neuroaxis Clin. Nucl. Med. 2024 49 9 15 10.1097/RLU.0000000000004966 38048554
51. Juntikka T. Vaittinen S. Vahlberg T. Jyrkkiö S. Minn H. Somatostatin Receptors and Chemokine Receptor CXCR4 in Lymphomas: A Histopathological Review of Six Lymphoma Subtypes Front. Oncol. 2021 11 710900 10.3389/fonc.2021.710900 34307181 PMC8299948
52. Endo A. Komatsu K. Akiyama Y. Saito R. Mikami T. Mikuni N. Primary Dural Lymphoma: A Rare Case with Rapidly Growing Lesions and Successful Treatment Through Biopsy and Chemotherapy Cureus 2025 17 e93761 10.7759/cureus.93761 41185806 PMC12579793
53. Inami K. Tsutsumi S. Hashizume A. Yamataka M. Sugiyama N. Ueno H. Ishii H. Dural-based large B-cell lymphoma masquerading as a tentorial meningioma Radiol. Case Rep. 2024 19 1661 1665 10.1016/j.radcr.2024.01.058 38384697 PMC10876468
54. Kurokawa R. Kurokawa M. Isshiki S. Harada T. Nakaya M. Baba A. Naganawa S. Kim J. Bapuraj J. Srinivasan A. Dural and Leptomeningeal Diseases: Anatomy, Causes, and Neuroimaging Findings Radiographics 2023 43 e230039 10.1148/rg.230039 37535461
55. Mowo-wale A.G. Akah O. Prajapati S.J. Shah P. Tripathi K.M. Kancherla N. Raj R. Primary Dural Diffuse Large B-Cell Lymphoma: A Report of a Rare Case and Review of the Literature Cureus 2026 18 e102290 10.7759/cureus.102290 41755948 PMC12933214
56. Matmati K. Matmati N. Hannun Y.A. Rumboldt Z. Patel S. Lazarchick J. Stuart R. Giglio P. Dural MALT lymphoma with disseminated disease Hematol. Rep. 2010 2 e10 10.4081/hr.2010.e10 22184513 PMC3222263
57. Kremer S. Grand S. Rémy C. Pasquier B. Benabid A.L. Bracard S. Le Bas J.F. Contribution of dynamic contrast MR imaging to the differentiation between dural metastasis and meningioma Neuroradiology 2004 46 642 648 10.1007/s00234-004-1194-2 15232661
58. Lui Y.W. Malhotra A. Farinhas J.M. Dasari S.B. Weidenheim K. Freeman K. LaSala P.A. Dynamic perfusion MRI characteristics of dural metastases and meningiomas: A pilot study characterizing the first-pass wash-in phase beyond relative cerebral blood volume AJR Am. J. Roentgenol. 2011 196 886 890 10.2214/AJR.10.5309 21427341
59. Weinberg B.D. Kuruva M. Shim H. Mullins M.E. Clinical Applications of Magnetic Resonance Spectroscopy in Brain Tumors: From Diagnosis to Treatment Radiol. Clin. N. Am. 2021 59 385 403 10.1016/j.rcl.2021.01.004 PMC8272438 33926682
60. Chourmouzi D. Potsi S. Moumtzouoglou A. Papadopoulou E. Drevelegas K. Zaraboukas T. Drevelegas A. Dural lesions mimicking meningiomas: A pictorial essay World J. Radiol. 2012 4 75 82 10.4329/wjr.v4.i3.75 22468187 PMC3314931
61. Panyaping T. Punpichet M. Tunlayadechanont P. Tritanon O. Usefulness of a Rim-Enhancing Pattern on the Contrast-Enhanced 3D-FLAIR Sequence and MRI Characteristics for Distinguishing Meningioma and Malignant Dural-Based Tumor AJNR Am. J. Neuroradiol. 2023 44 247 253 10.3174/ajnr.A7780 36732030 PMC10187810
62. Matias T.B. Cordeiro R.A. Duarte J.A. de Jarry V.M. Appenzeller S. Villarinho L. Reis F. Immune-Mediated Hypertrophic Pachymeningitis and its Mimickers: Magnetic Resonance Imaging Findings Acad. Radiol. 2023 30 2696 2706 10.1016/j.acra.2023.01.017 36882352
63. Nayak L. Bettegowda C. Scherer F. Galldiks N. Ahluwalia M. Baraniskin A. von Baumgarten L. Bromberg J.E.C. Ferreri A.J.M. Grommes C. Liquid biopsy for improving diagnosis and monitoring of CNS lymphomas: A RANO review Neuro Oncol. 2024 26 993 1011 10.1093/neuonc/noae032 38598668 PMC11145457
64. Hatiboglu M.A. Karacam B. Khan I. Akdur K. Elbasan E.B. Mahfooz S. Seyithanoglu M.H. Cetin G. Papaker M.G. Oztanir M.N. Liquid biopsy for CNS lymphoma: CSF exosomes and CSF exosomal miR-15a, miR-21, miR-155, miR-210, and miR-19b are promising biomarkers for diagnosis Mol. Biol. Rep. 2024 51 1035 10.1007/s11033-024-09967-8 39361107
65. Singh S. Charan M.L. Vojjala N. Kaur P. Mahesh K.V. Soundappan K. Takkar A. Prakash G. Gupta V. Lal V. Diagnostic Potential of Cerebrospinal Fluid Biomarkers in Diagnosis of Primary Central Nervous System Lymphoma: A Systematic Review and Meta-Analysis Ann. Indian Acad. Neurol. 2025 28 789 797 10.4103/aian.aian_335_25 41298320 PMC12798882
66. Kim Y. Cho H.-H. Kim S.T. Park H. Nam D. Kong D.-S. Radiomics features to distinguish glioblastoma from primary central nervous system lymphoma on multi-parametric MRI Neuroradiology 2018 60 1297 1305 10.1007/s00234-018-2091-4 30232517
67. Bathla G. Priya S. Liu Y. Ward C. Le N.H. Soni N. Maheshwarappa R.P. Monga V. Zhang H. Sonka M. Radiomics-based differentiation between glioblastoma and primary central nervous system lymphoma: A comparison of diagnostic performance across different MRI sequences and machine learning techniques Eur. Radiol. 2021 31 8703 8713 10.1007/s00330-021-07845-6 33890149
68. Zwanenburg A. Vallières M. Abdalah M.A. Aerts H.J.W.L. Andrearczyk V. Apte A. Ashrafinia S. Bakas S. Beukinga R.J. Boellaard R. The Image Biomarker Standardization Initiative: Standardized quantitative radiomics for high-throughput image-based phenotyping Radiology 2020 295 328 338 10.1148/radiol.2020191145 32154773 PMC7193906