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Journal de radiologie
Vol 86, N° 11  - novembre 2005
pp. 1659-1683
Doi : JR-11-2005-86-11-0221-0363-101019-200509130
Normal and abnormal meningeal enhancement: MRI features

JL Dietemann, R Correia Bernardo, A Bogorin, M Abu Eid, M Koob, Th Nogueira, MI Vargas, W Fakhoury, G Zöllner
[1] Service de Radiologie 2, Hôpitaux Universitaires, Hôpital de Hautepierre, Avenue Molière, 67098 Strasbourg Cedex.

To cite the present paper, use exclusively the following reference. Dietemann JL, Correia Bernardo R, Bogorin A, Abu Eid M, Koob M, Nogueira Th. Les prises de contraste méningées normales et pathologiques en IRM. (full text in english on J Radio 2005; 86: 1659-83.

Tirés à part : JL Dietemann,


Les prises de contraste méningées normales et pathologiques en IRM

Les auteurs rappellent l’anatomie et les aspects normaux avec quelques variantes des méninges et des espaces méningés. Les prises de contraste pathologiques au niveau des méninges sont soit de type arachnoïdo-dural, soit de type arachnoïdo-pial, diffuses ou localisées, soit dans certains cas de type mixte. Les données IRM de ces prises de contraste d’origine tumorale, infectieuses ou inflammatoires sont décrites et illustrées.


The authors describe normal imaging of the meninges and meningeal spaces and MR (magnetic resonance) imaging findings in tumoral and nontumoral diseases. Dural or/and pial enhancement may be related to tumoral, infectious or granulomatous diseases.

Mots clés : Méninges , Dure-mère , Arachnoïde , Pie-mère , IRM , Scanner

Keywords: Meninges , Dura , Arachnoid , Pia , MRI , CT

MRI is the best imaging modality to assess the intracranial and intraspinal meninges. MRI allows accurate evaluation of classical tumoral processes (meningiomas), cystic lesions (arachnoid and leptomeningeal cysts), post-traumatic or infectious subdural and extra-dural collections and inflammatory processes. MRI also allows demonstration of meningeal or CSF spread of primary CNS tumors, metastases from extra-cranial and extra-spinal tumors as well as inflammatory and infectious processes. The detection of meningeal pathology on MRI is based on the demonstration of dural and/or leptomeningeal enhancement. The presence of meningeal enhancement is non specific. Correlation between meningeal signal abnormalities and parenchymal signal abnormalities and clinical setting is mandatory for appropriate differential diagnosis.

The following topics will be discussed: (1) normal meninges and meningeal spaces, (2) pachymeningeal or dura-arachnoid enhancement, (3) focal and/or diffuse leptomeningeal or pia-subarachnoid enhancement (4) and rare or atypical lesions.

Normal meninges and meningeal spaces

The dura mater or pachymeninx corresponds to the outer meningeal layer (fig. 1) . At the cerebral convexity, it is composed of two layers [1]. The external layer, corresponding to the periosteum of the inner table, is highly vascularized and [2] the internal layer corresponding to the true meningeal dura mater. At the spinal level, only the internal dural layer is present that extends laterally into the intervertebral foramina to form the dural root sleeves which invest nerve roots and spinal ganglia. At the intracranial level, separations of both dural layers create the dural sinuses. The tentorium cerebelli, falx cerebri and falx cerebelli are dural reflections dividing the intracranial compartment [1].

The arachnoid and pia mater form the leptomeninges (fig. 1) . The arachnoid membrane rests on the dura. It is thin at the high convexity and thicker at the base of the brain. The pia is closely adherent to the surface of the brain and spinal cord. It is thicker at the spinal level [1].

The meningeal layers are separated by spaces: (1) the epidural space is a virtual space located between the inner table and dura, (2) the subdural space is a virtual space located between the dura and arachnoid (3) and the subarachnoid space is located between the arachnoid and pia and contains the cerebrospinal fluid (CSF). The subarachnoid space is filled with multiple trabeculae extending between arachnoid membrane and pia, including the basal cisterns. Some of these membranes, including the membrane of Liliequist, may be at the origin of arachnoid cysts [2], [3]. At the spinal canal, a retro-medullary sagittal midline membranous structure, the septum posticum, is present. The subarachnoid space extends to the dural sinuses and granulations of Pacchioni where CSF is absorbed into the venous blood. The perivascular spaces of Virchow-Robin contain CSF but are separated from the subarachnoid space by the pia and therefore do not directly communicate with the subarachnoid space (fig. 1) .

Imaging features

CT is of limited value for demonstrating the meninges. Only the falx cerebri and tentorium are routinely visualized on CT. CT may however be of value to confirm the presence of variants of normal including ossification of the falx and tentorium that may lead to diagnostic challenges on MRI because of the associated high T1W and T2W signal intensity related to fatty tissue (fig. 2) . CT is adequate to detect epidural and subdural collections but is poorly sensitive to detect enhancement of abnormally thickened meninges.

Normal dura can be demonstrated on MRI. On postcontrast T1W images, thin, and frequently discontinuous, enhancement along the inner table, falx and tentorium can be observed related to absent blood-brain barrier (fig. 3) . The conspicuity of meningeal enhancement is improved by increasing the volume of injected contrast material, reducing the slice thickness, selecting an optimal plane of section (coronal images to assess the dura along the high convexities and tentorium) and the use of fat suppressed spin echo sequences [1], [4]. On T1W inversion recovery images, the dura is hyperintense allowing visualization of the falx cerebri, tentorium, falx cerebelli, and margins of the superior sagittal sinus and cavernous sinuses [5] (fig. 4) . After craniotomy, thickening and enhancement of the dura and arachnoid is usually observed [6], [7] (fig. 5) . On thin slice 3D T2W sequences (3D CISS, 3D FSE), some of the subarachnoid trabeculae can be detected, including the membrane of Liliequist (fig. 6) extending through the interpeduncular cistern. Individuals with a high degree of pigmentation may have excess melanin deposition along the leptomeninges with corresponding areas of T2W hypointensity, especially along the medulla oblongata, that should be distinguished from abnormal deposition of melanin or iron (siderosis) [8].

Abnormal meningeal enhancement

Two types of enhancement pattern may be present (fig. 7) : dura-arachnoid and pia-subarachnoid enhancement [1]. In some instances, both types of enhancement may coexist [9]. The diffuse or focal nature of the enhancement and its location are useful for differential diagnosis.

Dura-arachnoid enhancement results from inflammatory ot tumoral thickening and appears as an area of linear enhancement along the inner table of the cranial convexity with involvement of the falx and tentorium. Regular and diffuse enhancement is suggestive of inflammation or intracranial hypotension, either spontaneous or following spinal tap, whereas irregular or focal enhancement is suggestive of tumor. This pattern of enhancement is mainly detected at the intracranial level.

Pia-subarachnoid enhancement closely follows the brain or cerebellar surface into sulci whereas linear enhancement is present along the surface of the braistem and spinal cord. This pattern of enhancement is more frequently seen in association with inflammatory diseases as opposed to tumors, especially when diffuse. This pattern of enhancement is seen with similar frequency at the intracranial and intraspinal levels.

Dura-arachnoid enhancement
Diffuse dura-arachnoid enhancement

Diffuse linear enhancement secondary to thickening of the arachnoid and dura is consistent with a chronic inflammatory process; this appearance is characteristic of diffuse pachymeningitis. This pattern of enhancement can be observed with some systemic diseases, including Wegener’s granulomatosis [10], but also with infectious (tuberculous pachymeningitis), granulomatous (sarcoidosis), and inflammatory auto-immune (rheumatoid arthritis) diseases [11], [12], [13], [14].

However, diffuse enhancing meningeal thickening along the convexities, falx and tentorium is more frequently the result of intracranial hypotension syndrome, either spontaneous, or more frequently following lumbar spinal tap (fig. 7 and 8) . Intracranial hypotension syndrome is characterized on MRI by the following features: small lateral ventricles with virtual third ventricle, brain settling with low lying cerebellar tonsils and brain stem, pituitary enlargement, enlargement of venous sinuses, supratentorial subdural collections, enlargement of upper cervical (C1, C2, C3) and lower lumbar (L5 and S1) antero-lateral spinal epidural veins, and subdural and extra-dural thoraco-lumbar collections [15]. Chronic intracranial hypotension, secondary to long-standing overshunting from a ventricular catheter in patients with neonatal hydrocephalus, may result in microcephaly, calvarial thickening, enlargement of the basal dural sinuses, and dural thickening, sometimes calcified and/or enhancing after gadolinum injection (fig. 9) ; this should not be confused with chronic calcified subdural hematoma.

Diffuse dura-arachnoid metastatic disease is infrequent and usually is seen in association with diffuse infiltration of the calvarium and skull base as sometimes seen with prostate carcinoma (fig. 10) . Metastatic infiltration of the skull is characterized by sclerosis of the skull base with thickening and loss of differentiation between cortex and diploic space.The adjacenet dura is thickened and enhances after gadolinium injection. Focal thickening may simulate meningioma. Involvement of the overlying scalp can occur as well. The falx and tentorium remain unaffected.

When no inflammatory, infectious or tumoral etiology or evidence of intracranial hypotension is present, a diagnosis of idiopathic pachymeningitis is considered, with possible dural calcifications. Dural thickening and enhancement are predominent at the posterior fossa and cervico-thoracic spinal canal. The thickened dura is T1W and T2W hypointense and shows enhancement after gadolinium injection. Peripheral enhancement at the site of active inflammatory reaction is sometimes present whereas calcified zones remain hypointense [16], [17] (fig. 11) . Dural thickening in the posterior fossa may cause mass effect with supratentorial hydrocephalus and intracranial hypertension.

Contrast material enhanced coronal T1W images are invaluable to differentiate between the three types of dura-arachnoid diseases [8], [10], [11]:

  • Diffuse symmetrical dural thickening along the cerebral convexities, skull base, falx and tentorium should first suggest a diagnosis of spontaneous or iatrogenic (spinal tap, ventricular shunt) intracranial hypotension syndrome; in patients with additional findings of skull thickening and prominent skull base and facial pneumatization, long-standing intracranial hypotension should be considered, typically secondary to chronic ventricular shunting for hydrocephalus.
  • Diffuse dural thickening along the cerebral convexities and eventually along the skull base without involvement of the falx or tentorium suggests diffuse tumor infiltration, most frequently associated with diffuse skull and skull base metastases, typically from prostate carcinoma.
  • Diffuse dural thickening predominently involving the posterior fossa and tentorium with associated calcifications suggests a diagnosis of idiopathic pachymeningitis.

Focal dura-arachnoid enhancement

Foca dural enhancement, associated with focal dural thickening, can often be observed in the setting of local or regional tumoral or inflammatory lesions: meningeal extension of an adjacent tumoral or inflammatory lesion of the brain or skull. The presence of a focal meningeal mass may cause diagnostic challenges. While meningioma is by far the most frequent dural based tumor (fig. 12) , other lesions (dural metastasis, meningeal sarcoidosis, meningeal lymphoma, hemangiopericytoma, plasmacytoma, plasma cell granuloma, inflammatory pseudotumors in patients with systemic disorders including rheumatoid arthritis and Castelman’s disease, solitary fibrous tumor, leptomeningeal melanocytic tumors, tuberculoma, primary meningeal sarcoma, gliosarcoma, most frequently temporal in location, leiomyosarcoma in the setting of immunosuppression, and Rosai-Dorfman disease) may have a similar appearance on CT and/or MR [18], [19], [20] (fig. 13- 19) . Meningeal tuberculosis may be unilateral and involve only one cerebral or cerebellar convexity [21].

Focal dura-arachnoid lesions appear on MRI as extra-axial T1W iso- to hypointense, T2W iso- to hyperintense intensely and homogeneously enhancing lesions. Meningeal sarcoidosis may sometimes be markedly T2W hypointense without demonstration of calcification on CT [22]. Sarcoid or lymphomatous lesions simulating meningioma may decrease in size with steroids [23]. Perfusion imaging, with the use of cerebral blood volume maps, may help differentiate lymphoma from hypervascular tumors [24].

The dural tail sign is not specific for meningioma and can be observed in association with many vascularized masses, either dural based or closely related to the dura [25].

Enhancing regional dural thickening is routinely observed following craniotomy [6], [26], [27].

Pia-subarachnoid enhancement

The differential diagnosis for focal and diffuse pia-subarachnoid enhancement is similar. Meningococcal meningitis is only associated with abnormal leptomeningeal enhancement when diagnosis is delayed. Marked meningeal enhancement is associated with pneumococcal and tuberculous meningitis mainly in the suprasellar cistern and sylvian fissures with extension to the high convexities and posterior fossa [28], [29] (fig. 20, 21) . Leptomeningeal thickening is more prominent in the basal cisterns in patients with cryptococcosis [30]. Irrespective of the underlying etiology for intracranial pia-subarachnoid enhancement, it is frequently associated with linear enhancement along the surface of the cord and diffuse enhancement along the cauda equina. Basal cistern meningitis from tuberculosis may be complicated by arteritis and brain infarcts. Viral encephalitis and meningo-encephalitis may be associated with focal or diffuse leptomeningeal enhancement (fig. 22) .

Leptomeningeal neurosarcoidosis is characterized by a similar pattern of enhancement. Enhancing nodular intra-axial lesions may involve the brain and cord, probably from extension of the leptomeningeal process along the perivascular spaces. Enhancing dural lesions may also be present [31], [32], [33], [34] (fig. 23) . Rapid regression of lesions frequently occurs with steroid treatment [35].

Leptomeningeal metastases may involve the brain and cord (fig. 24- 26) . Some imaging features are suggestive of metastatic disease: predominent enhancement in dependent regions (pericerebellar cisterns, lumbar dural sac), nodular enhancement of cranial nerves (mainly along the internal auditory canals and trigeminal nerves), along the spinal cord and cauda equina. Leptomeningeal metastases may originate from CSF spread of aggressive or immature primary brain or cord tumors (high grade glioma, medulloblastoma, germinoma, pinealoblastoma, PNET) or from non-CNS tumors (breast, lung and ovarian carcinomas, melanoma, lymphoproliferative disorders especially lymphoma…) [36]. FLAIR images show hyperintense signal in the sulci. The sensitivity of FLAIR imaging is nearly similar to that of postcontrast T1W imaging [37]. Postcontrast FLAIR imaging probably is the most sensitive sequence for detecting leptomeningeal lesions [38] (fig. 26) . In order to increase the sensitivity of MR imaging for detection of leptomeningeal disease, some authors have suggested using a double and even a triple dose of gadolinium contrast material [39], [40]. The association of leptomeningeal disease with enhancing intra-axial nodular lesions, especially intramedullary in location, is suggestive of metastatic disease and sarcoidosis. Leptomeningeal carcinomatosis may be complicated by hydrocephalus secondary to impaired CSF reabsorption [41].

The presence of symmetrical and bilateral enhancement of all spinal nerve roots and cranial nerves without associated focal tumor suggests a diagnosis of infectious or inflammatory meningoradiculitis (neuroborreliosis, Guillain-Barré) [42], [43] (fig. 27, 28) .

Leptomeningeal lesions, either inflammatory or neoplastic in nature, may be associated with subcortical low intensity areas on T2W and FLAIR images possibly secondary to free radical formation [44] (fig. 29) .

Correlation between MRI findings, clinical setting, CSF analysis and past medical history is mandatory for appropriate differential diagnosis.

Combined dura-arachnoid and pia-subarachnoid enhancement

In some cases, both types of meningeal enhancement may coexist, typically focal in location and in association with a vascularized extra-axial tumor including metastasis, lymphoma, focal tuberculous meningitis and sarcoidosis (fig. 30) .

Rare or atypical lesions
Tumoral lesions

Meningeal melanocytomas develop from pial melanocytes which are most concentrated over the ventral surface of the medulla [8]. The prognosis of meningeal melanocytomas is better than that of cutaneous melanomas. On MRI, the lesions are slightly T1W hyperintense and T2W hypointense [45].

Neurocutaneous melanosis may be complicated by hydrocephalus secondary to melanocytic proliferation obstructing the basal cisterns [46]. Diffuse moderately T1W hyperintense and enhancing leptomeningeal thickening at the cranial and spinal level is present [47].

Vascular lesions

Dural fistulas are characterized by the presence of enlarged meningeal and cortical vessels (fig. 31) . Hemorrhagic subarachnoid and intra-parenchymal complications may be detected on MRI. Leptomeningeal enhancement secondary to dilatation of pial collaterals may be observed in patients with moyamoya [48]. Diffuse leptomeningeal enhancement may be present in patients with vasculitis [49]. Wegener’s granulomatosis may be associated with pial and dural involvement [10], [50] (fig. 32) . Regional meningeal collateral flow may be present in patients with cerebral ischemia. Superior sagittal or transverse sinus thrombosis is associated with local dural enhancement secondary to venous stasis and collateral circulation (fig. 33) . Hypertrophic cranial pachymeningitis has been reported in association with aplastic anemia [51]. Unilateral leptomeningeal enhancement after carotid stent insertion has also been reported [52]. Leptomeningeal enhancement in Sturge-Weber disease (fig. 34) is usually posterior and ipsilateral to the side of facial angioma and associated with additional characteristic features of the disease: ipsilateral cerebral atrophy, ipsilateral choroid plexus enlargement, abnormal venous drainage and cortical calcifications (hyperdense gyriform cortical calcifications on CT with corresponding T2W and T2*W hypointense signal on MRI) [53].

Inflammatory and infectious lesions

Dural thickening may occur with Behcet’s disease [54]. Sinusitis and otomastoiditis may be complicated by pachymeningitis [55]. Focal leptomeningeal MR enhancement along the chiasm as a presenting sign of multiple sclerosis has been reported [56]. Involvement of spinal and posterior fossa leptomeninges by amyloid has also been reported [57].


MRI is valuable to demonstrate the presence of meningeal diseases. Postcontrast T1W and FLAIR images are most sensitive for its detection whereas T2W images may provide additional clues for lesion characterization. The distribution, morphological and MR signal intensity features of the lesions correlated with clinical and paraclinical (CSF analysis) findings frequently allow appropriate differential diagnosis.


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