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.
The dura mater or pachymeninx corresponds to the outer meningeal layer (fig. 1). At the cerebral convexity, it is composed of two layers [1Meltzer CC, Fukui MB, Kanal E, Smirniotopoulos JG. MR imaging of the meninges. Part I. Normal anatomic fetatures and nonneoplastic disease. Radiology 1996;201:297-308.
Click here to see the Library]. The external layer, corresponding to the periosteum of the inner table, is highly vascularized and [2Miyajima M, Arai H, Okuda O, Hishii M, Nakanishi H, Sato K. Possible origin of suprasellar arachnoid cysts: neuroimaging and neurosurgical observations in nine cases. J Neurosurg 2000;93:62-7.
Click here to see the Library] 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 [1Meltzer CC, Fukui MB, Kanal E, Smirniotopoulos JG. MR imaging of the meninges. Part I. Normal anatomic fetatures and nonneoplastic disease. Radiology 1996;201:297-308.
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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 [1Meltzer CC, Fukui MB, Kanal E, Smirniotopoulos JG. MR imaging of the meninges. Part I. Normal anatomic fetatures and nonneoplastic disease. Radiology 1996;201:297-308.
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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 [2Miyajima M, Arai H, Okuda O, Hishii M, Nakanishi H, Sato K. Possible origin of suprasellar arachnoid cysts: neuroimaging and neurosurgical observations in nine cases. J Neurosurg 2000;93:62-7.
Click here to see the Library], [3Zhang M, An PC. Liliquist’s membrane is a fold of the arachnoid mater: study using sheet plastination and scanning electron microscopy. Neurosurgery 2000; 47:902-8.
Click here to see the Library]. 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).
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 [1Meltzer CC, Fukui MB, Kanal E, Smirniotopoulos JG. MR imaging of the meninges. Part I. Normal anatomic fetatures and nonneoplastic disease. Radiology 1996;201:297-308.
Click here to see the Library], [4Quint DJ, Eldevik OP, Cohen JK. Magnetic resonance imaging of normal meningeal enhancement at 1.5 T. Acad Radiol 1996;3:463-8.
Click here to see the Library]. 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 [5Dietemann JL, Kehrli P, Maillot C, et al. Is there a dural wall between the cavernous sinus and the pituitary fossa ? Anatomical and MRI findings. Neuroradiology 1998;40:627-30.
Click here to see the Library](fig. 4). After craniotomy, thickening and enhancement of the dura and arachnoid is usually observed [6Burke JW, Podrasky AE, Bradley WG Jr. Meninges: benign postoperative enhacement on MR images. Radiology 1990; 174:99-102.
Click here to see the Library], [7Leach JL, Jones BV, Tomsick TA, Stewart CA, Balko MG. Normal appearance of arachnoid granulations on contraste-enhanced CT and MR of the brain: differentiation from dural sinus disease. AJNR Am J Neuroradiol 1997; 18: 594-5.
Click here to see the Library](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) [8Gebarski SS, Blaivas MA. Imaging of normal leptomeningeal melanin. AJNR Am J Neuroradiol 1996;17:55-60.
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Two types of enhancement pattern may be present (fig. 7): dura-arachnoid and pia-subarachnoid enhancement [1Meltzer CC, Fukui MB, Kanal E, Smirniotopoulos JG. MR imaging of the meninges. Part I. Normal anatomic fetatures and nonneoplastic disease. Radiology 1996;201:297-308.
Click here to see the Library]. In some instances, both types of enhancement may coexist [9Kioumehr F, Dadsetan MR, Feldman N, et al. Postcontrast MRI of cranial meninges: leptomeningitis versus pachymeningitis. J Comput Assist Tomogr 1995;19: 713-20.
Click here to see the Library]. 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.
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 [10Spranger M, Schwab S, Meinck HM, et al. Meningeal involvement in Wegener’s granulomatis confirmed and monitored by positive circulating antineutrophil cytoplasm in cerebrospinal fluid. Neurology 1997;48:263-5.
Click here to see the Library], but also with infectious (tuberculous pachymeningitis), granulomatous (sarcoidosis), and inflammatory auto-immune (rheumatoid arthritis) diseases [11Agildere AM, Tutar NU, Yucel E, Coskun M, Benli S, Aydin P. Parencyhmeningitis and optic neuritis in rheumatoid arthritis: MR findings. Br J Radiol 1999; 72:404-7.
Click here to see the Library], [12Cellerini M, Gabbrielli S, Maddali Bongi S, Cammelli D. MRI of cerebral rheumatoid parenchymeningitis: report of two cases with follow-up. Neuroradiology 2001;43:147-50.
Click here to see the Library], [13Demaerel P, Wilms G, Marchal G. MRI findings in tuberculous meningo-encephalitis. RÖFO Fortschr Röntgenstr 1990;152: 384-7.
Click here to see the Library], [14Goyal M, Scharma A, Mishra NK, Gaikwad SB, Sharma MC. Imaging apparearance of parechymeningeal tuberculosis. AJR Am J Roentgenol 1997; 169: 1421-4.
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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 [15Pannullo SC, Reich JB, Krol G, Deck D, Posner JB. MRI changes in intracranial hypotension. Neurology 1993;43: 919-26.
Click here to see the Library]. 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 [16Friedman DP, Flanders AE. Enhanced MR imaging of hypertrophic pachymeningitis. AJR Am J Radiol 1997;169: 1425-8.
Click here to see the Library], [17Bang OY, Kim DI, Yoon SR, Choi IS. Idiopathic hypertrophic pachymeningeal lesions: correlation between clinical patterns and neuroimaging characteristics. Eur Neurol 1998;39:49-56.
Click here to see the Library](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 [8Gebarski SS, Blaivas MA. Imaging of normal leptomeningeal melanin. AJNR Am J Neuroradiol 1996;17:55-60.
Click here to see the Library], [10Spranger M, Schwab S, Meinck HM, et al. Meningeal involvement in Wegener’s granulomatis confirmed and monitored by positive circulating antineutrophil cytoplasm in cerebrospinal fluid. Neurology 1997;48:263-5.
Click here to see the Library], [11Agildere AM, Tutar NU, Yucel E, Coskun M, Benli S, Aydin P. Parencyhmeningitis and optic neuritis in rheumatoid arthritis: MR findings. Br J Radiol 1999; 72:404-7.
Click here to see the Library]:
- 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.
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 [18Buttner A, Pfluger T, Weis S. Primary meningeal sarcomas in two children. J Neurooncol 2001;52:181-8.
Click here to see the Library], [19River Y, Schwartz A, Gomori JM, Schoffer D, Siegal T. Clinical significance of diffuse dural enhancement detected by magnetic resonance imaging. J Neurosurg 1996;85:777-83.
Click here to see the Library], [20Sandhu FA, Schellinger D, Martuza RL. A vascular sarcoid mass mimicking a convexity meningioma. Neuroradiology 2000;42:195-8.
Click here to see the Library](fig. 13-19). Meningeal tuberculosis may be unilateral and involve only one cerebral or cerebellar convexity [21Praharaj SS, Sharma MC, Prasad K, Misra NK, Mahapatra AK. Unilateral meningeal thickening: a rare presentation of tuberculous meningitis. Clin Neurol Neurosurg 1997;99:60-2.
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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 [22Buff BL Jr, Schick RM, Norregaar T. Meningeal metastasis of leiomyosarcoma mimicking meningioma: CT and MR findings. J Comput Assist Tomogr 1991; 15:166-7.
Click here to see the Library]. Sarcoid or lymphomatous lesions simulating meningioma may decrease in size with steroids [23Wilson JD, Castillo M, Van Tassel P. MRI features of intracranial sarcoidosis mimicking meningiomas. Clin Imaging 1994;18:184-8.
Click here to see the Library]. Perfusion imaging, with the use of cerebral blood volume maps, may help differentiate lymphoma from hypervascular tumors [24Kremer S, Grand S, Rémy C, et al. Contribution of dynamic contrast MR imaging to the differentiation between dural metastasis and meningioma. Neuroradiology 2004; 46: 642-8.
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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 [25Tien RD, Yan PJ, Chu PK. “Dural tail sign”: a specific MR sign for meningioma? J Comput Assist Tomogr 1991;15:64-6.
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Enhancing regional dural thickening is routinely observed following craniotomy [6Burke JW, Podrasky AE, Bradley WG Jr. Meninges: benign postoperative enhacement on MR images. Radiology 1990; 174:99-102.
Click here to see the Library], [26Hudgins PA, Davis PC, Hoffman JC Jr. Gadopentetate dimeglumine-enhanced MR imaging in children following surgery for brain tumor: spectrum of meningeal findings. AJNR Am J Neuroradiol 1991;12:301-7.
Click here to see the Library], [27Knauth M, Aras N, Wirtz CR, Dorfler A, Engelhorn T, Sartor K. Surgically induced intracranial contrast enhancement: potential source of diagnostic error in intraoperative MR imaging. AJNR Am J Neuroradiol 1999;20:1547-53.
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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 [28Villoria MF, De la Torre J, Fortea F, Munoz L, Hernandez T, Alarcon JJ. Intracranial tuberculosis in AIDS: CT and MRI findings. Neuroradiology 1992;34: 11-4.
Click here to see the Library], [29Tayfun C, Ucoz T, Tasar M, et al. Diagnostic value of MRI in tuberculous meningitis. Eur Radiol 1996;6:380-6.
Click here to see the Library](fig. 20, 21). Leptomeningeal thickening is more prominent in the basal cisterns in patients with cryptococcosis [30Arnder L, Castillo M, Heinz ER, Scatliff JG, Enterline D. Unusual pattern of enhancement in cryptococcal meningitis: in vivo findings with postmortem correlation. J Comput Assist Tomogr 1996;20: 1023-6.
Click here to see the Library]. 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 [31Fukui MB, Meltzer CC, Kanal E, Smirnioptopoulos JG. MR imaging of the meninges. Part II. Neoplasic disease. Radiology 1996;201:605-12.
Click here to see the Library], [32Bode MK, Tikkakoski T, Tuisku S, Kronqvist E, Tuominen H. Isolated neurosarcoidosis – MR findings and pathologic correlation. Acta Radiol 2001;42: 563-7.
Click here to see the Library], [33Pickhut D, Heywang-Kobrunner SH. Neurosarcoidosis: evaluation with MRI. J Neuroradiol 2000;27:185-8.
Click here to see the Library], [34Wilson JD, Castillo M. Magnetic resonance imaging of granulomatous inflammations: sarcoidosis and tuberculosis. Topic in Magnetic Resonance Imaging 1994;6:32-40.
Click here to see the Library](fig. 23). Rapid regression of lesions frequently occurs with steroid treatment [35Christoforidis GA, Spickler EM, Recio MV, Mehta BM. MR of CNS sarcoidosis: correlation of imaging features to clinical symptoms and response to treatment. AJNR Am J Neuroradiol 1999;20:655-69.
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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…) [36Gomori HL, Heching N, Siegal T. Leptomeningeal metastases: evaluation by gadolinium enhanced spinal magnetic resonance imaging. J Neurooncol 1998;36: 55-60.
Click here to see the Library]. FLAIR images show hyperintense signal in the sulci. The sensitivity of FLAIR imaging is nearly similar to that of postcontrast T1W imaging [37Adjenov V, Chapiron C, Asquier E, Vinikoff C, Lemarié E, Brunereau L. Imagerie des complications neurologiques du carcinome bronchique. J Radiol 2004;85: 599-609.
Click here to see the Library]. Postcontrast FLAIR imaging probably is the most sensitive sequence for detecting leptomeningeal lesions [38Griffiths PD, Coley SC, Romanowski CAJ, Hodgson T, Wilkinson ID. Contrast-enhanced fluid-attenuated inversion recovery imaging for leptomeningeal disease in children. AJNR Am J Neuroradiol 2003;24:719-23.
Click here to see the Library](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 [39Iaconetta G, Lamaida E, Rossi A, Signorelli F, Manto A, Giamundo A. Leptomeningeal carcinomatosis: review ot the litterature. Acta Neurol 1994;16:214-20.
Click here to see the Library], [40Kallmes DE, Gray L, Glass JP. High-dose gadolinium-enhanced MRI for diagnosis of meningeal metastases. Neuroradiology 1998;40:23-6.
Click here to see the Library]. 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 [41Watanabe M, Tanaka R, Takeda N. Correlation of MRI and clinical features in meningeal carcinomatosis. Neuroradiology 1993;35:512-5.
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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) [42Demaerel P, Wilms G, Van Lierde S, Delanote J, Baert AL. Lyme disease in childhoof presntint as primary leptomeningeal enhancement without parenchymal findings on MR. AJNR Am J Neuroradiol 1994;15:302-4.
Click here to see the Library], [43Nelson JA, Wolf MD, Yuh WT, Peeples ME. Cranial nerve involvement with Lyme borreliosis demonstrated by magnetic resonance imaging. Neurology 1992;42: 671-3.
Click here to see the Library](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 [44Lee JH, Na DG, Choi KH, et al. Subcortical low intensity on MR images of meningitis, viral encephalitis, and leptomeningeal metastasis. AJNR Am J Neuroradiol 2002;23:535-42.
Click here to see the Library](fig. 29).
Correlation between MRI findings, clinical setting, CSF analysis and past medical history is mandatory for appropriate differential diagnosis.
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).
Meningeal melanocytomas develop from pial melanocytes which are most concentrated over the ventral surface of the medulla [8Gebarski SS, Blaivas MA. Imaging of normal leptomeningeal melanin. AJNR Am J Neuroradiol 1996;17:55-60.
Click here to see the Library]. The prognosis of meningeal melanocytomas is better than that of cutaneous melanomas. On MRI, the lesions are slightly T1W hyperintense and T2W hypointense [45Châabane M, Ellouze S, Hamrouni A, Nlika N, Ben Hammouda M, Khoudja F. Une tumeur méningée rare : mélanocytome méningée. J Radiol 2003;84:415-6.
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Neurocutaneous melanosis may be complicated by hydrocephalus secondary to melanocytic proliferation obstructing the basal cisterns [46Orrison WW Jr. Neuroimaging. WB Saunders Compagny, édit., Philadelphia, 2000.
Click here to see the Library]. Diffuse moderately T1W hyperintense and enhancing leptomeningeal thickening at the cranial and spinal level is present [47Byrd SE, Darling CF, Tomita T, Chou P, de Leon GA, Radkowski MA. MR imaging of symptomatic neurocutaneous melanosis in children. Pediatr Radiol 1997; 27:39-44.
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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 [48Ohta T, Tanaka H, Kuroiwa T. Diffuse leptomeningeal enhancement, “ivy sign”, in magnetic resonance images of moyamoya disease in childhood: case repot. Neurosurgery 1995;37:1009-12.
Click here to see the Library]. Diffuse leptomeningeal enhancement may be present in patients with vasculitis [49Negishi C, Sze G. Vasculitis presenting as primary leptomeningeal enhancement with minim parenchymal findings. AJNR Am J Neuroradiol 1993;14: 26-8.
Click here to see the Library]. Wegener’s granulomatosis may be associated with pial and dural involvement [10Spranger M, Schwab S, Meinck HM, et al. Meningeal involvement in Wegener’s granulomatis confirmed and monitored by positive circulating antineutrophil cytoplasm in cerebrospinal fluid. Neurology 1997;48:263-5.
Click here to see the Library], [50Nusbaum AO, Morgello S, Atlas SW. Pial involvement in Wegener’s granulomatosis schown on MRI. Neuroradiology 1999;41:847-9.
Click here to see the Library](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 [51Asano T, Hayashida M, Ogawa K, Adachi K, Teramoto A, Yamamoto M. Hypertrophic cranial parenchymeningitis in a patient with aplastic anemia. Ann Hematol 1998;77:279-82.
Click here to see the Library]. Unilateral leptomeningeal enhancement after carotid stent insertion has also been reported [52Wilkinson ID, Griffiths PD, Hoggard N, Cleveland TJ, Gaines PA, Venables GS. Unilateral leptomeingeal enhancement after carotid stent insertion detected by magnetic resonance imaging. Stroke 2000;31: 2274-5.
Click here to see the Library]. 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) [53Sperner J, Schmauser I, Bittner R. MR-imaging findings in children with Sturge-Weber syndrome. Neuropediatrics 1990;21:146-52.
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Dural thickening may occur with Behcet’s disease [54Guma A, Aguilera C, Acebes J, Arruga J, Pons L. Meningeal involvement in Behcet’s disease: MRI. Neuroradiology 1998; 40:512-5.
Click here to see the Library]. Sinusitis and otomastoiditis may be complicated by pachymeningitis [55Nemzek W, Postma G, Poirier V, Hecht S. MR features of pachymeningitis presenting with sixth-nerve palsy secondary to sphenoid sinusitis. AJNR Am J Neuroradiol 1995;16:960-3.
Click here to see the Library]. Focal leptomeningeal MR enhancement along the chiasm as a presenting sign of multiple sclerosis has been reported [56Demaerel P, Robberecht W, Casteels I, et al. Focal leptomeningeal MR enchacement along the chiasm as a presenting sign of multiple sclerosis. J Comput Assist Tomogr 1995;19:297-8.
Click here to see the Library]. Involvement of spinal and posterior fossa leptomeninges by amyloid has also been reported [57Horowitz S, Thomas C, Gruener G, Nand S, Shea JF. MR of leptomeningeal spinal and posteriof fossa amyloid. AJNR Am J Neuroradiol 1998;19:900-2.
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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.
|The veins returning the blood from the cranial dura mater anastomose with the diploic veins and end in the various sinuses. Many of the meningeal veins do not open directly into the sinuses, but indirectly through a series of ampullæ, termed venous lacunæ. These are found on either side of the superior sagittal sinus, especially near its middle portion, and are often invaginated by arachnoid granulations; they also exist near the transverse and straight sinuses. They communicate with the underlying cerebral veins, and also with the diploic and emissary veins.|
|The nerves of the cranial dura mater are filaments from the semilunar ganglion, from the ophthalmic, maxillary, mandibular, vagus, and hypoglossal nerves, and from the sympathetic.|
|The Spinal Dura Mater (dura mater spinalis; spinal dura) (Fig. 767) forms a loose sheath around the medulla spinalis, and represents only the inner or meningeal layer of the cranial dura mater; the outer or endosteal layer ceases at the foramen magnum, its place being taken by the periosteum lining the vertebral canal. The spinal dura mater is separated from the arachnoid by a potential cavity, the subdural cavity; the two membranes are, in fact, in contact with each other, except where they are separated by a minute quantity of fluid, which serves to moisten the apposed surfaces. It is separated from the wall of the vertebral canal by a space, the epidural space, which contains a quantity of loose areolar tissue and a plexus of veins; the situation of these veins between the dura mater and the periosteum of the vertebræ corresponds therefore to that of the cranial sinuses between the meningeal and endosteal layers of the cranial dura mater. The spinal dura mater is attached to the circumference of the foramen magnum, and to the second and third cervical vertebræ; it is also connected to the posterior longitudinal ligament, especially near the lower end of the vertebral canal, by fibrous slips. The subdural cavity ends at the lower border of the second sacral vertebra; below this level the dura mater closely invests the filum terminale and descends to the back of the coccyx, where it blends with the periosteum. The sheath of dura mater is much larger than is necessary for the accommodation of its contents, and its size is greater in the cervical and lumbar regions than in the thoracic. On each side may be seen the double openings which transmit the two roots of the corresponding spinal nerve, the dura mater being continued in the form of tubular prolongations on them as they pass through the intervertebral foramina. These prolongations are short in the upper part of the vertebral column, but gradually become longer below, forming a number of tubes of fibrous membrane, which enclose the lower spinal nerves and are contained in the vertebral canal.|
|Structure.The spinal dura mater resembles in structure the meningeal or supporting layer of the cranial dura mater, consisting of white fibrous and elastic tissue arranged in bands or lamellæ which, for the most part, are parallel with one another and have a longitudinal arrangement. Its internal surface is smooth and covered by a layer of mesothelium. It is sparingly supplied with bloodvessels, and a few nerves have been traced into it.|
|The ArachnoidThe arachnoid is a delicate membrane enveloping the brain and medulla spinalis and lying between the pia mater internally and the dura mater externally; it is separated from the pia mater by the subarachnoid cavity, which is filled with cerebrospinal fluid.|
|The Cranial Part (arachnoidea encephali) of the arachnoid invests the brain loosely, and does not dip into the sulci between the gyri, nor into the fissures, with the exception of the longitudinal. On the upper surface of the brain the arachnoid is thin and transparent; at the base it is thicker, and slightly opaque toward the central part, where it extends across between the two temporal lobes in front of the pons, so as to leave a considerable interval between it and the brain.|
|The Spinal Part (arachnoidea spinalis) of the arachnoid is a thin, delicate, tubular membrane loosely investing the medulla spinalis. Above, it is continuous with the cranial arachnoid; below, it widens out and invests the cauda equina and the nerves proceeding from it. It is separated from the dura mater by the subdural space, but here and there this space is traversed by isolated connective-tissue trabeculæ, which are most numerous on the posterior surface of the medulla spinalis.|
|The arachnoid surrounds the cranial and spinal nerves, and encloses them in loose sheaths as far as their points of exit from the skull and vertebral canal.|
|Structure.The arachnoid consists of bundles of white fibrous and elastic tissue intimately blended together. Its outer surface is covered with a layer of low cuboidal mesothelium. The inner surface and the trabeculæ are likewise covered by a somewhat low type of cuboidal mesothelium which in places are flattened to a pavement type. Vessels of considerable size, but few in number, and, according to Bochdalek, a rich plexus of nerves derived from the motor root of the trigeminal, the facial, and the accessory nerves, are found in the arachnoid.|
|The Subarachnoid Cavity (cavum subarachnoideale; subarachnoid space) is the interval between the arachnoid and pia mater. It is occupied by a spongy tissue consisting of trabeculæ of delicate connective tissue, and intercommunicating channels in which the subarachnoid fluid is contained. This cavity is small on the surface of the hemispheres of the brain; on the summit of each gyrus the pia mater and the arachnoid are in close contact; but in the sulci between the gyri, triangular spaces are left, in which the subarachnoid trabecular tissue is found, for the pia mater dips into the sulci, whereas the arachnoid bridges across them from gyrus to gyrus. At certain parts of the base of the brain, the arachnoid is separated from the pia mater by wide intervals, which communicate freely with each other and are named subarachnoid cisternæ; in these the subarachnoid tissue is less abundant.|
|Subarachnoid Cisternæ (cisternæ subarachnoidales) (Fig. 768).The cisterna cerebellomedullaris (cisterna magna) is triangular on sagittal section, and results from the arachnoid bridging over the interval between the medulla oblongata and the under surfaces of the hemispheres of the cerebellum; it is continuous with the subarachnoid cavity of the medulla spinalis at the level of the foramen magnum. The cisterna pontis is a considerable space on the ventral aspect of the pons. It contains the basilar artery, and is continuous behind with the subarachnoid cavity of the medulla spinalis, and with the cisterna cerebellomedullaris; and in front of the pons with the cisterna interpeduncularis. The cisterna interpeduncularis (cisterna basalis) is a wide cavity where the arachnoid extends across between the two temporal lobes. It encloses the cerebral peduncles and the structures contained in the interpeduncular fossa, and contains the arterial circle of Willis. In front, the cisterna interpeduncularis extends forward across the optic chiasma, forming the cisterna chiasmatis, and on to the upper surface of the corpus callosum, for the arachnoid stretches across from one cerebral hemisphere to the other immediately beneath the free border of the falx cerebri, and thus leaves a space in which the anterior cerebral arteries are contained. The cisterna fossæ cerebri lateralis is formed in front of either temporal lobe by the arachnoid bridging across the lateral fissure. This cavity contains the middle cerebral artery. The cisterna venæ magnæ cerebri occupies the interval between the splenium of the corpus callosum and the superior surface of the cerebellum; it extends between the layers of the tela chorioidea of the third ventricle and contains the great cerebral vein.|
|The subarachnoid cavity communicates with the general ventricular cavity of the brain by three openings; one, the foramen of Majendie, is in the middle line at the inferior part of the roof of the fourth ventricle; the other two are at the extremities of the lateral recesses of that ventricle, behind the upper roots of the glossopharyngeal nerves and are known as the foramina of Luschka. It is still somewhat uncertain whether these foramina are actual openings or merely modified areas of the inferior velum which permit the passage of the cerebrospinal fluid from the ventricle into the subarachnoid spaces as through a permeable membrane.|
|The spinal part of the subarachnoid cavity is a very wide interval, and is the largest at the lower part of the vertebral canal, where the arachnoid encloses the nerves which form the cauda equina. Above, it is continuous with the cranial subarachnoid cavity; below, it ends at the level of the lower border of the second sacral vertebra. It is partially divided by a longitudinal septum, the subarachnoid septum, which connects the arachnoid with the pia mater opposite the posterior median sulcus of the medulla spinalis, and forms a partition, incomplete and cribriform above, but more perfect in the thoracic region. The spinal subarachnoid cavity is further subdivided by the ligamentum denticulatum, which will be described with the pia mater.|
|The cerebrospinal fluid is a clear limpid fluid, having a saltish taste, and a slightly alkaline reaction. According to Lassaigne, it consists of 98.5 parts of water, the remaining 1.5 per cent. being solid matters, animal and saline. It varies in quantity, being most abundant in old persons, and is quickly secreted.|
|The Arachnoid Villi (granulationes arachnoideales; glandulæ Pacchioni; Pacchionian bodies) (Fig. 769) are small, fleshy-looking elevations, usually collected into clusters of variable size, which are present upon the outer surface of the dura mater, in the vicinity of the superior sagittal sinus, and in some other situations. Upon laying open the sagittal sinus and the venous lacunæ on either side of it villi will be found protruding into its interior. They are not seen in infancy, and very rarely until the third year. They are usually found after the seventh year; and from this period they increase in number and size as age advances. They are not glandular in structure, but are enlarged normal villi of the arachnoid. As they grow they push the thinned dura mater before them, and cause absorption of the bone from pressure, and so produce the pits or depressions on the inner wall of the calvarium.|
|Structure.An arachnoidal villus represents an invasion of the dura by the arachnoid membrane, the latter penetrates the dura in such a manner that the arachnoid mesothelial cells come to lie directly beneath the vascular endothelium of the great dural sinuses. It consists of the following parts: (1) In the interior is a core of subarachnoid tissue, continuous with the meshwork of the general subarachnoid tissue through a narrow pedicle, by which the villus is attached to the arachnoid. (2) Around this tissue is a layer of arachnoid membrane, limiting and enclosing the subarachnoid tissue. (3) Outside this is the thinned wall of the lacuna, which is separated from the arachnoid by a potential space which corresponds to and is continuous with the subdural cavity. (4) And finally, if the villus projects into the sagittal sinus, it will be covered by the greatly thinned wall of the sinus which may consist merely of endothelium. It will be seen, therefore, that fluid injected into the subarachnoid cavity will find its way into these villi, and it has been found experimentally that it passes from the villi into the venous sinuses into which they project.|
|The Pia MaterThe pia mater is a vascular membrane, consisting of a minute plexus of bloodvessels, held together by an extremely fine areolar tissue and covered by a reflexion of the mesothelial cells from the arachnoid trabeculæ. It is an incomplete membrane, absent probably at the foramen of Majendie and the two foramina of Luschka and perforated in a peculiar manner by all the bloodvessels as they enter or leave the nervous system. In the perivascular spaces, the pia apparently enters as a mesothelial lining of the outer surface of the space; a variable distance from the exterior these cells become unrecognizable and are apparently lacking, replaced by neuroglia elements. The inner walls of these perivascular spaces seem likewise covered for a certain distance by the mesothelial cells, reflected with the vessels from the arachnoid covering of these vascular channels as they traverse the subarachnoid spaces.|
|The Cranial Pia Mater (pia mater encephali; pia of the brain) invests the entire surface of the brain, dips between the cerebral gyri and cerebellar laminæ, and is invaginated to form the tela chorioidea of the third ventricle, and the choroid plexuses of the lateral and third ventricles (pages 840 and 841); as it passes over the roof of the fourth ventricle, it forms the tela chorioidea and the choroid plexuses of this ventricle. On the cerebellum the membrane is more delicate; the vessels from its deep surface are shorter, and its relations to the cortex are not so intimate.|
|The Spinal Pia Mater (pia mater spinalis; pia of the cord) (Figs. 767,770) is thicker, firmer, and less vascular than the cranial pia mater: this is due to the fact that it consists of two layers, the outer or additional one being composed of bundles of connective-tissue fibers, arranged for the most part longitudinally. Between the layers are cleft-like spaces which communicate with the subarachnoid cavity, and a number of bloodvessels which are enclosed in perivascular lymphatic sheaths. The spinal pia mater covers the entire surface of the medulla spinalis, and is very intimately adherent to it; in front it sends a process backward into the anterior fissure. A longitudinal fibrous band, called the linea splendens, extends along the middle line of the anterior surface; and a somewhat similar band, the ligamentum denticulatum, is situated on either side. Below the conus medullaris, the pia mater is continued as a long, slender filament (filum terminale), which descends through the center of the mass of nerves forming the cauda equina. It blends with the dura mater at the level of the lower border of the second sacral vertebra, and extends downward as far as the base of the coccyx, where it fuses with the periosteum. It assists in maintaining the medulla spinalis in its position during the movements of the trunk, and is, from this circumstance, called the central ligament of the medulla spinalis.|
|The pia mater forms sheaths for the cranial and spinal nerves; these sheaths are closely connected with the nerves, and blend with their common membranous investments.|
|The ligamentum denticulatum (dentate ligament) (Fig. 767) is a narrow fibrous band situated on either side of the medulla spinalis throughout its entire length, and separating the anterior from the posterior nerve roots. Its medial border is continuous with the pia mater at the side of the medulla spinalis. Its lateral border presents a series of triangular tooth-like processes, the points of which are fixed at intervals to the dura mater. These processes are twenty-one in number, on either side, the first being attached to the dura mater, opposite the margin of the foramen magnum, between the vertebral artery and the hypoglossal nerve; and the last near the lower end of the medulla spinalis.|