中華放射醫誌 Chin J Radiol 2001; 26: 51-60 51

Intracranial Meningeal Carcinomatosis andNon-neoplastic Meningeal Diseases:Evaluation with Contrast-Enhanced MRImagingCHEN-PIN CHOU

1 PING-HONG LAI1,2 WEI-LIANG CHEN

1 HUAY-BEN PAN1,2 CLEMENT CHEN

1,2

CHIEN-FANG YANG1,2

Department of Radiology, Veterans General Hospital-Kaohsiung1, andNational Yang-Ming University2, Taipei, Taiwan, ROC

This study was performed to correlatemeningeal enhancement patterns withintracranial meningeal carcinomatosis and non-neoplastic meningeal diseases.

From 1993 to 1998, 48 patients with a clinicaldiagnosis of meningeal carcinomatosis and non-neoplastic meningeal diseases with abnormalmeningeal enhancement on MR imaging werereviewed. Two enhancement patterns of themeninges were characterized: pachymeningealand leptomeningeal. The distribution and shapeof the enhancement were also inspected. Themeningeal enhancement was classified into sixetiologic subgroups: carcinomatosis, infection,inflammation, cerebrovascular disease, reactivemeningitis, and chemical meningitis. Nineteenof the 48 patients with enhanced meninges hadcarcinomatosis of the meninges. The other 29patients without neoplasms included 10 withinfectious meningitis, 5 with inflammatorydisease, 8 with cerebrovascular disease (7 withearly brain infarction and 1 with Sturge-Weberdisease), 5 with reactive changes and 1 with

chemical meningitis. Pachymeningeal enhancement occurred in 11

patients with meningeal metastasis, 1 withamebic meningitis, 4 with inflammatorymeningeal disease, 7 with early infarction, 5with reactive meningeal disease, and 1 withchemical meningitis while leptomeningealenhancement was shown in 8 meningealmetastases, 9 with infectious meningitis, 2 withinflammatory changes and 2 with vasculardisease (1 with early brain infarction and 1with Sturge-Weber disease). Both enhancementpatterns were noted in 1 with inflammatorychanges (Wegener granulomatosis) and 1 withearly brain infarction.

Diffuse linear leptomeningeal enhancementfavored non-neoplastic etiologies whileenhanced leptomeningeal nodules indicatedmeningeal metastasis and some non-neoplasticdisease such as tuberculosis and neuro-sarcoidosis. Focal nodular pachymeningealenhancement presented mostly due tomeningeal carcinomatosis. Diffuse linearpachymeningeal enhancement could bemeningeal carcinomatosis or reactive meningealchange.

Key words: Meninges, Magnetic resonanceimaging, Meningitis, Meningeal metastasis.

Clinical evaluation of meningeal disorders haslimitations in nonspecific clinical presentationsand confusing cerebrospinal fluid (CSF) analysis.

ORIGINAL ARTICLE

Reprint requests to: Ping-Hong LaiDepartment of Radiology, Veterans General Hospital-Kaohsiung, 386 Ta-Chung first Rd. Kaohsiung 813,Taiwan, ROC.

Meningeal enhancement on MR imaging52

However, advances in magnetic resonance (MR)imaging have had great impact on the evaluationof the meninges [1]. Cranial meninges may beinvolved by varied pathological process leadingto carcinomatosis, infection, inflammation,vascular disease, reactive meningitis andchemical meningitis [2]. Anatomically, the cranialmeninges is composed of the dura, arachnoid andpia layers. Postcontrast images can visualize twodistinguishing enhancement patterns,leptomeningeal (pia-subarachnoid) andpachymeningeal (dura-arachnoid) [1]. Meningealenhancement shown by MR scanner is considereda sensitive aid for diagnosing meningeal diseases,selecting proper modalities for disease follow-upand providing high successful surgical biopsyrates [3]. The purpose of this study was toinvestigate the relationship between meningealenhancement patterns on MR imaging and variousmeningeal abnormalities.

MATERIALS AND METHODS

In this retrospective study, we reviewed theimaging studies of 48 cases with evidence ofabnormal meningeal enhancement on MR imagingwho were treated between 1993 and 1998. Therewere 18 women and 30 men with the ages rangingfrom six months to 74 years. The etiologies ofabnormal meningeal enhancement were classifiedinto six subgroups (Table 1): carcinomatosis,infection, inflammation, vascular disease,reactive meningitis and chemical meningitis.Three meningeal metastasis patients had positivemalignant cytology in the CSF. Another 16patients had a clinical diagnosis of meningealmetastasis by history of primary cancer. Sevenbrain infarction cases were diagnosed of patients’symptoms and correlated imaging findings. Teninfectious meningitis patients had CSF analysisfor diagnosis. Three patients had pathologicalevidence including neuro-sarcoidosis,hypertrophic cranial pachymeningitis, anddermoid cyst rupture. Post-neurologic surgery,subarachnoid hemorrhage or CSF pressurechanges (iatrogenic shunting or CSF leakage)were considered to be reactive changes in themeninges. The consequences of rupture ofintracranial dermoid or epidermoid cysts wereclassified as a chemical reaction. Meningealinvolvement due to collagen-vascular disease orneuro-sarcoidosis was considered inflammatory.Final diagnoses were based on medical histories,

surgical findings, pathology reports or CSFanalyses.

MR images were obtained with a 1.5 Teslasuperconductive magnet. T1-weighted spin echo(TR/TE 500-800/15-25), T2-weighted spin echo(TR/TE 2200-3000/80-120) and proton density(TR/TE 2200-3000/30-40) were routinelyobtained in the axial and coronal planes(parameters included: matrix size, 256X192;section thickness, 5mm; intersection gap, 2.5 mm;and field of view, 24 cm). After precontrastimages were obtained, gadopentetatedimeglumine (Magnevist) was administrated byintravenous injection at a dose of 0.1 mmol/kg.Multiplanar post contrast T1-weighted imagingwas obtained in the axial and coronal planes.Meningeal enhancement patterns weresubsequently divided into two categories: 1.leptomeningeal (pia-arachnoid ) enhancement,and 2. pachymeningeal (dura-arachnoid )enhancement. The enhancement area (focal ordiffuse) and shape (linear or nodular) were alsoinspected and distinguished by two radiologistsunaware of the final diagnoses.

RESULTS

Pachymeningeal enhancement was seen in 11patients with meningeal metastasis, 1 with amebicmeningitis, 1 with hypertrophic cranialpachymeningitis, 1 with Wegener granulomatosis,2 with Tolosa-Hunt syndrome, 7 with earlyinfarction, 4 who were postoperative change, 1with intracranial hypotension and 1 with chemicalmeningitis while leptomeningeal enhancementwas found in 8 with meningeal metastasis, 9 withinfectious meningitis, 1 with neuro-sarcoidosis, 1with Sturge-Weber syndrome and 2 with vasculardisease (1 with early brain infarction and 1 with

Table 1. Different etiologies and enhancement of meningealdiseases on MR imaging in 48 patients

Type Total Pachymeningeal LeptomeningealCarcinomatosis 19 11 8Non-neoplastic 29

Infectious 10 1 9Inflammatory 5* 4 2

Vascular 8# 7 2Reactive 5 5 0Chemical 1 1 0

*One Wegener granulomatosis showed both enhancementpatterns.

# One brain infarction showed both enhancementpatterns.

Meningeal enhancement on MR imaging 53

Sturge-Weber disease). Both enhancementpatterns were identified in 1 patient with Wegenergranulomatosis and 1 with early brain infarction.MR imaging findings of the six etiologic groupsare described below.

Meningeal Carcinomatosis

Nineteen patients with primary malignancywere subsequently considered to have meningealtumor involvement. Lung carcinoma, breastcarcinoma and melanoma were the commonprimary malignancies. Of eleven patients withpachymeningeal carcinomatosis, eight had focalnodular pachymeningeal enhancement and theother three patients presented diffuse linearpachymeningeal patterns (Fig. 1). All eightleptomeningeal carcinomatosis patients hadnodular leptomeningeal enhancement (Fig. 2).

Infection

Nine of the ten infectious meningitis casesshowed leptomeningeal enhancement, including 3with bacterial, 3 with tuberculosis (TB), 2 withcryptococcus and 1 with Angiostrongylusmeningitis. Two cases of TB meningitis (Fig. 3)and one case of cryptococcus meningitis showedbasal cistern leptomeningeal nodularenhancement. One case of bacterial meningitiswas complicated with empyema and the MRimages showed linear leptomeningealenhancement with subdural fluid collection.

One case of amebic (Acanthamoeba) meningitishad focal pachymeningeal nodular enhancement(Fig. 4).

Inflammatory Meningeal Disease

Inflammatory meningitis was seen in 2 patientswith Tolosa-Hunt syndrome, 1 with neuro-sarcoidosis, 1 with hypertrophic cranialpachymeningitis and 1 with Wegenergranulomatosis. Two Tolosa-Hunt syndrome caseshad temporal base focal nodular pachymeningealenhancement adjacent to the cavernous sinus (Fig.5). One neuro-sarcoidosis case showed diffusenodular leptomeningeal enhancement. OneWegner granulomatosis case displayed bothenhancement pattens (Fig. 6). One Sjogrensyndrome revealed diffuse linear pachymeningealthickening with strong enhancement andhypertrophic cranial pachymeningitis wasdiagnosed on biopsy.

Figure 2. Postcontrast coronal T1WI in a breastcarcinoma patient with intracranial metastasis showsmultiple nodular leptomeningeal enhancement (arrows).

Figure 1. Prostate carcinoma with pachymeningealmetastasis. Postcontrast coronal T1WI shows diffuselinear pachymeningeal enhancement (arrows).

Figure 3. Postcontrast T1WI of TB meningitis showsnodular leptomeningeal enhancement around basalcisterns (arrows) and mild ventricular dilatation.

Meningeal enhancement on MR imaging54

Cerebrovascular Disease

Most cerebrovascular diseases with abnormalmeningeal enhancement in our study were earlyinfarction (within one week after clinical ictus).All abnormal meningeal enhancements wereassociated with cerebral or cerebellar large-territory infarction. The seven cases of earlyinfarction showed focal pachymeningealenhancement and four cases showed variousdegrees of parenchyma enhancement at theinvolved area. In one case, leptomeninges wasalso involved (Fig.7a and b). One Sturge-Webersyndrome case displayed linear leptomeningealenhancement (Fig. 8).

Reactive Meningitis

All of the reactive meningitis in our study hadthe either focal or diffuse linear pachymeningealenhancement pattern. Three post-craniotomycases showed focal pachymeningeal enhancementadjacent to the previous surgery regions (Fig. 9).One case of post ventricle-peritoneum (V-P)shunting disclosed diffuse linear pachymeningealenhancement (Fig.10). One case of intracranialhypotension showed diffuse linearpachymeningeal enhancement (Fig. 11).

Chemical Meningitis

One case of dermoid cyst rupture into ventricleand subarachnoid space showed focal linearpachymeningeal enhancement.

DISCUSSION

The meninges consists of the dura, arachnoidand pia matter. The dura matter is the outermostlayer of the meninges. The outer layer of the durais a fibrous layer of skull bone and the inner layerof dura is the meninges layer [1]. The falx cerebriis composed of the double layers of inner durabetween the cerebral hemispheres at the midline.The tentorium cerebelli is a doubled durapartition located within the transverse fissureseparating the occipital lobe and cerebellarhemispheres.

The leptomeninges is composed of arachnoid

Figure 5. Tolosa-Hunt syndrome. A 53-year-old patientpresented with symptoms of painful right-sidedophthalmoplegia. Postcontrast coronal T1WI revealsabnormal tissue enhancement around the right cavernoussinus and adjacent pachymeninges (arrows). The soft-tissue lesions resolved after treatment with steroids.

Figure 6. Wegener granulomatosis. Postcontrast coronalT1-weighted MR imaging (T1WI) shows leptomeningealenhancement (arrows) and pachymeningeal enhancementwith diffuse dura thickening (arrowheads).

Figure 4. Postcontrast axial T1WI in a case of amebic(Acanthamoeba) meningitis shows focal nodularpachymeningeal enhancement (arrows).

Meningeal enhancement on MR imaging 55

and pia matter. The subarachnoid space is thetrabecular space between the arachnoid and piamatter and contains CSF. Short-segment convexlymeningeal enhancement is commonly seen andmost likely represents intravascular contrastmaterial in normal meningeal vessels. Long-segment (> 3 cm), diffusely convexly or acontinuous meningeal enhancement patternusually suggests meningeal abnormality and iscorrelated with clinical illness [4]. Two distinctpatterns of meningeal enhancement may beobserved in postcontrast MR imaging.Leptomeningeal enhancement extends into thedepths of the sulci while pachymeningeal

enhancement follows the inner surface of theskull. Meningeal enhancement surrounding thebrain stem always indicates the leptomeningealtype because of the corresponding location ofbasal cistern pia-arachnoid space [1].

Different etiologies of meningeal enhancementare discussed below:

Meningeal Carcinomatosis

Dural metastasis may be caused by invasiondirectly from bone metastasis or hematogenousspreading to the dura [5]. Subarachnoid tumordeposits are due to hematogenous dissemination,

Figure 7. Early braininfarction. A 60-year-oldman with sudden onsetof consciousnessdisturbance. (a) T2WIcoronal views 3 daysafter onset show highsignal intensity in theright temporal-parietalregion. (b) Postcontrastcoronal T1WI showspachymeningeal,leptomeningeal andparenchymalenhancement in the righttemporal-parietal region.

7a 7b

Figure 8. Sturge-Weber syndrome. Postcontrast T1WIshows atrophy of the right hemisphere. Theleptomeningeal angiomatosis is strongly enhanced(arrows). An enlarged ipsilateral choroid plexus(arrowhead) is also noted.

Figure 9. A 57- year-old patient with a history ofintracranial hemorrhage post surgery. Follow-uppostcontrast axial T1WI shows right frontal lobeencephalomalacia, diffuse linear pachymeningealenhancement (arrows), and a craniotomy in the rightparietal region (arrowheads).

Meningeal enhancement on MR imaging56

perineural spread and seeding of CSF fromcerebral and ependymal metastasis [6]. Szedescribed normal Gd-MR images being normal innearly one-third of the cases clinically diagnosedas meningeal carcinomatosis [7]. They suggestedthese may be in the early stage of leptomeningealcarcinomatosis [7].

In our study, pachymeningeal metastasis werecommonly presented as solitary or multiple duralmasses at the cerebral convexity adjacent to theskull or diffuse linear dural thickening. Inpatients with dura metastasis withoutleptomeninges invasion or negative CSF findings,image diagnosis can help in early diagnosis andtreatment. MR allows us to assess the outcomebecause diffuse leptomeningeal orpachymeningeal involvement confers a poorprognosis.

Infectious Meningitis

Infectious meningitis can be direct extensionfrom a contiguous extracerebral infection (otitismedia or sinusitis) or hematogenous infectionfrom the bloodstream [8]. In our study, the mostcommon imaging finding of bacterial meningitiswas leptomeningeal enhancement. Farhad et al.found all of their infectious meningitis cases(including bacteroids, virus and fungus) showedleptomeningeal enhancement only [2]. Howeverthere was some limitation in separatingleptomeningeal and pachymeningeal enhancementwhen the infectious process progressed andinvolved all three layers of the meninges.

Tuberculosis meningitis was found in elderly

patients in our study series. Tuberculousmeningitis was characterized of the presence ofinflammatory meningeal exudate involving thebasal cistern meningeal surfaces and CSF spaces[9]. Inflammatory meningeal exudate showedintense nodular leptomeningeal contrastenhancement (Fig. 3). The exudate revealed amicroscopic hypervascular nature ofinflammatory neovessel leakage. Communicatinghydrocephalus is the most common complicationof cranial TB meningitis secondary to obstructionof CSF flow by meningeal exudates in the basalcistern [9,10].

Central nervous system (CNS) cryptococcususually occurs in aged or immunocompetentpatients. Meningitis is the most common findingof CNS cryptococcosis in AIDS patients [11].Basal cistern leptomeningeal enhancement incryptococcus meningitis was less common thanTB meningitis in our study. Meningealenhancement was less common compared to othermeningitis, probably due to a lack of hostreaction and immunosuppressive effect of theorganism capsule [1,12,13].

Bacterial meningitis with subdural empyema isa neurosurgical emergency. Gadolinium-enhancedMR imaging has proven to be more sensitive thanCT for detection of meningeal enhancement,parenchymal change and subdural fluid collection[1,14,15].

The leptomeningeal enhancement pattern is themost common feature of infectious meningitiswhile pachymeningeal enhancement is rare.

Figure 10. Post V-P shunting surgery shows diffusepachymeningeal enhancement on postcontrast coronalT1WI (arrows).

Figure 11. Intracranial hypotension. Postcontrast axialT1WI reveals diffuse linear pachymeningealenhancement.

Meningeal enhancement on MR imaging 57

Although the CSF analysis is the gold standardfor meningitis, MR images can offer moreinformation about other intracranial abnormalitiesor contraindications for lumbar puncture. Weknow normal imaging cannot exclude meningitis,but it can help with patient management whenmeningitis is clinically suspected in patients withleptomeningeal enhancement.

Inflammatory meningeal disease

Inflammatory pachymeningitis is a raredisorder, with neuro-sarcoidosis, Wegenergranulomatosis and syphilis being the mostcommonly considered etiologies.

Sarcoidosis involves the CNS in about 5% ofthe patients. In neurosarcoidosis, the pia isinvolved more frequently than the dura [1]. Whensarcoidosis involves the CNS, multiple smallnodular granulomas usually infiltrate theleptomeninges and the underlying brainparenchyma [16]. One patient showed diffusenodular leptomeningeal enhancement.

Hypertrophic cranial pachymeningitis (HCP)was found in one patient with Sjogren syndrome.HCP is granulomatous thickening of thepachymeninges and has a wide range ofetiologies. There is uniformly, dense and linearcontrast enhancement of the thicken duralmembrane [17].

Wegener granulomatosis is a multisystemdisorder characterized by necrotizing granulomasand systemic vasculitis. Cerebral and meningealinvolvement were uncommon [18,19]. Bothdiffuse pachymeningeal and leptomeningealenhancement were present in our patient ofWegener granulomatosis, consisting with diffuseinvolvement of the whole layer meninges (Fig.6).

Tolosa-Hunt syndrome is characterized bypainful ophthalmoplegia caused by cavernoussinus inflammation which is responsive to steroidtherapy [20]. MRI revealed a convex enlargementof the symptomatic cavernous sinus by abnormaltissue which was isointense with gray matter onT1 weighted images and isohypointense on T2weighted images. This abnormal tissue showedmarkedly increased signal intensity after contrastinjection (Fig. 5) [21].

Cerebrovascular Disease

The two earliest signs of acute infarction areintravascular and meningeal enhancement, whichtend to occur during the first week after stroke[22]. Abnormal enhancement of the meninges

adjacent to the infarction area occurs due tocollateral vascular enlargement, sluggish flow,and early breakdown resulting from underlyinginfarction. Enhancement is not seen in thebrainstem or in deep cerebral (basalganglia/internal capsule) infarctions [23].Enhancement is seen mostly with largeinfarctions [24]. In all of our cases, enhancementpresented as focal linear pachymeningeal patternadjacent to the cortical infarction region with avarious degree of early parenchymal enhancementor leptomeningeal enhancement (Fig.7).

Sturge-Weber syndrome is a neurocutaneoussyndrome characterized by facial andleptomeningeal angiomas. MR findings includepial angiomatosis, cerebral atrophy, decreased incortical veins, enlargement of deep veins,enlargement of the choroid plexus (Fig. 8), andparenchymal calcification [25]. On MR images,the most characteristic finding is diffuse linearleptomeningeal enhancement, believed torepresent leakage of contrast medium through theanomalous pial vessel due to Blood brain barrier(BBB) disruption or enhancement of a pialangioma [25,26].

Reactive Meningitis

Irritation caused by bleeding into thesubarachnoid space or physical disruption of theintegrity of the meninges may cause meningealenhancement after craniotomy. Elster studied 46postoperative patients and found that nearly everypostcraniostomy patient had nonneoplasticmeningeal enhancement on MR images [27].Enhancement of the brain or pia mater wasinconspicuous and normally lasted less than 1year while dural enhancement might persist forseveral years [27]. Postoperatively, the durausually shows focal linear enhancement near thecraniotomy site, but diffuse extensive durathickening could also be found. Nodularpachymeningeal enhancement or persistentleptomeningeal enhancement is suggestive ofrecurrence [27].

Spontaneous intracranial hypotension ischaracterized by posture headache responding toepidural blood patch. The diagnosis is made whenthe pressure CSF is less than 60 mm H2O [1]. MRimages reveal a bilateral subdural fluid collectionand extensive diffuse pachymeningealenhancement (Fig. 11) [1]. One patient in ourstudy presented with posture headache anddiffuse pachymeningeal enhancement on MR

Meningeal enhancement on MR imaging58

images. Low CSF pressure was measured andnuclear medicine study showed CSF leakage inthe thoracic spine region.

Post V-P shunting surgery can be thought of asthe same mechanism as decreased intracranialpressure or over-shunting. Diffuse linearpachymeningeal enhancement has also beenidentified.

A pachymeningeal enhancement pattern andpathogenesis similar to postcraniotomy occurs inpatients with subarachnoid hemorrhage (SAH) ofany cause (trauma or aneurysm rupture). Wefound the reactive meningeal change due tosurgery, shunting, intrathecal therapy, SAH orintracranial hypotension commonly presents thepachymeningeal rather than the leptomeningealpattern. The intact intracranial BBB withincreased granulation tissue and vascularity of thepachymeninges might explain the pachymeningealenhancement.

Chemical Meningitis

Chemical meningitis has been reported afterintrathecal injection of a variety of foreignsubstances or rupture of an infectious cyst [2].Rarely chemical meningitis may develop as aconsequence of rupture of an intracranial dermoidtumor, epidermoid tumor or craniopharyngiomas.The pattern is thought to be due to irritation bycholesterin crystals and keratin material. T1-weighted MR images can give the diagnosis byvisualization of tumor rupture and high signallipid material in the CSF [2].

CONCLUSION

The higher contrast provided by gadolinium-enhanced MR imaging, coupled with lack ofbeam-hardening artifact suggests that contrast-enhanced MRI is the most sensitive diagnosticimaging modality for meningeal diseases.Meningeal enhancement patterns are mostly non-specific findings and correlation with clinicalhistory is necessary. In this study, we founddiffuse linear leptomeningeal enhancementfavored non-neoplastic etiologies while enhancedleptomeningeal nodules suggested meningealmetastasis and some non-neoplastic diseases suchas tuberculosis and neuro-sarcoidosis. Focalnodular pachymeningeal enhancement representedmostly meningeal carcinomatosis. Diffuse linearpachymeningeal enhancement could be meningealcarcinomatosis or reactive meningeal change. ◆

REFERENCES

1. Meltzer CC, Fukui MB, Kanal E, et al. MR imaging ofthe meninges. Part I. Normal anatomic features andnonneoplastic disease. Radiology 1996; 201: 297-308

2. Kioumehr F, Dadsetan MR, Feldman N, et al.Postcontrast MRI of cranial meninges: leptomeningitisversus pachymeningitis. J Comput Assist Tomogr 1995;19: 713-720

3. Cheng TM, O'Neill BP, Scheithauer BW, et al. Chronicmeningitis: the role of meningeal or cortical biopsy.Neurosurgery 1994; 34: 590-595

4. Quint DJ, Eldevik OP, Cohen JK. Magnetic resonanceimaging of normal meningeal enhancement at 1.5 T.Acad Radiol 1996; 3: 463-468

5. Watanabe M, Tanaka R, Takeda N. Correlation of MRIand clinical features in meningeal carcinomatosis.Neuroradiology 1993; 35: 512-515

6. Kallmes DF, Gray L, Glass JP. High-dose gadolinium-enhanced MRI for diagnosis of meningeal metastases.Neuroradiology 1998; 40: 23-26

7. Sze G, Soletsky S, Bronen R, et al. MR imaging of thecranial meninges with emphasis on contrastenhancement and meningeal carcinomatosis. AJR 1989;153: 1039-1049

8. Tunkel AR, Wispelwey B, Scheld WM. Pathogenesisand pathophysiology of meningitis. Infect Dis ClinNorth Am 1990; 4: 555-581

9. Jinkins JR, Gupta R, Chang KH, et al. MR imaging ofcentral nervous system tuberculosis. Radiol Clin NorthAm 1995; 33: 771-786

10. Ozates M, Kemaloglu S, Gurkan F, et al. CT of thebrain in tuberculous meningitis. A review of 289patients. Acta Radiol 2000; 41: 13-17

11. Miszkiel KA, Hall-Craggs MA, Miller RF, et al. Thespectrum of MRI findings in CNS cryptococcosis inAIDS. Clin Radiol 1996; 51: 842-850

12. Tien RD, Chu PK, Hesselink JR, et al. Intracranialcryptococcosis in immunocompromised patients: CTand MR findings in 29 cases. AJNR 1991; 12: 283-289

13. Mathews VP, Alo PL, Glass JD, et al. AIDS-relatedCNS cryptococcosis: radiologic-pathologic correlation.AJNR 1992; 13:1477-1486

14. Nathoo N, Nadvi SS, van Dellen JR, et al. Intracranialsubdural empyemas in the era of computed tomography:a review of 699 cases. Neurosurgery 1999; 44: 529-535

15. Pruitt AA. Infections of the nervous system. NeurolClin 1998; 16: 419-447

16. Christoforidis GA, Spickler EM, Recio MV, et al. MRof CNS sarcoidosis: correlation of imaging features toclinical symptoms and response to treatment. AJNR1999; 20: 655-669

17. Goyal M, Malik A, Mishra NK, et al. Idiopathichypertrophic pachymeningitis: spectrum of the disease.Neuroradiology; 1997; 39: 619-623

18. Provenzale JM, Allen NB. Wegener granulomatosis: CTand MR findings. AJNR 1996; 17: 785-792

19. Murphy JM, Gomez-Anson B, Gillard JH, et al.Wegener granulomatosis: MR imaging findings in brainand meninges. Radiology 1999; 213: 794-799

20. Yousem DM, Atlas SW, Grossman RI, et al. MRimaging of Tolosa-Hunt syndrome. AJNR 1989; 10:1181-1184

21. Pascual J, Cerezal L, Canga A, et al. Tolosa-Hunt

Meningeal enhancement on MR imaging 59

syndrome: focus on MRI diagnosis. Cephalalgia 1999;19 Suppl 25: 36-38

22. Elster AD. Magnetic resonance contrast enhancement incerebral infarction. Neuroimaging Clin of North Am1994; 4: 89-100

23. Elster AD. MR contrast enhancement in brainstem anddeep cerebral infarction. AJNR 1991; 12: 1127-1132

24. Elster AD, Moody DM. Early cerebral infarction:gadopentetate dimeglumine enhancement. Radiology1990; 177: 627-632

25. Benedikt RA, Brown DC, Walker R, et al: Sturge-Weber

syndrome: cranial MR imaging with Gd-DTPA. AJNR1993; 14: 409-415

26. Vogl TJ, Stemmler J, Bergman C, et al. MR and MRangiography of Sturge-Weber syndrome. AJNR 1993;14: 417-425

27. Elster AD, DiPersio DA. Cranial postoperative site:assessment with contrast-enhanced MR imaging.Radiology 1990; 174: 93-99

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顱內腦膜腫瘤轉移與非腫瘤腦膜疾病：以注射顯影劑的磁振造影評估

周春平1 賴炳宏1,2 陳威良1 潘慧本1,2 陳坤煌1,2 楊建芳1,2

高雄榮民總醫院　放射線部1 國立陽明大學2

本文在討論腦膜腫瘤轉移與非腫瘤轉移腦膜疾病，在注射顯影劑後不正常磁振造影影像之分析。

從1993年至1998年間，共收集48例有臨床診斷且有不正常腦膜磁振造影影像的病人。注射顯影劑後區分為軟腦膜及硬腦膜增強並觀察增強之分佈及形狀。同時我們將病人疾病歸納為6項分類: 腫瘤轉移，感染，發炎性反應，腦血管疾病，反應性病變，化學性反應。

48位病人中，19例腦膜腫瘤轉移。其他29例非腫瘤疾病有10例腦膜感染，5例腦膜發炎性反應，8例腦血管疾病（7例早期腦梗塞，1例Sturge-Weber疾病），5例反應性腦膜病變，1例化學性腦膜炎。

結果顯示呈現硬腦膜增強的共有11例腦膜腫瘤轉移，1例阿米巴腦膜炎，4例腦膜發炎性反應，7例腦梗塞，5例反應性腦膜病變及1例化學性腦膜炎。而呈現軟腦膜增強的共有8例腦膜腫瘤轉移， 9 例腦膜感染， 2 例腦膜發炎性反應及 2 例腦血管疾病（1 例早期腦梗塞及 1 例Sturge-Weber 疾病）。同時出現兩種腦膜增強的有一例腦膜發炎性反應（Wegenergranulomatosis）及一例早期腦梗塞。

分析結果認為廣泛線型的軟腦膜增強較偏向非腫瘤腦膜疾病。結節狀軟腦膜造影增強可以是腫瘤的轉移或其他疾病，如結核腦膜炎，中樞系統的結節病。局部結節狀硬腦膜增強大部份為腫瘤轉移。廣泛線型的硬腦膜增強則要考慮腫瘤轉移或反應性腦膜病變。

關鍵詞：腦膜，磁振造影，腦膜炎，腦膜腫瘤轉移