Meningiomas

The most common extra-axial brain tumours are meningiomas, although haemangiopericytomas, sarcomas, lymphomas and metastasis are also frequent. They account for 20 - 25 % of all intracranial tumours and are found approximately twice as often in women as in men [41]. Meningiomas are classified as WHO grade I, grade II or atypical meningiomas, and grade III or anaplastic meningiomas. Atypical variant has increased mitotic activity, high cellularity and foci of necrosis. The distinction between typical and atypical variant is clinically relevant, because benign meningiomas recur in about 7-20 % of cases, whereas atypical variants recur in 29-41% of cases [42, 43]. There are characteristic MRI features that distinguish meningiomas from intra-axial neoplasms, such as buckling of adjacent cortex, widening of cerebrospinal fluid spaces, and displacement of subarachnoid veins [41-43]. Although meningiomas are extra-axial and usually benign, they are often accompanied by brain oedema that causes clinical symptoms and is one of the most serious complications in the management of these tumours.

The pathogenetic mechanism of oedema is not clear. However, oedema is correlated with large tumour size, disappearance of peritumoral rim, irregular tumour margins, and hyperintensity on T2 images. The disappearance of peritumoral rim and the irregularity of tumour margins indicate cortical penetration of the tumour, which can favour the extent of oedema into white matter [44]. 'H-MRSI, DWI and PWI represent useful tools in the distinction of typical from atypical variants [43] and in the differentiation of meningiomas from other tumoral lesions [18, 45-47]. *H-MRSI generally shows marked reduction or absence of NAA and Cr and a variable amount of Cho (Fig. 18.7). The multiplet signal from glutamate and glutamine (Glx) is considered a prominent feature of meningiomas, as well as the signal from glutathione (GSH). Cho and LL levels relate directly to the malignancy of meningiomas [3, 46]. ADC values in meningioma are similar to or slightly higher than those of normal white matter, while in peritumoral hyperintense regions, generally consisting of vasogenic oedema, they are significantly higher [47]. rCBV may be grossly estimated due to the complete lack of blood-brain barrier in tumour capillaries. Meningio-

Fig. 18.6. Contrast-enhanced T1-weighted (a), T2-weighted (b) and FLAIR (e) images, ADC (c), rCBV (d), Cho (f ),NAA (g), Cr (h) and LL (i) maps, and proton MR spectra (1-9) from selected ROIs in the same patient as Fig. 18.5, after 3 months. Note that in the right occipital lobe the lesion has acquired the features of malignant glioma, with diffuse contrast-enhancement and evidence of necrotic core. ROIs are ROI with necrotic aspect (1);perienhancing ROIs with „tumour" (2-4) and „oedema" (5,6) pattern; ROIs in the remaining lesion (8, 7) without relevant modification compared to previous examination (Fig. 18.5); and contralateral (8, 9) normal ROIs. Note: the low level of Cho and the high LL peak in the necrotic core; the abnormal Cho/NAA ratio in tumoral ROIs; the normal Cho/NAA ratio and the lower metabolite levels in the „oedema" ROI, as compared to the contralateral normal ROI; and the similarity of spectra in ROIs 8 and 7, as compared to ROIs 6 and 7 in Fig. 18.5

Fig. 18.6. Contrast-enhanced T1-weighted (a), T2-weighted (b) and FLAIR (e) images, ADC (c), rCBV (d), Cho (f ),NAA (g), Cr (h) and LL (i) maps, and proton MR spectra (1-9) from selected ROIs in the same patient as Fig. 18.5, after 3 months. Note that in the right occipital lobe the lesion has acquired the features of malignant glioma, with diffuse contrast-enhancement and evidence of necrotic core. ROIs are ROI with necrotic aspect (1);perienhancing ROIs with „tumour" (2-4) and „oedema" (5,6) pattern; ROIs in the remaining lesion (8, 7) without relevant modification compared to previous examination (Fig. 18.5); and contralateral (8, 9) normal ROIs. Note: the low level of Cho and the high LL peak in the necrotic core; the abnormal Cho/NAA ratio in tumoral ROIs; the normal Cho/NAA ratio and the lower metabolite levels in the „oedema" ROI, as compared to the contralateral normal ROI; and the similarity of spectra in ROIs 8 and 7, as compared to ROIs 6 and 7 in Fig. 18.5

mas are highly vascular and their capillaries are highly leaky and permeable. The latter produces the immediate contrast agent leakage, during the first-pass contrast agent bolus, without any substantial recovery of

T2* signal loss back to the baseline, and renders the in-travascular compartmentalization of contrast agent impossible [48].

Fig. 18.7. Contrast-enhanced T1-weighted (a), FLAIR (b) and T2-weighted (e) images, ADC (c) and rCBV (d) maps, and proton MR spectra (1 -9) from selected ROIs in a 54-year-old man with a grade II frontoparietal meningioma. ROIs are tumour mass (1,2) andmargin (3), vasogenic oedema (4), homolateral (5) andcontralateral (6-9) normal ROIs. Note that the vasogenic oedema ROI presents a normal Cho/NAA ratio, metabolite peaks lower than mirrored normal ROIs (7,8), and an ADC higher and an rCBV lower than contralateral normal white matter; rCBV in meningioma mass is overestimated due to the leakage phenomenon during the first pass of contrast agent bolus

Fig. 18.7. Contrast-enhanced T1-weighted (a), FLAIR (b) and T2-weighted (e) images, ADC (c) and rCBV (d) maps, and proton MR spectra (1 -9) from selected ROIs in a 54-year-old man with a grade II frontoparietal meningioma. ROIs are tumour mass (1,2) andmargin (3), vasogenic oedema (4), homolateral (5) andcontralateral (6-9) normal ROIs. Note that the vasogenic oedema ROI presents a normal Cho/NAA ratio, metabolite peaks lower than mirrored normal ROIs (7,8), and an ADC higher and an rCBV lower than contralateral normal white matter; rCBV in meningioma mass is overestimated due to the leakage phenomenon during the first pass of contrast agent bolus

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