Diffusionweighted imaging findings of intracranial tumors relationship between

Diffusion-weighted imaging findings of intracranial tumors relationship between T 2 and diffusibility Hiwatashi A, Moritani T University of Rochester, NY

Introduction Routine magnetic resonance (MR) imaging is sensitive method of detecting tumors of the brain. Diffusion-weighted imaging (DWI) can differentiate between tumor and infection (1 -51) and can help the characterization and grading of brain tumors. This exhibit demonstrates DWI characteristics of intracranial tumors.

Gliomas (Figs 1 -6) The signal intensity of gliomas on DWI is variable and depends mainly on their T 2 and apparent diffusion coefficient (ADC) values (1 -22). Thus, some gliomas are hyperintense on DWI with decreased ADC, which reflects reduced volume of extracellular space. Other gliomas have normal or increased ADC which causes T 2 shinethrough effect.

High Grade Tumors It has been reported that high-grade gliomas tends to show high signal on DWI with decreased ADC (3, 8 -10, 12, 13, 19). High tumor cellularity is probably the major cause (3, 8, 12, 18). There are still controversies regarding how well DWI can differentiate between high grade primary brain tumor and metastasis (6, 18, 46). In lymphoma, ADC have been reported to be lower than in high grade gliomas (16), but in the clinical situation there is often overlap between lymphoma and high-grade glioma.

Peritumoral infiltration The value of DW imaging for the delineation of peritumoral invasion in primary brain tumors is controversial (3, 4, 10 -12, 18, 19). The poor delineation is probably due to conjoined effects of T 2 and ADC. Diffusion tensor imaging may add more information about tumor infiltration.

Fig 1 A. GBM 69 -year-old female with left side weakness Postcontrast T 1 WI shows heterogeneous enhancement (arrow).

Fig 1 B. GBM 69 -year-old female with left side weakness DWI shows hyperintensity in enhancing (arrow) and hyperintensity in cystic/necrotic portions (arrowhead).

Fig 1 C. GBM 69 -year-old female with left side weakness ADC map shows heterogeneous hyperintensity (0. 74 -0. 85 x 10 -3 mm 2/s; arrow) in enhancing portion compared to surrounding vasogenic edema. Cystic/necrotic portion (arrowhead) is hyperintense. These findings may correspond to high cellularity of enhancing tumor and increased diffusibility of cystic/necrotic portion.

Fig 2 A. GBM 51 -year-old male with right side weakness T 2 WI shows hyperintense mass in left basal ganglia and thalamus (arrow).

Fig 2 B. GBM 51 -year-old male with right side weakness T 1 WI shows hyperintensity (arrow).

Fig 2 C. GBM 51 -year-old male with right side weakness Postcontrast T 1 WI shows heterogeneous enhancement posteriorly (arrow).

Fig 2 D. GBM 51 -year-old male with right side weakness DWI shows hyperintensities (arrows). Areas of marked hyperintensity on DWI does not show contrast enhancement in this patient.

Fig 2 E. GBM 51 -year-old male with right side weakness ADC map shows heterogeneous hyperintensity (0. 58 -0. 89 x 10 -3 mm 2/s; arrows).

Fig 3 A. GBM 80 -year-old female with personality change T 2 WI shows hyperintense mass which involves genu of corpus callosum (butterfly tumor).

Fig 3 B. GBM 80 -year-old female with personality change Postcontrast T 1 WI shows irregular ring-like enhancement.

Fig 3 C. GBM 80 -year-old female with personality change DWI shows hyperintensity (arrow).

Fig 3 D. GBM 80 -year-old female with personality change ADC map shows heterogeneous intensity. Note hyperintensity in center of lesion (arrow). These findings may correspond to the cellularity.

Fig 4 A. JPA 14 -year-old male with headache T 2 WI shows hyperintense mass in cerebellum (arrow). Mural nodule is seen (arrowhead).

Fig 4 B. JPA 14 -year-old male with headache Postcontrast T 1 WI shows enhancement in nodule (arrowhead).

Fig 4 C. JPA 14 -year-old male with headache DWI shows hyperintensity in cystic component (arrow) and mild hyperintensity in nodule (arrowhead).

Fig 4 D. JPA 14 -year-old male with headache ADC map shows hyperintensity in cyst (arrow) and mild hyperintensity in nodule (1. 18 x 10 -3 mm 2/s; arrowhead).

Fig 5 A. Brain stem glioma 8 -year-old female with headache T 2 WI shows hyperintense lesion (arrow) with surrounding edema in pons.

Fig 5 B. Brain stem glioma 8 -year-old female with headache Postcontrast T 1 WI shows no significant enhancement.

Fig 5 C. Brain stem glioma 8 -year-old female with headache DWI shows iso-intensity in the lesion (arrow).

Fig 5 D. Brain stem glioma 8 -year-old female with headache ADC map shows hyperintensity (arrow). Iso-intensity on DWI is caused by a balance between increased T 2 and ADC.

Fig 6 A. Low-grade oligoastrocytoma 48 -year-old female with seizures T 2 WI shows a hyperintense lesion in the right temporal lobe (arrow).

Fig 6 B. Low-grade oligoastrocytoma 48 -year-old female with seizures Postcontrast T 1 WI shows slightly hyperintense lesion and no enhancement (arrow).

Fig 6 C. Low-grade oligoastrocytoma 48 -year-old female with seizures DWI shows hyperintensity (arrow).

Fig 6 D. Low-grade oligoastrocytoma 48 -year-old female with seizures ADC map shows hyperintensity (0. 98 -1. 19 x 10 -3 mm 2/s; arrow).

Epidermoid tumor (Fig 7) Epidermoid tumors are benign neoplasms of ectodermal origin with stratified squamous epithelium and keratinaceous debris (13, 24 -31). They are hyperintense on DWI with decreased ADC. The ADC of epidermoid tumors has been reported to be lower than cerebrospinal fluid and equal or higher than brain parenchyma (24 -26, 28, 29, 31). Therefore, the hyperintensity of epidermoid tumors on DWI is primarily caused by T 2 shine-through effect.

Fig 7 A. Epidermoid 9 -year-old asymptomatic female T 2 WI shows hyperintense mass near in midline (arrow).

Fig 7 B. Epidermoid 9 -year-old asymptomatic female T 1 WI shows hyperintensity (arrow).

Fig 7 C. Epidermoid 9 -year-old asymptomatic female DWI shows hyperintensity (arrow).

Fig 7 D. Epidermoid 9 -year-old asymptomatic female ADC map shows heterogeneous hyperintensity.

Arachnoid cysts (Fig 8) Arachnoid cysts have a similar appearance on routine MR imaging as epidermoid tumors, but it is well-known that DWI can distinguish the two (24 -31). Arachnoid cysts are hyperintense on DWI and their MR signal characteristics are similar to cerebrospinal fluid.

Fig 8 A. Arachnoid cyst 9 -year-old female with developmental delay T 2 WI shows large hyperintense lesion in right cerebellopontine angle (arrow).

Fig 8 B. Arachnoid cyst 9 -year-old female with developmental delay T 1 WI shows hyperintensity (arrow).

Fig 8 C. Arachnoid cyst 9 -year-old female with developmental delay DWI shows hyperintensity (arrow).

Fig 8 D. Arachnoid cyst 9 -year-old female with developmental delay ADC map shows hyperintensity due to increased diffusibility (3. 07 -3. 12 x 10 -3 mm 2/s; arrow).

Primitive neuroectodermal tumor (PNET) (Fig. 9) PNET is a group of histologically similar tumors that occur mostly in children. They include embryonal, largely undifferentiated tumors, such as medulloblastoma, neuroblastoma, pineoblastoma, ependymoblastoma and medulloepithelioma. These tumors have a high cellular density and are typically hyperintensity on DWI with decreased ADC (32 -35).

Fig 9 A. PNET 20 -month-old female with lethargy and nausea T 2 WI shows a well demarcated and heterogeneous intense mass in right frontal lobe.

Fig 9 B. PNET 20 -month-old female with lethargy and nausea T 1 WI shows heterogeneous hyperintensity.

Fig 9 C. PNET 20 -month-old female with lethargy and nausea DWI shows hyperintensity.

Fig 9 D. PNET 20 -month-old female with lethargy and nausea ADC map shows heterogeneous hyperintensity (0. 54 -0. 74 x 10 -3 mm 2/s) representing hypercellularity.

Meningiomas (Figs 10, 11) Most benign meningiomas are iso-intense on DWI and ADC maps, but some are slightly hyperintense on both DWI and ADC maps. Malignant or atypical meningiomas have markedly increased signal intensity on DWI and decreased ADC due to a high tumor cellularity (12, 18, 36). However, other factors, such as multifocal areas of necrosis, numerous abnormal mitoses and cytologic pleomorphism may also cause the high DWI signal (11, 12, 18, 36, 37).

Fig 10 A. Benign meningioma 72 -year-old female with visual disturbance T 2 WI shows hyperintense mass near frontal falx.

Fig 10 B. Benign meningioma 72 -year-old female with visual disturbance Postcontrast T 1 WI shows homogeneous enhancement.

Fig 10 C. Benign meningioma 72 -year-old female with visual disturbance DWI shows hyperintensity.

Fig 10 D. Benign meningioma 72 -year-old female with visual disturbance ADC map shows mild hyperintensity (0. 73 -0. 78 x 10 -3 mm 2/s).

Fig 11 A. Atypical meningioma 45 -year-old female with headache T 2 WI shows heterogeneous intense mass in left temporal lobe (arrow).

Fig 11 B. Atypical meningioma 45 -year-old female with headache Postcontrast T 1 WI shows heterogeneous enhancement (arrows).

Fig 11 C. Atypical meningioma 45 -year-old female with headache DWI shows heterogenous hyperintensity (arrows).

Fig 11 D. Atypical meningioma 45 -year-old female with headache ADC map shows hyperintensity especially in left side (0. 51 x 10 -3 mm 2/s; arrows).

Malignant lymphomas (Fig. 12) Most lymphomas are iso- or hyperintense on T 2 WI and show homogeneous enhancement in immunocompetent patients. But in immunosuppressed patients a rim enhancement is a more common finding (18, 38 -40). The enhancing components of lymphomas are generally hyperintense on DWI (16, 18, 41). ADC of lymphomas is often lower than in high grade gliomas (16). As mentioned before, this corresponds to the hypercellularity and might help in differentiating between lymphomas and high grade gliomas (16).

Fig 12 A. Lymphoma 64 -year-old male with seizures T 2 WI shows slightly hyperintense mass (arrow) with surrounding edema in left frontal lobe.

Fig 12 B. Lymphoma 64 -year-old male with seizures Postcontrast T 1 WI shows heterogeneously enhancing mass (arrow).

Fig 12 C. Lymphoma 64 -year-old male with seizures DWI shows hyperintensity (arrow).

Fig 12 D. Lymphoma 64 -year-old male with seizures ADC map shows hyperintensity (0. 51 -0. 71 x 10 -3 mm 2/s; arrow).

Craniopharyngiomas (Fig. 13) Craniopharyngiomas typically show a combination of contrast enhancement, cyst formation and calcifications. Signal intensity on DWI depends on ADC and T 2 values (42).

Fig 13 A. Craniopharyngioma 8 -year-old male with panhypopituitarysm T 2 WI shows hyperintense mass (arrow) in suprasellar region.

Fig 13 B. Craniopharyngioma 8 -year-old male with panhypopituitarysm DWI shows hyperintensity (arrow).

Fig 13 C. Craniopharyngioma 8 -year-old male with panhypopituitarysm ADC map shows hyperintensity (2. 25 -2. 38 x 10 -3 mm 2/s; arrow).

Metastases (Fig 14) The signal intensity of solid components of metastases on DWI is variable and depends on their T 2 and ADC (2, 6, 11, 12, 18, 19, 30, 43 -51). DWI findings of metastasis are similar to that of gliomas, probably reflecting the cellularity of the primary tumor (6, 11, 18, 30). Common signal intensity of necrotic/cystic components of metastases may relate to an increase in free water, showing hyperintensity on DWI with increased ADC. However, in the presence of extracellular methemoglobin and/or increased viscosity, DWI can show hyperintensity with decreased ADC (18, 43 -51).

Fig 14 A. Metastasis 59 -year-old female with adenocarcinoma of lung T 2 WI shows heterogenous mass (arrow) with surrounding edema in right temporal lobe.

Fig 14 B. Metastasis 59 -year-old female with adenocarcinoma of lung Postcontrast T 1 WI shows heterogeneous ring-like enhancement (arrow).

Fig 14 C. Metastasis 59 -year-old female with adenocarcinoma of lung DWI shows hyperintensity in solid (arrowhead) and hyperintensity in the cystic/necrotic portions (arrow).

Fig 14 D. Metastasis 59 -year-old female with adenocarcinoma of lung ADC map shows hyperintensity in solid (0. 971. 00 x 10 -3 mm 2/s; arrowhead) and hyperintensity (2. 21 -2. 35 x 10 -3 mm 2/s; arrow) in necrotic portions.

Conclusion DW imaging can provide additional information about tumor cellularity and help in the characterization and grading of tumors. The ability of specific tumor differentiation and determination of tumor infiltration is difficult in most situations.

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