malignes intraventrikuläres Meningeom
Malignant intraventricular meningioma with craniospinal dissemination and concurrent pulmonary metastasis. Primary MIVM and first local recurrence. (A) CT scan, showing a huge hyperdense mass lesion in the trigone with central necrosis. (B) MRI scan, demonstrating heterogeneous enhancement of the lesion. (C) Histopathological findings revealing anaplastic meningioma with cellular pleomorphism, nuclear atypia, and geographic necrosis (H & E 400×). (D) Postoperative MRI scan, displaying no residual tumor. (E) MRI scan, disclosing local recurrence. (F) MRI scan, showing a huge residual cavity after the second craniotomy.
Malignant
intraventricular meningioma with craniospinal dissemination and concurrent pulmonary metastasis. Primary MIVM and first local recurrence. (A) CT scan, showing a huge hyperdense mass lesion in the trigone with central necrosis. (B) MRI scan, demonstrating heterogeneous enhancement of the lesion. (C) Histopathological findings revealing anaplastic meningioma with cellular pleomorphism, nuclear atypia, and geographic necrosis (H & E 400×). (D) Postoperative MRI scan, displaying no residual tumor. (E) MRI scan, disclosing local recurrence. (F) MRI scan, showing a huge residual cavity after the second craniotomy.
Cerebrospinal fluid dissemination of anaplastic intraventricular meningioma: report of a case presenting with progressive brainstem dysfunction and multiple cranial nerve palsies. Brain MRI of the present patient at admission (a –c), and 17 days (d–f) and 40 days (g–i) after admission. Fluid attenuated inversion recovery (FLAIR) images at admission showed no gross abnormality, including in the brainstem and cranial nerves (a, b), although a mass-enhancing lesion was observed in the trigone of the left lateral ventricle on T1-weighted imaging (c). 17 days after admission, FLAIR images revealed slight hyperintensity in the exit for the trigeminal nerve and the left cerebellar hemisphere (d, e), and diffusion-weighted imaging (DWI) showed hyperintensity in the left cerebellar hemisphere (f). At the final MRI at 40 days after admission, diffuse high-intensity lesions and hydrocephalus were observed in the brainstem and cerebellum on FLAIR (g, h) and DWI revealed multiple hyperintense lesions in the bilateral cerebellar hemispheres (i)
Cerebrospinal
fluid dissemination of anaplastic intraventricular meningioma: report of a case presenting with progressive brainstem dysfunction and multiple cranial nerve palsies. Brain MRI of the present patient at admission (a –c), and 17 days (d–f) and 40 days (g–i) after admission. Fluid attenuated inversion recovery (FLAIR) images at admission showed no gross abnormality, including in the brainstem and cranial nerves (a, b), although a mass-enhancing lesion was observed in the trigone of the left lateral ventricle on T1-weighted imaging (c). 17 days after admission, FLAIR images revealed slight hyperintensity in the exit for the trigeminal nerve and the left cerebellar hemisphere (d, e), and diffusion-weighted imaging (DWI) showed hyperintensity in the left cerebellar hemisphere (f). At the final MRI at 40 days after admission, diffuse high-intensity lesions and hydrocephalus were observed in the brainstem and cerebellum on FLAIR (g, h) and DWI revealed multiple hyperintense lesions in the bilateral cerebellar hemispheres (i)
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Assoziationen und Differentialdiagnosen zu malignes intraventrikuläres Meningeom: 