Meningioma with Leptomeningeal Dissemination

Most meningiomas are benign (WHO Grade I), with <10% being aggressive (WHO Grade II) and malignant (WHO Grade III) tumors.

WHO Grade

• I – benign
• II – aggressive
• III – malignant

Distant metastases are rare, and are usually associated with aggressive or malignant meningomas. The most common route of metastases is blood-borne. Other routes include via the paravertebral venous plexus, lymphatic vessels and rarely, CSF. Common locations for blood-borne metastases include the liver, lungs, pleura and lymph nodes.

Distant mets:

1. Blood-borne (via jugular vein) – liver, lung, pleura, lymph nodes
2. CSF – leptomeningeal dissemination – intracranial, spinal
3. paravertebral venous plexus
4. lymphatic vessels

A. pre-op MRI, R cerebellopontine angle meningioma. B. post-op MRI. C and D. f/u MRI (2 months) local recurrence + new lesions (posterior fossa, suprasella, spinal). E. spinal MRI, multiple leptomeningeal dissemination.

A. preop MRI, L sphenoidal ridge meningioma. B. f/u MRI (4months) local recurrence.

C&D. f/u MRI (18 months), multiple meningomas around bilateral convexity.

A. pre-op MRI, meningioma in trigone of L lateral ventricle. B. f/u MRI 1.7y later, local recurrence. C. enhanced MRI, new lesions R cavernous sinus, posterior fossa. D. post-op MRI (2nd surgery). E. f/u PET CT (4 months later), multiple extraneuronal metastases in skull base, ribs, spines, pelvic bone. F. spinal MRI, leptomeningeal dissemination.

Notes:

1. Time to dissemination involving intraventricular meningiomas is shortest compared to other intracranial and spinal meningiomas. Ventricular location is an important site for dissemination through CSF.
2. histologically, factors that predict metastases: high cellularity, cellular hereogeneity, high mitosis rate, nuclear pleomorphism, tumor necrosis, invasion of adjacent blood vessels.
3. histologic transformation / aggressive transformations: meningiomas progress from benign to malignant state by accumulation of genetic alterations
   1. 1p loss of heterozygosity
   2. p73/RASSF1A promotor methylation
4. surgical resection initiates metastatic spread? counter arguments:
   1. low incidence despite so many tumors being operated on
   2. cases describing CSF dissemination but no surgical intervention
   3. **surgical resection could theoretically influence malignant transformation.
5. ?screening spinal MRI – consider between 6mos and 12mos after local recurrence of non-benign intraventricular meningioma
6. (+) intracranial LD of malignant intraventricular meningioma – recommends:
   1. whole spinal MRI immediately
   2. f/u spinal MRI between 3-6mos after dissemination
7. Treatment
   1. multimodal treatments (multiple surgery, chemotherapy, radiotherapy) have been performed, but prognosis in literature still dismal
   2. aggressive chemotherapy?
      1. systemic therapy (temozolomide, irinotecan, IFN-alpha, cyclophosphamide, bevacizumab)
      2. concurrent regional chemotherapy (intraventricular liposomal cytosine arabinoside, busulfan, thiotepa)
   3. radiotherapy to symptomatic areas?
   4. chemotherapy with agents that cross BBB or delivered directly into CSF?

Reference:

Park, K., Kim, K., Park, S., Hwang, J., & Lee, D. (2015). Intracranial Meningioma with Leptomeningeal Dissemination : Retrospective Study with Review of the Literature. Journal Of Korean Neurosurgical Society, 57(4), 258. doi: 10.3340/jkns.2015.57.4.258

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Perclose device deployment