NEUROFIBROMATOSIS TYPE-2 - GROWTH-STIMULATION OF MIXED ACOUSTIC SCHWANNOMA BY CONCURRENT ADJACENT MENINGIOMA - POSSIBLE ROLE OF GROWTH-FACTORS - CASE-REPORT

Citation
R. Pallini et al., NEUROFIBROMATOSIS TYPE-2 - GROWTH-STIMULATION OF MIXED ACOUSTIC SCHWANNOMA BY CONCURRENT ADJACENT MENINGIOMA - POSSIBLE ROLE OF GROWTH-FACTORS - CASE-REPORT, Journal of neurosurgery, 89(1), 1998, pp. 149-154
Citations number
59
Categorie Soggetti
Surgery,"Clinical Neurology",Neurosciences
Journal title
ISSN journal
00223085
Volume
89
Issue
1
Year of publication
1998
Pages
149 - 154
Database
ISI
SICI code
0022-3085(1998)89:1<149:NT-GOM>2.0.ZU;2-P
Abstract
The authors report the case of a young man suffering from neurofibroma tosis type 2 (NF2) who harbored bilateral acoustic schwannomas and a p arasellar meningioma. Neuroimaging studies performed during a 4-year f ollow-up peri od showed that the bilateral schwannomas had grown very little and at similar rates. However, after the meningioma had infiltr ated the tentorium and approached the ipsilateral schwannoma at the in cisura, both Schwann cell tumors started to grow rapidly, particularly the one adjacent to the meningioma, of which the percentage of annual growth rate increased by approximately a factor of 10(2). At the same time, magnetic resonance imaging showed that this tumor also changed its features. During surgery, the acoustic schwannoma was firmly adher ent to both meningioma and tentorium. Histological examination reveale d meningotheliomatous cells in the schwannoma adjacent to the meningio ma. Antiphosphotyrosine immunoblotting of PC12 cells was compatible wi th the presence of an epidermal growth factor (EGF)-like molecule in t he cerebrospinal fluid !CSF) of the patient. This factor was not detec ted in the CSF of five other NF2 patients, two of whom bore associated bilateral acoustic schwannomas and meningioma in remote locations. It is hypothesized that the meningotheliomatous cells infiltrating the s chwannoma triggered an autocrine/paracrine growth-stimulatory mechanis m that involved an EGF-like factor.