Cerebellar Hemorrhage due to a Direct Carotid–Cavernous Fistula after Surgery for Maxillary Cancer

Infratentorial cerebral hemorrhage due to a direct carotid–cavernous fistula (CCF) is very rare. To our knowledge, only four such cases have been reported. Cerebellar hemorrhage due to a direct CCF has not been reported. We describe a 63-year-old female who presented with reduced consciousness 3 days after undergoing a maxillectomy for maxillary cancer. Computed tomography showed a cerebellar hemorrhage. Magnetic resonance angiography showed a left-sided direct CCF draining into the left petrosal and cerebellar veins through the left superior petrosal sinus (SPS). Her previous surgery had sacrificed the pterygoid plexus and facial vein. Increased blood flow and reduced drainage could have led to increased venous pressure in infratentorial veins, including the petrosal and cerebellar veins. The cavernous sinus has several drainage routes, but the SPS is one of the most important routes for infratentorial venous drainage. Stenosis or absence of the posterior segment of the SPS can also result in increased pressure in the cerebellar and pontine veins. We emphasize that a direct CCF with cortical venous reflux should be precisely evaluated to determine the hemodynamic status and venous drainage from the cavernous sinus.

Assessment of epidermal growth factor receptor status in glioblastomas

Our previous study showed that a newly designed tracer radioiodinated 6-[3-morpholinopropoxy]-7-ethoxy-4-[3'-iodophenoxy]quinazoline [[[125]I]PYK] is promising for the evaluation of the epidermal growth factor receptor [EGFR] status and prediction of gefitinib treatment of non-small cell lung cancer. EGFR is over-expressed and mutated also in glioblastoma. In the present study, the expressions and mutation of EGFR were tested with [[125]I] PYK in glioblastoma in vitro and in vivo to determine whether this could be used to predict the sensitivity of glioblastoma to gefitinib treatment. Glioblastoma cell lines with different expression of EGFR were tested. Growth inhibition of cell lines by gefitinib was assessed by the 3-[4, 5-dimethylthiazol-2-yl]-2, 5-diphenyltetrazolium bromide [MTT] colorimetric assay. Uptake levels of [[125]I]PYK were evaluated in cell lines in vitro. Tumor targeting of [[125]I]PYK was examined by a biodistribution study and imaging by single photon emission computed tomography [SPECT]. High concentrations of gefitinib were needed to suppress EGFR-mediated proliferation. The uptake of [[125]I] PYK in cell lines in vitro was low, and showed no correlation with EGFR expression or mutation status. Biodistribution study and SPECT imaging with [[125]I]PYK for xenografts showed no [[125]I]PYK uptake. The results showed prediction of gefitinib effectiveness was difficult in glioblastoma by [[125]I]PYK, which might be due to the complicated expression of EGFR status in glioblastoma. Thus, new tracers for sites downstream of the mutant EGFR should be investigated in further studies