Cystic trochlear nerve schwannoma. Case report.

BACKGROUND: Twenty-six cases of pathologically verified schwannomas of the trochlear nerve have been reported in the literature. Five of them had a large cystic component and a smaller solid portion. Complex skull base approaches have been usually applied for their removal. CASE DESCRIPTION: We report on a rare case of cystic trochlear schwannoma in a 52-year-old female patient. The patient presented with double vision, facial palsy, decreased hearing, hemiparesis on the right side, and severe gait instability. Magnetic resonance imaging revealed a 2.5-cm left-sided extra-axial lesion compressing the brain stem at the lower midbrain and upper pontine level. Total resection was performed via a retrosigmoid craniotomy. After the surgery, the neurological deficit diminished considerably. At 28 months follow-up, her only complaint was mild double vision when walking down the stairs and hypesthesia in the right half of her face. CONCLUSIONS: This case represents a rare pontomesencephalic lesion removed successfully via the simple retrosigmoid route.

Advanced glycation end products induce angiogenesis in vivo.

Advanced glycation end products (AGEs) have been thought to participate in diabetic microangiopathy. However, the effects of AGEs on angiogenesis have so far been mainly examined either in vitro or by using cultured cells. In the present study, we have analyzed whether AGEs induce angiogenesis in vivo by using the chorioallantoic membrane (CAM) assay. The CAM assay was carried out in embryonated hen eggs to determine the effects of AGEs. Following generation of AGEs based on bovine serum albumin (BSA), either AGE-BSA or nonglycated BSA was administered to the CAM and their effects on angiogenesis were assessed, together with an inhibitory effect of an anti-AGE antibody against AGE-BSA-induced angiogenesis. The histological features of AGE-induced vascular lumens were examined by immunohistochemical analysis for Factor VIII and smooth muscle alpha-actin. AGE-BSA induced angiogenesis in CAM in a dose- and time-dependent manner. AGE-induced angiogenesis on CAM was neutralized by the anti-AGE antibody. Immunohistochemical analysis demonstrated that AGE-induced vascular lumens were devoid of pericytes. Our data demonstrated that AGEs are an angiogenetic factor and that our system of AGE-induced abnormal vessels in CAMs is useful in further investigations of the mechanism of diabetic retinal angiogenesis and can also be used to provide a therapeutic model for diabetic angiopathy.