Temporal crescent syndrome is a monocular visual field defect involving the temporal crescent of one eye caused by a retrochiasmal lesion. The most anterior portion of the striate cortex is the only area where the retrochiasmal lesion produces a monocular visual field defect. The authors present the case of a 9-year-old boy who presented with mild headache. MRI revealed a cyst with cerebrospinal fluid signal intensity, occupying the body and trigone of the right lateral ventricle. Conservative treatment with regular clinical and radiological follow-up was chosen because neurological examination findings were normal. Three years later, the patient experienced blurred vision with a temporal crescent defect in the left eye. Endoscopic cyst fenestration was performed, and the pathological findings indicated a glioependymal cyst. After surgery, the monocular temporal crescent disorder was resolved. MRI indicated shrinkage of the cyst and improvement in the narrowing of the anterior calcarine sulcus. These findings suggested that the temporal crescent syndrome was caused by a lateral ventricular glioependymal cyst. This is the first known report of temporal crescent syndrome caused by a lateral ventricular glioependymal cyst. In patients with monocular temporal crescent disorder without intraocular disease, a retrochiasmal lesion in the most anterior portion of the striate cortex should be considered.
Izumi Yamaguchi, Kyong-Hon Pooh, Mai Azumi, and Yasushi Takagi
Tadashi Yamaguchi, Takeshi Miyamoto, Keiko T. Kitazato, Eiji Shikata, Izumi Yamaguchi, Masaaki Korai, Kenji Shimada, Kenji Yagi, Yoshiteru Tada, Yoshihito Matsuzaki, Yasuhisa Kanematsu, and Yasushi Takagi
The pathogenesis of intracranial aneurysm rupture remains unclear. Because it is difficult to study the time course of human aneurysms and most unruptured aneurysms are stable, animal models are used to investigate the characteristics of intracranial aneurysms. The authors have newly established a rat intracranial aneurysm rupture model that features site-specific ruptured and unruptured aneurysms. In the present study the authors examined the time course of changes in the vascular morphology to clarify the mechanisms leading to rupture.
Ten-week-old female Sprague-Dawley rats were subjected to hemodynamic changes, hypertension, and ovariectomy. Morphological changes in rupture-prone intracranial arteries were examined under a scanning electron microscope and the association with vascular degradation molecules was investigated.
At 2–6 weeks after aneurysm induction, morphological changes and rupture were mainly observed at the posterior cerebral artery; at 7–12 weeks they were seen at the anterior Willis circle including the anterior communicating artery. No aneurysms at the anterior cerebral artery–olfactory artery bifurcation ruptured, suggesting that the inception of morphological changes is site dependent. On week 6, the messenger RNA level of matrix metalloproteinase–9, interleukin-1β, and the ratio of matrix metalloproteinase–9 to the tissue inhibitor of metalloproteinase–2 was significantly higher at the posterior cerebral artery, but not at the anterior communicating artery, of rats with aneurysms than in sham-operated rats. These findings suggest that aneurysm rupture is attributable to significant morphological changes and an increase in degradation molecules.
Time-dependent and site-dependent morphological changes and the level of degradation molecules may be indicative of the vulnerability of aneurysms to rupture.