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A 40-year-old female was admitted to the hospital with complaints of headache worsening gradually over a 1-month duration. Her past history included surgery to treat a left cerebellar cystic lesion 3 years before, and an untreated small solid right supracerebellar lesion of 1 cm diameter. On admission, magnetic resonance imaging showed that the right cerebellar lesion had grown to approximately 4 cm diameter abutting the tentorium and causing obstructive hydrocephalus. She also had two more small lesions, a right supratentorial solid lesion with cystic component near the splenium and an intramedullary cystic lesion at the C-2 level. Right suboccipital craniectomy was done. The vascular attachments between the superior aspect of the tumor and the tentorium were coagulated and the tumor was totally removed. C1-2 laminectomy was also performed to drain the intramedullary cyst. The patient deteriorated and lost consciousness with respiratory arrest 6 hours postoperatively and was reoperated for intracerebellar hematoma due to oozing from the tentorial vessels. Histological investigation revealed hemangioblastoma. Dural tentorial vascular attachments in solid hemangioblastomas located subjacent to the tentorium may cause early postoperative complications of hematoma at the site of vascular attachment following the resection. Computed tomography study in the early postoperative period is helpful to identify this problem.

A 17-year-old male presented with a wound on the right temporal region, oozing hemorrhagic necrotic brain tissue and cerebrospinal fluid, following a fall. Computed tomography showed temporoparietal and petrous apex fractures on the right. Neurological examination revealed abducens nerve paresis, ptosis, and myosis on the right side. The patient was treated surgically for the removal of the free bony fragments at the fracture site and to close the dural tear. The abducens nerve paresis, ptosis, and myosis persisted at the 3rd monthly postoperative follow-up examination. The anatomy of the abducens nerve at the petroclival region was studied in four cadaveric heads. Two silicone-injected heads were used for microsurgical dissections and two for histological sections. The abducens nerve has three different angulations in the petroclival region, located at the dural entrance porus, the petrous apex, and the lateral wall of the cavernous segment of the internal carotid artery. The abducens nerve had fine anastomoses with the trigeminal nerve and the periarterial sympathetic plexus. There were fibrous connections extending inside the venous space of the petroclival area. The abducens nerve seems to be vulnerable to damage in the petroclival region, either directly by trauma to its dural porus and petrous apex or indirectly by stretching of the nerve through the nervous and/or fibrous connections. Concurrent functional loss of the abducens nerve and the periarterial sympathetic plexus clinically manifested as incomplete Horner's syndrome in our patient.

A 39-year-old woman was admitted with complaints of headache and nasal discharge on the left for 3 months which was later on proved to be cerebrospinal fluid (CSF). Neurological examination found no abnormalities except bilateral papilledema. Neuroimaging demonstrated enlargement of the lamina cribrosa foramina through which the olfactory nerves pass, as well as empty sella and cerebral cortical atrophy. Bone mineral densitometry showed osteopenia. CSF Ca++ and blood parathyroid hormone levels were elevated. CSF pressure was 280 mmH2O. Bilateral frontal craniotomy was performed to expose the anterior fossa. Foraminal enlargement at the lamina cribrosa was confirmed, and islands of extra-osseous calcifications on the arachnoid membrane were identified. The base of the anterior fossa was repaired intradurally with fascial graft and fibrin glue on both sides. No CSF leakage was noted at 1-year follow up. Spontaneous CSF leakage probably resulted from enlargement of the foramina at the lamina cribrosa due to Ca++ mobilization from bones and pseudotumor cerebri not to the extent of hydrocephalus caused by poor CSF absorption at the arachnoid granulations obliterated by extra-osseous calcareous accumulation.