The authors conclude that the endoscopic management of patients with pineal region masses and hydrocephalus may be a preferred initial strategy.

Objective: Slit ventricle syndrome (SVS) has been described in hydrocephalus patients who continue to have shunt malfunction-like symptoms in the presence of a functioning shunt system and small ventricles on imaging studies. These symptoms usually present years after shunt placement or revision and can consist of headache, nausea and vomiting, lethargy and decreased cognitive skills. Treatments offered range from observation, medical therapy (migraine treatment) and shunt revision to subtemporal decompression or cranial vault expansion. We describe a subset of patients with SVS who were symptomatic with high intracranial pressure (ICP) as measured by sedated lumbar puncture and whose symptoms completely resolved after lumboperitoneal shunt (LPS) placement. Methods: Seven patients with a diagnosis of SVS underwent lumboperitoneal shunting. The age at shunting ranged from 3 to 18 years. Most had undergone recent ventriculoperitoneal shunt (VPS) revisions for presentation of shunt malfunction-like symptoms. Despite this, all remained symptomatic and underwent a sedated lumbar puncture to measure opening pressure (OP). All had high OP in spite of a functional VPS and underwent LPS placement. Results: All 7 patients had a prolonged period of overdrainage symptoms after lumboperitoneal shunting that resolved completely over several weeks. The initial etiology of hydrocephalus was reported to include trauma, aqueductal stenosis and intraventricular hemorrhage of prematurity. Two patients required revision of their LPS, after which their symptoms again resolved. Conclusion: In a certain subset of patients with SVS who are symptomatic from increased ICP, placement of an LPS is an effective treatment option. It appears that this subgroup of patients previously treated with ventriculoperitoneal shunting behave in a fashion similar to pseudotumor cerebri patients and respond well to lumboperitoneal shunting.

✓The authors describe a medial supraorbital craniotomy performed through a medial eyebrow skin incision to approach an epidural abscess located in the medial anterior fossa of the skull. An 8-year-old boy presented with fevers and facial swelling. Imaging demonstrated pansinusitis and an epidural fluid collection adjacent to the frontal sinus. A medial supraorbital craniotomy was performed to access and drain the epidural abscess. The supraorbital nerve laterally and the supratrochlear nerve medially were preserved by incising the frontalis muscle vertically, parallel to the course of the nerves, and dissecting the subperiosteal plane to mobilize the nerves. This approach may be a useful access corridor for other lesions located near the medial anterior fossa.

The authors report on a 54-year-old man who presented with a lumbar vertebral body lesion and an adjacent epidural lesion that was found to be hairy cell leukemia (HCL). The patient presented with gradual onset of back pain and intermittent lower-extremity radicular symptoms. He did not have splenomegaly or peripheral blood count abnormalities. Admission MR imaging revealed an L-5 vertebral body lesion and a lumbar epidural lesion extending from L-3 to S-2. An [18F]fluorodeoxyglucose–PET study showed numerous sites of osseous involvement. The patient underwent minimally invasive surgical biopsy sampling of the epidural lesion. Histopathological examination revealed extranodal HCL. After treatment with a 5-day course of cladribine, the patient's symptoms resolved, and at the 16-week follow-up visit there was no radiographic or metabolic evidence of disease. Hairy cell leukemia rarely involves neurological structures, but this patient responded well to standard treatment. This case demonstrates the value of tissue biopsy procedures instead of aggressive resection and the use of minimally invasive techniques to treat an HCL spinal lesion.

Pleomorphic xanthoastrocytoma (PXA) is a rare primary central nervous system tumor which frequently harbors mutations in BRAF. Anaplastic PXA follow a more aggressive course than their nonanaplastic counterparts. We present the case of an anaplastic PXA initially treated with the BRAF inhibitor vemurafenib. After progression of disease the MEK inhibitor trametinib was added to the regimen leading to radiographic improvement. The rationale for combined BRAF and MEK inhibition in PXA is reviewed.