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Endoscopic third ventriculostomy (ETV) has been accepted for obstructive hydrocephalus (OH). We herein present a case of OH and optic nerve sheath edema (ONSE). Although ETV was successful, ONSE worsened. Discussion is focused on the relationship among intracranial hypertension (IH), ETV, and ONSE. The patient was a 19-year-old woman with complaints of headache and emesis. Papilledema was prominent. Radiological examination showed OH as an aqueductal tumor. Endoscopic tumorectomy and ETV were accomplished. Although headache and emesis disappeared, papilledema persisted. On the 4th day, the patient lost light perception. On magnetic resonance imaging, the third ventricular stroma and aqueduct were patent. Nevertheless, ONSE was prominent. After lumbar drainage, her vision was restored. Finally, ventriculoperitoneal shunting was performed, following which ONSE disappeared. IH is not always accompanied by ONSE. However, once it occurs, it may act separately from IH, and ETV may even exacerbate ONSE due to alteration of cerebrospinal fluid (CSF) flow into the chiasmatic cistern. In the optic nerve sheath, CSF pressure is not easily transmitted across different areas; this should explain the dissociation between ONSE and other symptoms of IH. Furthermore, we suggest that ONSE and acute optic dysfunction should be considered an independent crisis as “hydronervus opticus.”

Background context Noninfectious nontumorous retro-odontoid masses are rare, and masses have not been reported to extensively compress the spinal cord. We encountered a case of a large retro-odontoid lesion that extensively compressed the spinal cord. Case report A 76-year-old-man reported experiencing a sudden onset of neck pain, hand and foot paresthesia, dysarthria, and dysphagia. When symptoms had not eased by 10 days of treatment with external stabilization and bed rest, he was referred to our hospital. Dynamic radiographs of the cervical spine showed that the atlantodental interval widened from 2 mm on extension to 7 mm on flexion. Computed tomography did not reveal abnormality of the odontoid process or the presence of a high-density area that could suggest calcification in or near the cystic mass. Fluid-attenuated inversion recovery axial magnetic resonance image showed a mass that was 3.0-cm wide, 2.7-cm high, and 2.5-cm thick that severely compressed the lower brain stem. T2-weighted magnetic resonance imaging showed that the mass contained a solid part posterior to the C2 dense area, extending rostrally, compatible with the presence of degenerated and hypertrophic ligaments. We performed surgical decompression of the lesion combined with atlantoaxial fixation. The partly cystic mass, which was located extradurally, had xanthochromic content, indicating microbleeding. Dysarthria and dysphagia immediately disappeared, and neurologic symptoms disappeared by 1 month. At 1-year follow-up, the patient remained symptom free, and computed tomography scans did not show recurrence of the mass. The pathologic diagnosis of degenerative ligament tissue with chronic recurrent microbleeding and associated granulation was made. Discussion A possible explanation why the cyst grew to an exceptionally large size is that the transverse ligament of axis became degenerated and hypertrophic because of chronic mechanical stress by atlantoaxial subluxation. Then, a part of the ligament developed reactive granulation with small vessel formation. Finally, rupture of these small vessels caused repeated episodes of microbleeding, resulting in formation of a large cyst. The observation of degenerative ligament tissue, granulation formation, and microbleeding differentiated it from a synovial cyst or a ganglion cyst. The presence of hemosiderin deposits suggested chronic recurrent microbleeding. Taking all our findings together, we believe that our case of retro-odontoid cystic mass is different from the others that have been reported. Atlantoaxial instability may cause a large mass, such as we described here, so that careful observation is important.

Chronic subdural hematoma (CSDH) is an angiogenic disease that is recognized as a cause of treatable dementia with unknown pathogenesis. Vascular endothelial growth factor (VEGF), a potent growth factor regulating angiogenesis through the phosphatidylinositol 3-kinase (PI3-kinase)/Akt pathway, has been implicated in its etiology. The status of this signaling pathway in CSDH outer membranes was examined in the present study, using outer membranes obtained during trepanation surgery. Expressions of PI3-kinase, PKB-kinase, Akt, phosphorylated Akt at Ser(473) (p-Akt), endothelial nitric oxide synthase (eNOS), vascular endothelial-cadherin (VE-cadherin), and actin were examined by Western blot analysis, together with their immunohistochemistry. PI3-kinase, Akt, eNOS, and VE-cadherin were detected in all cases. The magnitude of the expression of p-Akt varied among cases; however, the localization was revealed to be present in endothelial cells of vessels in CSDH outer membranes, together with VEGF and VE-cadherin detected in endothelial cells of vessels. These findings suggest that the PI3-kinase/Akt signaling is activated in CSDH outer membranes, and indicate the possibility that the PI3 kinase/Akt pathway might be activated by VEGF and play a critical role in the angiogenesis of CSDH.

There are mainly two surgical methods for lumbar foraminal stenosis, simple decompression of the extra-foraminal portion or decompression with fixation surgery. However the indication of either method is controversial. The aim of this study is to show our surgical method and results.In six cases diagnosed as lumbar foraminal stenosis with or without far lateral disc herniation by X-ray, CTscan, MRI and nerve conduction velocity, decompression surgery was performed by our paramedian method (Wiltse approach). The apex and lateral portion of the superior articular facet (one third to one fourth) and the transforaminal ligament without fixation for lumbar foraminal stenosis. All patients were followed up for more than 10 months after the surgery. Japanese Orthopaedic Association (JOA) score and Visual Analogue Scale (VAS) were assessed before surgery and more than 10 months after the surgery. Postoperative radiological assessments were examined by neutral, flexion and extension X-ray.Foraminal stenosis was successfully decompressed in all cases. The postoperative JOA score and VAS were significantly improved in comparison to the preoperative score (Recovery Rate ware of 74.9% and 85.8%). There was no recurrence of symptoms or necessity for secondary surgery. The radiological evaluation did not indicate significant instability or decrease in the disc height.Our surgical method, removing the apex and lateral part of the superior articular process and transforaminal ligament without fusion led to a good outcome and recurrence 10 months after the surgery had not occurred.