Unilateral facet cyst at the atlantoaxial joint leading to cervical myelopathy: A case report and review of literature.

Background: Spinal synovial cysts are rare in the cervical spine where they may cause myeloradiculopathy. Contrast MR studies help differentiate these from other lesions. The optimal treatment is often surgical removal. Case Description: A 47-year-old male presented with axial neck pain, numbness, and left-hand paresthesia. When the MR study showed dorsolateral cord compression due to a left-sided C1-C2 facet cyst, he underwent a unilateral decompression/fusion. Adequate cyst removal/excision was documented on a postoperative MR performed 2 weeks and 3 months postoperatively. Conclusion: A 47-year-old male presented with myelopathy attributed to an MR-documented dorsolateral C1/ C2 facet cyst. Following excision/decompression of the cyst and posterior fusion, the patient's symptoms/signs resolved.

Endoscopic endonasal transclival resection of a ventral pontine cavernous malformation: technical case report.

Brainstem cavernous malformations are challenging due to the critical anatomy and potential surgical risks. Anterolateral, lateral, and dorsal surgical approaches provide limited ventral exposure of the brainstem. The authors present a case of a midline ventral pontine cavernous malformation resected through an endoscopic endonasal transclival approach based on minimal brainstem transection, negligible cranial nerve manipulation, and a straightforward trajectory. Technical and reconstruction technique advances in endoscopic endonasal skull base surgery provide a direct, safe, and effective corridor to the brainstem.

The protective role of heme oxygenase-1 in cerebral ischemia.

Cerebral ischemia is one of the leading causes of death and disability in industrialized countries, with no curative treatments to date. Identification of potential targets and elucidation of their physiological role under stress conditions may give support to the development of drugs and strategies to contend with this pathology. In the last years, Heme oxygenase-1 (HO-1) has been considered by many groups as a potential target in ischemic damage. HO-1 is the enzyme responsible for the conversion of the heme group to billiverdin, carbon monoxide and iron; a highly regulated cytoprotective enzyme able to respond to numerous chemical or physical stressors, many of which decrease oxygen availability and generate oxidative stress. The disruption of HO-1 activity has been widely associated with a bad outcome in many disorders, and a protective role through its heme catabolism products has been observed in transplantation, cardiac ischemia, limb ischemia/reperfusion and different alterations that involve ischemia and reperfusion events. Here, we review recent reports supporting the protective role of HO-1 in cerebral ischemia. Results on the endogenous HO-1 response, overexpression of HO-1 and compounds that reduce ischemic damage through the induction of HO-1 in cerebral ischemia in in vivo and in vitro models are analyzed.