Shahzada K. Ahmed

Chordomas are rare malignant tumors arising from embryonic remnants of the primitive notochord, around which the skull base and vertebral column develop. They are locally aggressive but metastasize rarely. To our knowledge, this is the first reported case of synchronous intraosseous chordomas. A 32-year-old man presented with intermittent double vision secondary to a right-side abducent nerve palsy. Imaging revealed a clivus chordoma and an asymptomatic synchronous second primary chordoma in the fifth lumbar vertebra. Both chordomas were surgically excised: the clivus using the endonasal, endoscopic route and the L5 vertebra by total vertebral excision and replacement with a titanium prosthesis. The patient made an uneventful and complete recovery. We have modified our departmental practice as we believe that all patients diagnosed with chordoma should have magnetic resonance imaging of their entire spinal tract to exclude a second primary chordoma.

Pituitary apoplexy is a potentially fatal condition that can have serious consequences even after successful treatment. One of the potential complications of this syndrome is occlusion of the internal carotid arteries, which causes cerebral ischaemia. This can occur through one of two mechanisms—direct compression of the artery or vasospasm caused by factors released from haemorrhagic or necrotic material. We illustrate two examples of cerebral ischaemia with pituitary apoplexy, one with compression and one with vasospasm, both ending in a successful resolution. In both, magnetic resonance imaging, angiography, and hormonal studies allow diagnosis, and urgent surgical decompression should be the treatment of choice. We review the literature and discuss the mechanisms.

The process of embedding tissue in paraffin degrades many important molecules involved in respiratory epithelial remodelling. We therefore examined alternative methods. Inferior turbinate and nasal polyp biopsies were either placed in formalin or immediately snap-frozen in the operating theatre. Novel protocols for staining remodelling markers were compared with current methods. Our method, using a mixture of three lectins, stained a significantly greater proportion of samples, compared with using Ulex europeaus lectin alone (84 vs 62 per cent; p < 0.005). Comparison of different proliferation markers showed that Ki67 was more suitable than proliferating cell nuclear antigen for frozen sections. This study indicates that our robust, repeatable methods for examining whole mounts and for staining capillaries, cell proliferation and nuclei on the same section of nasal mucosa are superior to current methods. The use of fresh tissue that has not been paraffin-embedded would allow a greater suite of epitopes to be examined in the future.

Background: Nasal polyposis is a common disease of which little is currently known. Recent studies have shown up-regulation of several proangiogenic factors. The aim of this study was to assess and quantify how much angiogenesis occurs in nasal polyps and therefore whether angiogenesis is involved in the etiology of polyposis. Methods: Biopsy specimens of polyp tissue and inferior turbinate (IT) were taken from patients undergoing polypectomy and compared with IT samples from control patients. Five patients were used per study group. Biopsy specimens were either stained with a fluorescent lectin for confocal microscopy or snap frozen and sectioned for histology for the examination of multiple measures of angiogenesis. Results: No significant differences in capillary density, capillary-associated proliferation, capillary surface density, or capillary volume density were seen between the three study groups, and the regression of surface density versus volume density described a linear relationship. Polyp samples showed increases in capillary diameter and interstitial proliferation. Conclusion: These results show no active angiogenesis occurring in the polyp or changes in capillary bed architecture, although capillaries seem more edematous in the polyp. As the capillary supply increases in line with the physiological needs of the growing polyp, we conclude that angiogenesis is not a driving force in the etiology of nasal polyposis.