Computed tomography findings in patients with primarily unknown causes of severe or recurrent epistaxis.

OBJECTIVE: In addition to rhinoscopy, computed tomography of paranasal sinuses (CT) may be performed on patients with primary unknown cause of severe epistaxis (SE) or recurrent epistaxis (RE) to further assess the potential cause of bleeding. The aim of this study was to evaluate CT findings during the work-up of intractable epistaxis patients. METHODS: 6937 patients were treated in our emergency department with acute epistaxis between 2009-2018. 304/6937 patients underwent CT and rhinoscopy due to intractable SE or RE. 33 patients presented with head trauma prior to epistaxis and were excluded from the final analysis. In 271 cases the primary causes of SE (n = 252) or RE (n = 19) remained unknown. Two observers retrospectively evaluated CT scans for potential sources of epistaxis. Disagreement was settled by consensus. CT and rhinoscopy findings were compared. RESULTS: In 247/271 (91.1%) SE patients no related pathology was found on CT. A possible cause for epistaxis was found in all RE patients, but only in 5/252 (1.9%) patients with SE. Most tumours (10/11) and inflammatory conditions (9/10) were found in patients with RE. In three SE cases, a tumour was suspected on CT, from which two suspicions were refuted during rhinoscopy. CT revealed 10 cases of inflammatory conditions of the sinus and anatomical variant as potential cause of bleeding. CONCLUSION: For patients with unknown causes of epistaxis, supplementary CT imaging may be a useful diagnostic add-on to rhinoscopy in the event of RE, tumour suspicion or inflammation of the paranasal sinuses. However, in most cases of first-time SE, CT does not necessarily add to the diagnosis. In these cases, the marginal benefit of CT needs to be weighed carefully against its risks.

Gonadotropin-releasing hormone regulates spine density via its regulatory role in hippocampal estrogen synthesis.

Spine density in the hippocampus changes during the estrus cycle and is dependent on the activity of local aromatase, the final enzyme in estrogen synthesis. In view of the abundant gonadotropin-releasing hormone receptor (GnRH-R) messenger RNA expression in the hippocampus and the direct effect of GnRH on estradiol (E2) synthesis in gonadal cells, we asked whether GnRH serves as a regulator of hippocampal E2 synthesis. In hippocampal cultures, E2 synthesis, spine synapse density, and immunoreactivity of spinophilin, a reliable spine marker, are consistently up-regulated in a dose-dependent manner at low doses of GnRH but decrease at higher doses. GnRH is ineffective in the presence of GnRH antagonists or aromatase inhibitors. Conversely, GnRH-R expression increases after inhibition of hippocampal aromatase. As we found estrus cyclicity of spine density in the hippocampus but not in the neocortex and GnRH-R expression to be fivefold higher in the hippocampus compared with the neocortex, our data strongly suggest that estrus cycle-dependent synaptogenesis in the female hippocampus results from cyclic release of GnRH.