This study aimed to examine the relationship of the accessory sphenoidal septum with surrounding vital structures and their variations.

This cross-sectional retrospective study investigated the prevalence of accessory sphenoidal septa and their relationship with variations in surrounding vital structures in coronal and axial paranasal computed tomography images.

Coronal and axial computed tomography images of 347 patients were assessed to evaluate the presence of accessory sphenoidal septa. Accessory sphenoidal septa originated from the internal carotid artery in 47.7 per cent of patients and from the optic nerve in 17.5 per cent. These structures were significantly associated with protrusion of the optic nerve, internal carotid canal or Vidian nerve canal.

Accessory sphenoidal septa can originate from the internal carotid artery or the optic nerve. Therefore, the presence of an accessory sphenoidal septum indicates an increased risk of surgical complications including internal carotid artery injury and loss of vision due to optic nerve injury.

To evaluate the presence of carotid thickening and its relationship with the Pathobiological Determinants of Atherosclerosis in Youth score.

We carried out a cross-sectional study involving 512 brazilian adolescents. Variables such as sex, body mass index, concentrations of non-high-density lipoprotein and high-density lipoprotein cholesterol, blood pressure, blood glucose and glycated haemoglobin A1c levels that make up the score, and carotid thickening through the intima-media complex measured by ultrasound were evaluated. We adopted two cut-off points to evaluate carotid thickening, being considered altered for those higher or equal to the z-score 2+ and ⩾75th percentile. The association was assessed using the χ2 test and univariate and multivariate logistic regression analyses.

High cardiovascular risk was present in 10.2% of the adolescents; carotid thickness was present in 4.3% determined by the z-score 2+ and in 25.0% determined by the 75th percentile. When measured by the z-score, carotid thickening was associated with high systolic blood pressure (p=0.024), high-non-high density lipoprotein cholesterol (p=0.039), and high cardiovascular risk assessed by the score and by the 75th percentile, with body mass index >30 (p=0.005). In the multivariate analysis, high cardiovascular risk was found to be independently associated with the presence of carotid thickness evaluated by the z-score, with risk four times greater (p=0.010) of presenting with this condition compared with individuals with low risk, and this fact was not observed when factors were analysed alone.

The presence of high cardiovascular risk in adolescents assessed by the Pathobiological Determinants of Atherosclerosis in Youth score was associated with marked thickening of the carotid artery in healthy adolescents.

To describe an unusual cause for hearing loss in an adult.

A 37-year-old man presented with a year's history of right-sided hearing loss. He had no history of trauma, or local or systemic infection. He was otherwise well, took no medication and had no allergies. He had a two-year history of low back pain. On examination, he had a retracted right tympanic membrane with no perforation, and a middle-ear effusion. Nasendoscopy was normal. Examination of other systems was unremarkable. Computed tomography of the temporal bones with contrast demonstrated a large, right, intra-cerebral internal carotid artery aneurysm compressing the eustachian tube. After a balloon occlusion test, he underwent endovascular occlusion of the parent vessel. He made a good post-operative recovery. A subsequent abdominal ultrasound excluded an abdominal aneurysm as a cause of his low back pain. His hearing had not improved three days post-operatively, and was to be formally assessed and monitored in the clinic.

A carotid aneurysm is a rare cause of eustachian tube compression but must be considered in the differential diagnosis of conductive hearing loss. Aneurysms may have systemic causes, and their presence in other systems should be excluded as they may be multiple.

We report a rare case of epistaxis resulting from a ruptured internal carotid artery aneurysm, and present a successful treatment method.

A 72-year-old woman was admitted following recurrent massive epistaxis. There was no history of trauma or surgery. Radiographic imaging demonstrated a large internal carotid artery aneurysm. An attempt was made to occlude the aneurysm with endovascular coils. Despite this, the patient went on to have further epistaxis. Endovascular ablation of the feeding internal carotid artery led to complete resolution.

This case demonstrates that spontaneous epistaxis from intra-cavernous carotid artery aneurysms can be managed using endovascular techniques. To our knowledge, we report the first use of interventional radiological techniques to assess the collateral circulation to the brain and subsequently undertake endovascular ablation of the internal carotid artery.