RESUMO
An abnormal communication between the subarachnoid spaces and the tympanic cavity and mastoid cells can determine a cerebrospinal fluid (CSF) leak in the air spaces of the temporal bone. The etiology of CFS leak in the temporal air cells includes acquired, congenital and spontaneous causes. Spontaneous CSF leak, defined as a leak without a manifest cause, is present in about 4% of cases and often occurs in the middle cranial fossa. We describe a case of spontaneous CSF leak in the right temporal air cells that mimicked a skull fracture in a subject with headache and apparent rhinorrhea after a head trauma. Both CT and MRI play a key role in the differential diagnosis between post-traumatic temporal CSF leak due to a fracture and spontaneous leak: traumatic CSF leak often does not require a surgical approach, whereas spontaneous CSF leak may need surgical treatment because of the risk of meningitis.
RESUMO
Aggressive hemangiomas are rare and can compress the spinal cord, nerve roots or both, producing myelopathy or radiculopathy. This report describes an aggressive and compressive hemangioma of the body of the Th9 vertebra in a woman with symptoms of medullary sufferance, treated with embolization of the afferent vessels of the lesion followed by radiotherapy.
RESUMO
AIM: Based on the known effect of metformin (MET) in improving insulin sensitivity in type 2 diabetes, with the scope to focus the effects on glycaemic and free fatty acids (FFA) levels, we studied the effects of a short-term treatment with this drug in obese subjects and obese patients with diabetes or family history of diabetes (FHD). We used a method to allow us to evaluate the possible difference of insulin sensibility with regard to the insulin action on glycaemia and blood FFA, both in the basal state and during oral glucose tolerance test (OGTT). METHODS: Insulin sensitivity was investigated before and after MET treatment (850 mg bid for 10 days) in seven obese subjects with normal glucose tolerance and without FHD and 13 obese patients with diabetes (n=7) or FHD (n=6). By using specifically designed formulae, we calculated four insulin-sensitivity indices (ISI) from basal level (b) and area values (a) (during OGTT) of insulinaemia, glycaemia (gly) or FFA (ffa), namely: ISI (gly)-b, ISI (gly)-a, ISI (ffa)-b and ISI (ffa)-a. RESULTS: In patients with diabetes or FHD, MET improved ISI (gly)-b (0.79 +/- 0.06 vs. 0.59 +/- 0.07, p<0.001) and ISI (gly)-a (0.69 +/- 0.09 vs. 0.51 +/- 0.07, p<0.05), whereas only minor changes occurred for ISI (ffa)-b and ISI (ffa)-a. In contrast, in simple obese subjects, MET induced further deterioration of both ISI (gly)-a (0.47 +/- 0.07 vs. 0.64 +/- 0.10, p<0.01) and ISI (ffa)-a (0.43 +/- 0.07 vs. 0.55 +/- 0.08, p<0.05). Fasting level and total area of lactate were high in the obese patients and were not affected by MET. A statistically significant increase (p<0.01), however, was observed for the 'decremental' area of lactate in obese subjects with diabetes or FHD, which might probably contribute to the reduction of insulin resistance induced by the drug in these patients. CONCLUSIONS: Although the low number of subjects studied precludes absolute conclusions, data would suggest that MET improved ISI towards glucose but not towards FFA, in the diabetic and 'prediabetic' obese patients, whereas worsened it in the obese subjects without FHD. Therefore, the effects of MET would not be secondary to changes of FFA but rather to a primary action of MET on glucose metabolism. Thus, utilization of MET to treat the insulin resistance in obesity is indicated only in the presence of alterations of glucose metabolism or FHD.