Objective
We describe our experience for repair septal perforation with a septal flap and we analyse the route of the septal branch of the anterior ethmoidal artery (AEA) in the septum area with a ...radiological anatomy study in order to perform this flap.
Study design
We carry out a prospective analysis with computed tomography scan in the cadaver heads and we perform an endoscopic technique in the patients.
Methods
Ten nasal cavities were analysed in five adult cadaveric heads and two patients diagnosed with anterior septal perforation were surgically treated. Measurements in the cadaveric heads were obtained from a sagittal plane of the nasal septum. The anterior point corresponds to the projection of the anterior insertion of the middle turbinate in the frontal process of the maxilla over the nasal septum. The posterior point was obtained with a vertical line passing through the entrance of the AEA in the nasal septum.
Results
The mean distance between the anterior point and the posterior point was 7.35 mm with a standard deviation of 0.95 mm. The lowest value was 5.5 mm and the highest value was 8.7 mm. We observed good epithelialisation and closure of the perforation in all patients.
Conclusion
The unilateral septal flap pedicle by anterior ethmoidal artery may be used for small and medium perforations with a pedicle smaller than 1 cm posterior to the axilla.
While prior studies have established various interacting mechanisms and neural consequences (i.e. monoaminergic nerve terminal damage) that might contribute to the adverse effects caused by ...methamphetamine administration, the precise mechanisms that mediate relapse during withdrawal remain unknown. This study evaluated the long‐term consequences of binge methamphetamine administration (three pulses/day, every 3 hours, 4 days, i.p.; dose–response: 2.5, 5 and 7.5 mg/kg) in adult Sprague–Dawley rats at two behavioral levels following 25 days of withdrawal: (1) negative affect (behavioral despair—forced‐swim test, and anhedonia—1% sucrose consumption, two‐bottle choice test) and (2) voluntary methamphetamine consumption (20 mg/l, two‐bottle choice test). Striatal and hippocampal brain samples were dissected to quantify monoamines content by high‐performance liquid chromatography and to evaluate neurotoxicity (dopaminergic and serotonergic markers) and neuroplasticity markers i.e. cell fate regulator (Fas‐associated protein with death domain) FADD by Western blot. The results showed that methamphetamine administration induced dose‐dependent negative effects during prolonged withdrawal in adult rats. In particular, rats treated repeatedly with methamphetamine (7.5 mg/kg) showed (1) enhanced negative affect—increased anhedonia associated with behavioral despair, (2) increased voluntary methamphetamine consumption, (3) enhanced neurotoxicity—decreased dopamine and metabolites in striatum and decreased serotonin in hippocampus, (4) altered neuroplasticity markers—decreased FADD protein and increased p‐FADD/FADD balance selectively in hippocampus and (5) higher consumption rates of methamphetamine that were associated with lower FADD content in hippocampus. These results confirm that methamphetamine withdrawal dose‐dependently induced negative affect and decreased monoamines content, while also increased voluntary methamphetamine consumption and suggested a role for hippocampal FADD neuroplasticity in these drug‐withdrawal adaptations.
Methamphetamine administration induced dose‐dependent negative effects during prolonged withdrawal in adult rats. Mainly, rats treated repeatedly with methamphetamine (7.5 mg/kg) showed: (1) enhanced negative affect—increased anhedonia associated with behavioral despair, (2) increased voluntary methamphetamine consumption, (3) enhanced neurotoxicity—decreased brain dopamine and serotonin, (4) altered neuroplasticity—decreased hippocampal FADD protein, and (5) higher consumption rates of methamphetamine were associated with lower hippocampal FADD content. Thus, these results suggested a role for hippocampal FADD neuroplasticity in these drug‐withdrawal adaptations.
