Facial nerve edema is an important finding in Bell's palsy patients. Inflammation may cause facial nerve edema, and mechanical compression and ischemic change of the facial nerve may occur in the facial nerve canal. A few studies have reported the dimensions of the facial nerve canal using conventional computed tomography or human temporal bone sections. However, the cross-sectional area of the facial nerve canal has not been fully understood. Therefore, the cross-sectional area of the facial nerve canal was measured in patients with unilateral Bell's palsy by computer tomography with multiplanar reconstruction. Sixteen patients with unilateral Bell's palsy were enrolled. Computed tomography of the temporal bone was performed, and perpendicular images to the facial nerve canal were reconstructed by the multiplanar reconstruction technique. The cross-sectional area of the facial nerve canal on the affected and unaffected sides was measured at the labyrinthine segment, the horizontal segment, and the mastoid segment. Both in the labyrinthine and horizontal segments, the mean cross-sectional area of the facial nerve canal was significantly smaller on the affected side than on the unaffected side. There was no significant difference between the affected and unaffected sides in the cross-sectional area of the facial nerve canal in the mastoid segment. The labyrinthine segment was the narrowest segment in the facial nerve canal. These findings suggest that the facial nerve is vulnerable, especially in the labyrinthine segment of the facial nerve canal, and a narrow facial nerve canal may be one of the risk factors for Bell's palsy.
A 17-year-old male with poststreptococcal acute glomerulonephritis (PSAGN) superimposed on the course of IgA nephropathy is presented. The histological findings of the first renal biopsy showed mild IgA nephropathy with a mesangial deposition of IgA and C3. Eighteen months later, acute nephritic syndrome with hypocomplementemia and rising antihyaluronidase titer occurred 10 days following the onset of an upper respiratory infection. The second renal biopsy revealed severe diffuse endocapillary proliferative and exudative glomerulonephritis with cellular crescents in 70% of the glomeruli. Immunofluorescence showed granular staining of C3 alone along the capillary walls. The pre-existing IgA deposits had disappeared. Typical ‘humps’ were observed by electron microscopy. The symptoms were gradually resolved by intensive steroid and anticoagulant therapy. Five months after the episode of acute nephritic syndrome, the patient was clear of symptoms except for mild proteinuria and hematuria. The third renal biopsy at that time showed morphologic changes similar to those of the first renal biopsy with mild mesangial IgA deposits.
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