McNab A A
The Royal Melbourne Hospital and Royal Victorian Eye and Ear Hospital, Melbourne, Australia.
J Clin Neurosci. 1998 Apr;5(2):186-92. doi: 10.1016/s0967-5868(98)90036-4.
Optic neuropathy affects a small proportion of patients with Graves' eye disease. It is due to optic nerve compression by enlarged extraocular muscles and can be treated by corticosteroids, irradiation or surgical orbital decompression. The current report evaluates the effectiveness of extracranial orbital decompression performed by one surgeon for optic neuropathy in Graves' eye disease. The records of 21 patients (33 orbits) undergoing extracranial orbital decompression for Graves' optic neuropathy were analysed for changes in visual acuity and colour vision and reduction in proptosis. Visual acuity and colour vision improved in all 33 eyes in the short-term postoperatively (4 weeks), but later deteriorated in 5 eyes (6.6%) of 4 patients (19%). The remainder maintained improved vision for the duration of the follow-up period (mean 22, range 3-54 months). Proptosis decreased by a mean 5.0 mm (range 1-8). Extraocular muscle imbalance and diplopia worsened in 9 21 patients (43%) and improved in 2 21 (9.5%). The patients having medial wall and floor decompressed all had worse diplopia (5 5 ), those with medial and lateral wall worsened in 4 10 cases and improved in 1 10 , and those having all three walls decompressed had no cases of worsening diplopia and 1 6 improved. All patients with symptomatic diplopia achieved binocular single vision in a useful range after one and sometimes two squint procedures. No patient lost vision as a result of the extracranial orbital decompression, but one lost vision in one eye after transfrontal decompression following failed extracranial decompression. Extracranial orbital decompression is effective in improving vision and reducing proptosis in most patients with optic neuropathy in Graves' eye disease, but induces or worsens diplopia in a high proportion of patients. The diplopia is readily correctable, and the change to decompressions that include the lateral wall may reduce the risk of postoperative diplopia.
视神经病变在一小部分格雷夫斯眼病患者中出现。它是由眼外肌增大对视神经的压迫所致，可通过皮质类固醇、放疗或手术眼眶减压进行治疗。本报告评估了由一位外科医生进行的颅外眼眶减压术对格雷夫斯眼病视神经病变的疗效。分析了21例（33只眼眶）因格雷夫斯视神经病变接受颅外眼眶减压术患者的视力、色觉变化以及眼球突出度的降低情况。术后短期内（4周），所有33只眼的视力和色觉均有改善，但4例（19%）患者的5只眼（6.6%）后来视力恶化。其余患者在随访期间（平均22个月，范围3 - 54个月）视力保持改善。眼球突出度平均降低5.0毫米（范围1 - 8毫米）。21例患者中有9例（43%）眼外肌失衡和复视加重，2例（9.5%）改善。接受内侧壁和眶底减压的患者复视均加重（5/5），接受内侧壁和外侧壁减压的患者中4/10例加重，1/10例改善，接受三壁减压的患者无复视加重病例，1/6例改善。所有有症状性复视的患者在进行一次有时两次斜视手术后，在有效范围内实现了双眼单视。没有患者因颅外眼眶减压术而失明，但1例在颅外减压失败后经额部减压，一只眼失明。颅外眼眶减压术对大多数格雷夫斯眼病视神经病变患者改善视力和降低眼球突出度有效，但在很大一部分患者中会诱发或加重复视。复视很容易矫正，采用包括外侧壁的减压术可能会降低术后复视的风险。
