A 28-year-old Japanese woman positive for TSH receptor antibody and anti-nuclear antibody complained of difficulty seeing nearby objects, severe throbbing retro-orbital pain, diplopia, blepharoptosis and upward gaze palsy when she became hypothyroid during treatment with 30 mg methylmercaptoimidazole for Graves’ hyperthyroidism. Brain magnetic resonance imaging revealed slightly swollen bilateral inferior rectus muscles, suggesting the external ophthalmoplegia due to the muscle pathology commonly encountered in Graves’ disease. The retro-orbital pain was associated with marked accommodation failure and the pupillary abnormalities. The left and/or right eye showed intermittent, asymmetric and fluctuating mydriasis, being unresponsive to ordinary light but slowly responsive to strong sunlight and slowly responsive in a dark room. During the 5-year period, mydriasis was observed 9 times on both sides, 11 times only on the right side and 4 times only on the left side. Internal ophthalmoplegia with tonic pupils and accommodation failure affecting both the pupillary sphincter muscle and ciliary muscle due to damage to the parasympathetic outflow to these muscles was suggested. Autoimmune mechanism and/or the mechanism underlying channelopathy affecting the ciliary ganglion or short ciliary nerves might be responsible for this fluctuating complication. This very rare panophthalmopathy affecting both external and internal muscles occurred when the patient was suffering from iatrogenic hypothyroidism during the 30 mg methylmercaptimidazole treatment for Graves’ disease.

一名 TSH 受体抗体和抗核抗体阳性的 28 岁日本女性，在接受 30 mg 甲基巯基咪唑治疗期间甲状腺功能减退时，主诉难以看清附近物体、严重的眶后痛、复视、上睑下垂和向上凝视麻痹。格雷夫斯甲状腺机能亢进症。脑磁共振成像显示双侧下直肌轻度肿胀，提示由于 Graves 病常见的肌肉病理导致的眼外肌麻痹。眶后疼痛与明显的调节失败和瞳孔异常有关。左眼和/或右眼出现间歇性、不对称和波动性瞳孔散大，对普通光无反应，但对强光反应缓慢，在暗室反应缓慢。5年间双侧散瞳9次，右侧11次，左侧4次。建议由于对这些肌肉的副交感神经流出的损害，导致瞳孔括约肌和睫状肌的强直性瞳孔和调节功能障碍的内部眼肌麻痹。自身免疫机制和/或影响睫状神经节或短睫状神经的通道病的潜在机制可能是造成这种波动性并发症的原因。这种影响外部和内部肌肉的非常罕见的全眼病发生在患者在 30 毫克甲基巯基咪唑治疗格雷夫斯病期间患有医源性甲状腺功能减退症时。仅右侧 11 次，仅左侧 4 次。建议由于对这些肌肉的副交感神经流出的损害，导致瞳孔括约肌和睫状肌的强直性瞳孔和调节功能障碍的内部眼肌麻痹。自身免疫机制和/或影响睫状神经节或短睫状神经的通道病的潜在机制可能是造成这种波动性并发症的原因。这种影响外部和内部肌肉的非常罕见的全眼病发生在患者在 30 毫克甲基巯基咪唑治疗格雷夫斯病期间患有医源性甲状腺功能减退症时。仅右侧 11 次，仅左侧 4 次。建议由于对这些肌肉的副交感神经流出的损害，导致瞳孔括约肌和睫状肌的强直性瞳孔和调节功能障碍的内部眼肌麻痹。自身免疫机制和/或影响睫状神经节或短睫状神经的通道病的潜在机制可能是造成这种波动性并发症的原因。这种影响外部和内部肌肉的非常罕见的全眼病发生在患者在 30 毫克甲基巯基咪唑治疗格雷夫斯病期间患有医源性甲状腺功能减退症时。建议由于对这些肌肉的副交感神经流出的损害，导致瞳孔括约肌和睫状肌的强直性瞳孔和调节功能障碍的内部眼肌麻痹。自身免疫机制和/或影响睫状神经节或短睫状神经的通道病的潜在机制可能是造成这种波动性并发症的原因。这种影响外部和内部肌肉的非常罕见的全眼病发生在患者在 30 毫克甲基巯基咪唑治疗格雷夫斯病期间患有医源性甲状腺功能减退症时。建议由于对这些肌肉的副交感神经流出的损害，导致瞳孔括约肌和睫状肌的强直性瞳孔和调节功能障碍的内部眼肌麻痹。自身免疫机制和/或影响睫状神经节或短睫状神经的通道病的潜在机制可能是造成这种波动性并发症的原因。这种影响外部和内部肌肉的非常罕见的全眼病发生在患者在 30 毫克甲基巯基咪唑治疗格雷夫斯病期间患有医源性甲状腺功能减退症时。