A case of ocular myasthenia gravis and Miller-Fisher syndrome

<jats:p>A40-year-old Chinese man with myasthenia gravis presented to the emergency department with worsening of ocular symptoms and the authors were asked for an opinion. He first presented 7 years ago with diplopia and ptosis that were responsive to edrophonium. His acetylcholine receptor antibody titre was elevated at 0.8 optical density unit (ODU) (laboratory reference <0.43 ODU), although repetitive nerve stimulation study did not produce a significant motor potential decrement. He improved with regular pyridostigmine (40 mg three times a day) but there was still mild ptosis and limited abduction of his left eye.</jats:p> <jats:p>His condition did not change in the last few years. For the current presentation, he had progressive deterioration of ocular movements over 1 week. Physical examination showed complete ophthalmoplegia bilaterally, partial ptosis of the left eye and absent pupillary light reflex in the right. Intravenous edrophonium 10 mg produced minimal improvement in right eye abduction.</jats:p> <jats:p> On further questioning, he also complained of numbness of his extremities, difficulties in fine hand functions, and unsteadiness while walking. He recalled a flu-like illness 2 weeks before the neurological symptoms. All his tendon reflexes were unobtainable and he had an ataxic gait. There was no demonstrable limb or facial weakness. Cerebrospinal fluid analysis showed increased protein concentration at 1.33 g/litre (reference range 0.12–0.6 g/litre) with total cell count of <1×10 <jats:sup>6</jats:sup> /litre. Anti-GQ1b antibody level was elevated at 43 enzyme immunoassay (EIA) Units (reference range <10 EIA). Nerve conduction studies only showed marginal reduction of F-wave persistence in the upper limbs. Magnetic resonance imaging of his brain revealed no abnormalities. </jats:p> <jats:p>Miller-Fisher syndrome (MFS) was diagnosed. He was treated with three sessions of plasmapheresis. His symptoms started to improve over the next week and he subsequently made a full clinical recovery. Moreover, he was completely free from his myasthenia gravis-related ophthalmoplegia in the following 2 months. Pyridostigmine was later recommenced when his baseline symptoms returned.</jats:p>