Share this article on:

Generalized Myasthenia Gravis Triggered by Cataract Surgery

Sahai-Srivastava, Soma MD; Lin, Tina C DO

Journal of Neuro-Ophthalmology: December 2007 - Volume 27 - Issue 4 - p 311-312
doi: 10.1097/WNO.0b013e31815bfd42
Letters to the Editor

Department of Neurology Los Angeles County and University of Southern California Medical Center Los Angeles, California

There have been many case reports describing onset of myasthenia gravis (MG) after cardiac surgery (1-3) and after administration of neuromuscular blocking agents in preparation for surgery (4). We describe a patient in whom severe generalized MG developed immediately after cataract surgery, requiring thymectomy and long-term immunosuppressive therapy.

A 52-year-old right-handed white man developed progressive weakness 1 day after outpatient cataract surgery on the right eye. His past medical history was significant for insulin-dependent diabetes treated with an insulin infusion pump. He had diabetic peripheral neuropathy.

Before surgery, he reported no other neurologic symptoms. The cataract surgery was uncomplicated, and routine topical analgesics had been applied on the eye before the procedure. The patient noticed nothing unusual until he removed the eye patch the day after surgery and experienced diplopia followed by bilateral ptosis. Over the next 2 weeks, he noted progressive fatigue and limb weakness. A Tensilon test performed 3 weeks after surgery showed subjective and objective strength improvement, and pyridostigmine and prednisone were started. One week later, he developed neck weakness and difficulty swallowing and was hospitalized.

On admission, he had 4 mm of ptosis bilaterally. The right eye had no movement in any direction. The left eye had 80% adduction and abduction and full vertical ductions. He was hoarse and had difficulty swallowing liquids. He had 4/5 weakness in distal and proximal muscles. His reflexes were 1+ throughout. Plantar reflexes were flexor. Sensory signs included bilateral decreased temperature, vibration, and joint position sense distal to the knees.

Results of laboratory studies were negative for acetylcholine receptor binding and blocking antibody, anti-striated muscle antibody, anti-muscle-specific tyrosine kinase (MuSK) antibody, serum cytomegalovirus (CMV) IgG and IgM, and anti-ganglioside GD1a IgG and IgM antibody. Results of a paraneoplastic workup were negative. A chest CT scan was negative for thymoma, and cerebrospinal fluid (CSF) showed a red blood cell count of 0, white blood cell count of 1, glucose of 157 mg, and protein of 89 mg.

Slow repetitive nerve stimulation (3 Hz) of the bilateral median nerve at rest and 1 minute after exercise showed compound muscle action potential (CMAP) amplitude decrements of 35% and 20%, respectively, consistent with a diagnosis of neuromuscular junction disorder. The baseline CMAP amplitude was normal without an incremental response of CMAP amplitude after 10 seconds of maximum isometric contraction, making it less likely to be a presynaptic condition. Sensory nerve action potentials were absent, indicating a polyneuropathy. Surprisingly, the patient had moderate to severely prolonged CMAP onset latencies with decreased conduction velocity in all extremities and preserved CMAP amplitudes, indicating a demyelinating polyneuropathy, which is unlike the findings seen in typical diabetic neuropathy.

The patient was treated with a course of plasmapheresis and his bulbar symptoms improved. Three months after his initial symptoms, he underwent thymectomy, with the specimen showing normal thymic tissue. With 60 mg prednisone, 80 mg pyridostigmine 3 times/day, and 250 mg mycophenolate mofetil 2 times/day, he continues to have binocular oblique diplopia that is worse in up-and-left gaze and is ambulatory with minimal assistance.

It is rare to identify a trigger for the onset of MG. With respect to cardiothoracic surgery (1-3), it has been presumed that manipulation of thymic remnants provided a trigger for autoimmune damage. It is possible that damage induced during the surgical procedure could induce a new wave of autoantibody production that is not readily subject to immune regulation in susceptible individuals.

A well-documented effect of neuromuscular blockade agents such as vecuronium, which are administered during tracheal intubation, is to unmask undiagnosed MG. The diagnosis is made when patients fail to maintain adequate spontaneous ventilation after the procedure (4,5). Subsequently, it is discovered that such patients have a history of ptosis, diplopia, dysphagia, dysarthria, fatigue, and weakness.

We postulate that the cataract surgery itself or local anesthetics triggered an autoimmune response or aggravated a preexisting subclinical MG in this patient.

Soma Sahai-Srivastava, MD

Tina C. Lin, DO

Department of Neurology, Los Angeles County and University of Southern California Medical Center Los Angeles, California

Back to Top | Article Outline


1. Resatoglu AG, Tok M, Yemisci M, et al. Autoimmune myasthenia gravis after coronary artery bypass surgery. Ann Thorac Surg 2006;81:725-6.
2. Scopetta C, Onorati P, Eusebi F, et al. Autoimmune myasthenia gravis after cardiac surgery. J Neurol Neurosurg Psychiatry 2003;74:392-3.
3. Sleeman K, Rajani R, Chabers J, et al. Autoimmune neurological disease after cardiac surgery. J Neurol Neurosurg Psychiatry 2004;75:1078-9.
4. Dunsire MF, Clarke SG, Stedmon JJ. Undiagnosed myasthenia gravis unmasked by neuromuscular blockade. Br J Anaesth 2001;86:727-30.
5. Bailey C, Menon G, Saxena H. An unusual first presentation of myasthenia gravis. Anaesthesia 2004;59:515-6.
© 2007 Lippincott Williams & Wilkins, Inc.