Open Access Mini Review

Autoimmune Ocular Myasthenia Gravis: Diagnostic Utility of Autoantibodies to The Neuromuscular Junction in Eye Disorders

Pankaj Kumar1 and Hans Frykman2*

Department of Medicine, University of British Columbia, Vancouver, British Columbia, Canada

Corresponding Author

Received Date: September 03, 2020;  Published Date: October 23, 2020


Keywords: Myasthenia Gravis (MG), Autoantibodies (Abs), Achr, Musk, LRP4, RIPA, Cbas


Myasthenia gravis (MG) is a neuromuscular disease, mediated by autoantibodies (Abs) that targets functionally important proteins at the postsynaptic neuromuscular junction (NMJ) [1]. MG patients are typically subgrouped according to their clinical symptoms as well as serum Abs profile, which differs significantly in terms of immunopathology, and their distinct response to treatments. Although MG patients can develop a range of symptoms, however, the hallmark of the disease is the fluctuating muscle weakness which is highly variable in severity [1]. Circulating MG Abs can potentially target any skeletal muscle of the body, however, for the majority of patients, initial weakness starts with extraocular muscles (Ocular MG (OMG)), with a classic presentation of unilateral or bilateral drooping of the upper eyelid (ptosis) and rapidly progressive double vision (diplopia) [1,2]. OMG patients typically complain of weakness and heaviness around eyes that worsens as daygoes on. Patients often raise their eyebrows and chin to lift the eyelid in order to see properly. In approximately 15% of patients, the muscle weakness remains strictly ocular, however, for the majority of the patients (85%) the symptoms progress to other parts of the body including, facial, neck, bulbar and limb muscle weakness, resulting in generalized MG (GMG), which usually happens within the first 2 years of disease onset [1,3]. Respiratory muscles can also be affect ed by GMG [1]. Thus, prompt and accurate diagnosis of OMG patients is critical as the likelihood of generalization can be reduced with early interventions. Progression to GMG is unlikely if the OMG patients do not generalize within the first three years of the disease onset [2]s.

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