If MG is confined to the ocular muscles for more than 3 years, there is a 94% likelihood that the symptoms will not worsen or generalize.Aside from asymmetric ptosis (which becomes worse with fatigue, sustained upgaze, and at the end of the day) and variable limitation of extraocular muscles/diplopia, other clinical signs of ocular MG include gaze-evoked nystagmus (rapid, involuntary, oscillatory motion of the eyeball) and Cogan’s lid twitch (upper lid twitch present when patient looks straight ahead after looking down for 10–15 seconds). Pathophysiology
Normally, muscle contraction is a result of electrical signals sent from the central nervous system to muscle fibers via nerve impulses. At the neuromuscular junction, this electrical message is converted into a chemical message as acetylcholine is released from nerve fibers and attaches to corresponding receptors on the muscle fiber. In MG, antibodies are produced that block acetylcholine receptors, preventing the molecule from binding to the receptor and leading to a breakdown in communication between the nervous system and the muscle, resulting in muscle fatigue, and sometimes paralysis. Autoantibodies against acetylcholine receptors are detectable in 70–90% of patients with generalized MG, but only 50% in ocular MG.

Predilection for eye muscles
The precise reasons for the preferential involvement of eye muscles in MG is not well understood, but there are several lines of thought. Functional hypotheses propose that although multiple muscles may be affected, a deficit may be more readily apparent in the eyes for several reasons.
Significant correlation between treatment-associated molecular changes and PASI improvement was observed in the risankizumab treated patients.The efficacy, safety and tolerability was further investigated in a phase III program comprising four clinical trials which compared risankizumab to ustekinumab, adalimumab and placebo in the indication of plaque psoriasis. The results of these trials confirmed the efficacy and tolerability of risankizumab. History
Risankizumab was approved by the U.S. Food and Drug Administration (FDA) for treatment of moderate-to-severe plaque psoriasis in April 2019.The FDA approved risankizumab based on evidence primarily from five clinical trials (Trial 1/NCT0202684370, Trial 2/NCT02684357, Trial 3/NCT02672852, Trial 4/ NCT02694523 and Trial 5/NCT02054481) of 1606 patients with moderate to severe plaque psoriasis. The trials were conducted in Asia, Canada, Europe, Mexico, South America, and the United States. References
External links
"Risankizumab". Drug Information Portal. U.S. National Library of Medicine.