“…The ICA occlusion observed in the present case should be attributed to the comorbid NPSLE, while the exact underlying mechanisms of ICA occlusion in this case are unclear. Several possible pathophysiological mechanisms could be raised, such as premature atherosclerosis, thrombosis, vasculopathy, emboli, dissection of the carotid artery, and antiphospholipid syndrome [ 1 , 2 , 4 , 6 , 7 , 8 , 9 , 10 ]. There would have been atherosclerosis and thrombosis process following the chronic inflammation, and rarely, these pathological changes can result in ICA dissection [ 1 , 8 , 9 ].…”