The diverse pathology of disease-associated TM is evident from studies showing that lupus-associated TM could be associated with central nervous system vasculitis or thrombotic infarction of the spinal cord [ 4,20-24 ]. Other studies have also described the role of autoantibodies in patients with neuromyelitis optica and recurrent TM [ 25-28 ]. Autoantibodies have been implicated in activating other components of the immune system by crossing the blood-brain barrier. The high prevalence of various autoantibodies seen in such patients suggests polyclonal derangement of the immune system. It may also be that some autoantibodies initiate a direct and selective injury of neurons that express antigens that cross-react with antibodies directed against infectious pathogens [ 4 ].