Abstract:

TDL is a brain damage characterized by a mass effect with a diameter of 2 cm or more, perilesial swelling and wing structure. TDL is sometimes observed in patients with multiple sclerosis (MS) and neuromyelitis optics (NMO). We scaned anti-normal and neuronal cell surface antibodies in patients with TDL (relapsing-remitting MS; RRMS) to determine whether the antibodies produced against Aquaporin 4 (Aqp-4) and neuronal surface antibodies (ion channels and other neuronal membrane proteins) play a role in TDL pathogenesis. In this study; 7 RRMS patients with neurological symptoms characterized by TDL (6 women, 1 men; average age±standard deviation 42.2±11. 7) and 40 RRMS that have no age-gender matching TDL, 40 autoimmune limbic encephalitis, antibodies known 25 NMO patients and 50 healthy control serums have been used. In either MS patient with or without TDL and in any healthy controls, no antibodies have been observed against any cell surface antigen that is expressed in well characterized neuronal surface antigen or neurons in cell culture. Nevertheless, as expected, various anti-normal antibodies (5 Aqp-4, 3 CASPR2, 3 LGI1, 5 NMDAR, 2 AMPAR, 2 GABABR, 5 GAD antibodies) were detected in autoimmune encephalitis and NMO patient serums. Our study has not shown a relationship between the formation of TDL and the neuronal surface antibodies. The absence of anti-normal antibodies connected to the surface antigens of the neuron membrane in our cell culture results indicates that antibodies-related mechanisms do not play a role in TDL patients.

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