SUBPOPULATIONS OF ACETYLCHOLINE RECEPTOR ANTIBODY -- DETERMINATION AND ITS CL1NICAL SIGNIFICANCE X-H Xu, W-Y Li, B-Y Xu, Z Wn, M-Q. Zhao, Y Li, Y-K Hu, X-G Wang, M-X Tan. Die. Neuroimmunol., Dept. NeuroL, PUMC Hosp/.tal, Beijing 100730, China Total acetylcholine receptor antibody (AChR Abt) and AChR Ab co1~taining carbohydrate moiety (AChR Abe) were determ/ned by routine ELISA (a-BuTx w~s coa:ed et firs:, then imman AC~LR, patient's sample and so on) and Con A method respectively. AChR Ab without AChR blocking AB was determined by competiflveiy inmut:sosuppr',,gsive ELISA (patient's sample was preincabated with excess of AChR which had been preinenbated with excess a-BuTx--"treated patient's sample H, the determining procedure is essentially as the same as routine ELISA for AChR Abt except treated patient'~ sample instead of patient's sample). The assay for AChR blocking Ab (AChR Abb) is not quantitative for antibody determination in sample, and is expressed as the percentage inhibition of toxin binding under the specific conditions cf the experiment, the inhibition greater than 20% was considered to be abnormal. The 3 subpopulatious of AChR Ab were determined in 50 patients with definite generalized myasthenia gravis (MGg) and in 50 normal controls (NCs--blood donors). The positive rate of AChR Abt, AChR Abb, and AChR Abc ,- ~re °00%, 75% and 40% respectively in 50 patients w;_th MGg: but they were ~egative in all NCs. Most of the patients showed positive AChR Abb were early cases with MGg. The detective rate of ACbR Ab could be raised to 96% for patients with MGg, using combination of AChR Abt and AChR Abb. Conclusions: the best detecting method for patients with MGg is combination of AChR Abt and AChR Abb, the main AChR Ab in early case with MGg is AChR Abb. AChR Abe is not very helpful for the diagnosis of MOg.

INTRATHECAL SYNTHESIS OF AChR Ab MAY CAUSE PYRAMIDAL SIGN X-H Xu, Z Wu, W-Y Gu, X-G Wang, Y-K Itu, Y Li, M Xia, M-X Tan. Department of Neurology, PUMC Hespital, Beijing 100730, China 11 myasthenie patien~ with pyramidal sign (MGPS) were treated by ihymectomy ~nd other immlmotherapy. Their pyrar~idal sigr, disappeared while their MG was improved. Thei~ VEI', BAEP and SSEP were normal. IgG in CSF in MOPS (0.0699/-0.04) was significantly ~,igi~er (p<0.05, t=2.34, df=13) than that in myasthenic patients without pyramidal sign (MGoPS) (0.025+1-0.03) and in normal controls (NC--0.0245+1-0.014). Intrathecal de nero synthesis of IgO (IgGsyn) is significantly higher (p<0.01, tffi4.14, df= 13) in MOPS (5.999+/-5) than in MOoPS (5.65+/-5.84) and NC (5.6+/-5.9). Bu*~ in IgG in serum, there is no significant difference among MOPS (10.04+/-2.49), MOoPS (11.05+/-2.5) and NC (11.31+/- 2.52); and in Albcsf/Albs, among MOPS (0.004465+/- 0.009366), MOoPS (0.0031+/-0.0025) and NC (0.00229+1-0.00185). The increased IgGcsf i n MOPS is due neither to increased lgGs nor to increased permeability of BBB, but to increased IgGsyn. In MOPS, AChR Abcst/AChR Abs (0.02155+/-0.00657) is significantly higher (p<0.01, t=1.23, df= 16). Our data are the circumstantial evidence of that AChR Absyn in.some MG patients may in turn cause the functional disturbance of cholinergic neurons in the pyramidal tract and pyramidal sign. Of course, it does not me,,qn the possibility of generalized autoimmune causing pyramidal sign could be ruled out.