Neuropathy target esterase (NTE), the putative target enzyme for organophos
phate induced delayed polyneuropathy (OPIDP), can be measured in lymphocyte
s but has rarely been assessed in acute human poisoning, Serum autoantibodi
es to nervous system proteins develop in hens poisoned with neuropathic ins
ecticides and also have not been studied after human poisoning. Serial lymp
hocyte NTE (LNTE) was measured in a 16-year-old boy after acute poisoning w
ith methamidophos for evaluation as a predictor of subsequent neuropathy. T
he profiles of serum autoantibodies to neurofilament triplet proteins, myel
in basic protein, and glial fibrillary acidic protein were measured in orde
r to characterize changes occurring as a result of OPIDP, Clinical neuropat
hy characterized by steppage gate and profound lower extremity weakness, de
creased grip and pinch strength, and decreased ulnar and absent tibial comp
ound muscle action potentials developed 2 weeks following poisoning. Sensor
y examination and nerve conduction studies were normal. On day 3 following
poisoning LNTE was depressed (77% compared with subsequent baseline enzyme
activity). Marked increases in serum immunoglobulin G (IgG) autoantibodies
to glial fibrillary acidic protein and to neurofilament 200 were observed a
fter the development of OPIDP. We conclude that inhibition of lymphocyte NT
E is predictive of subsequent OPIDP, Serum autoantibody titers to nervous s
ystem proteins may be useful markers of neuropathy.