MLR recordings from a group of 11 high-functioning adult autistic subj
ects were compared with those from a control group of 11 normal subjec
ts. Components selected for analysis were "Pa," the maximum positivity
in the 25-40 msec latency range following stimulus onset, "P1," the m
aximum positivity within the 50-65 msec latency range, and "Nb," the m
aximum negative deflection in the 40-50 msec latency range. Statistica
l analyses of amplitude and latency data were conducted using repeated
measures analysis of variance and t test group comparisons. The Pa co
mponent showed no significant difference between autistic and control
groups. However, 2 types of abnormality were noted in the P1 component
: (1) the P1 component was significantly smaller in the autistic subje
cts at slow rates of stimulation, and (2) the autistic P1 did not chan
ge as rates of click stimulation increased from 0.5 to 10/sec, in cont
rast to the normally produced P1 decrement. Data from the P1 model in
the cat, and complementary data from the human, closely link the gener
ator substrate of the P1 potential to cholinergic components of the as
cending reticular activating system (RAS) and their thalamic target ce
lls. This is the first report of abnormal P1 responses in autism and s
trongly suggests that the RAS and/or its post-synaptic thalamic target
s may be dysfunctional in this syndrome.