The effects of convulsive doses of 1,1-dimethylhydrazine (UDMH) on somatosensory evoked responses were studied in cats with chronically implanted electrodes in n. ventralis posterolateralis (VPL), in primary somatic cortex (SI), and cerebellar cortex. Stimulation was either to ulnar nerve or to thalamocortical afferent fibers. EEG recordings were made from cerebral cortex and hippocampus. Intraperitoneal administration of UDMH in doses sufficient to produce generalized seizures resulted in a small, inconstant increase of the primary positive evoked response and a large, consistent increase in the primary negative response in SI. The enhancement of cortical evoked responses prior to a seizure is due to increased excitability of superficial cortical layers rather than increased afferent inflow from VPL. The first two waves of the cerebellar evoked response were unaffected by UDMH, while the third wave was depressed prior to seizures. These results are consistent with previous suggestions that UDMH and other hydrazines block production of gamma-aminobutyric acid. Paroxysmal EEG activity sometimes began in the limbic system and then spread to cerebral cortex. The large and consistent increase of SI negative response amplitude prior to seizures is a good predictor of seirure onset. Some possible applications of such a predictor for neurochemical studies of convulsive agents and in epileptic patients are discussed.