Pancuronium decreases the minimal alveolar anesthetic concentration (MAC) of halothane in humans, while atracurium has a metabolite, laudanosine, which is a known cerebral stimulant. To determine if these muscle relaxants significantly alter cerebral function, their effects on cerebral metabolic rate (CMRO2), cerebral blood flow (CBF), intracranial pressure (ICP), EEG, and the cerebral energy state were studied in halothane-anesthetized dogs. Group A dogs (n = 6) were maintained at 0.86% end-expired (1.0 MAC) halothane. Thereafter, a sequence of 1) pancuronium 0.1 mg.kg-1; 2) reversal of neuromuscular blockade with neostigmine plus glycopyrrolate; and 3) pancuronium 0.2 mg.kg-1produced no changes in CMRO2CBF, ICP, or EEG. Group B dogs (n = 6) also were maintained at 0.86% end-expired halothane and received the following in sequence: 1) atracurium 0.5 mg.kg-1; 2) reversal of neuromuscular blockade with neostigmine plus glycopyrrolate; 3) atracurium 1.0 mg.kg-1; and 4) atracurium 2.5 mg.kg-1. There were no changes in CMRO2, CBF, or ICP; EEG evidence of cerebral arousal occurred in only one dog with the final dose of atracurium. Group C dogs (n = 6) received tetracaine spinal anesthesia and the minimal halothane concentration (mean ± SE = 0.69 ± 0.03% end-expired) that would maintain an “anesthetic” EEG pattern. Each Group C dog received the following in sequence: 1) atracurium 1.0 mg.kg-1, and 2) atracurium 2.5 mg.kg-1. EEG evidence of cerebral arousal occurred in all six Group C dogs. Arousal was not accompanied by significant increases in CBF, CMRO2, or ICP. In Groups B and C, neuromuscular blockade always preceded arousal. Once arousal occurred, the EEG never returned to the asleep pattern. Cerebral stimulation by atracurium in the dog is modest in magnitude, is probably independent of the neuromuscular effects of the drug, and is presumed to be secondary to the metabolite laudanosine.