Long-term alcohol use confers neurochemical changes in response to alcohol's exogenous inhibitory effects. Downregulation and decreased sensitivity of γ-aminobutyric acid receptors render benzodiazepines less effective at controlling psychomotor agitation. Propofol has been reported to have successfully relieved alcohol withdrawal syndrome (AWS) symptoms in part because of activation of γ-aminobutyric acid channels in combination with antagonism of excitatory amino acids such as N-methyl-D-aspartate. Successful use of propofol in refractory AWS in patients with endotracheal intubation and mechanical ventilation has been reported. We present a case of resolution of AWS symptoms in a benzodiazepine-refractory, nonintubated, non-mechanically ventilated alcohol withdrawal patient with low-dose, continuous-infusion propofol.