Drug-induced oculogyric crisis (OGC) is ordinarily discussed from a neuropharmacological point of view. It is usually controlled without difficulty by adjusting the dosage, changing the neuroleptic, or adding antiparkinson medications. When these traditional methods failed to control this symptom in the authors' patient, it became clear other models must be considered. They included conversion and psychophysiological models. The psychophysiological model proved to be most useful. It was hypothesized that a tendency for OGC was drug-induced. When combined with an increased state of emotional arousal and/or a reduction in the ability of the neuromuscular system to compensate, the OGC would occur. The increased state of emotional arousal could result from either internal or external stress. Internal stresses occurred when there was diminished external stimuli to aid repression. Fatigue was the most obvious factor altering the ability of the neuromuscular system to compensate. The psychophysiological model provided a frame-work to formulate an effective treatment program to deal with the various contributing factors.