The mechanisms underlying pathologic pain states such as phantom limb pain remain a mystery. Observations that 1) pain may persist indefinitely; 2) trigger zones may spread to healthy parts of the body; and 3) pain may be abolished by either decreasing or increasing the sensory input cannot be explained solely in terms of peripheral causes or abnormal activity restricted to the spinal cord. This paper proposes that a portion of the brainstem reticular formation exerts a tonic inhibitory effect on transmission at all levels of the somatic projection system. The loss of sensory input after amputation would decrease the tonic inhibition and increase the probability of self-sustaining neural activity. The self-sustaining activity, its capacity to recruit adjacent neurons, and its occurrence at several transmission levels would underlie prolonged pain and spread of trigger zones. Modulation of the sensory input by anesthetic blocks or intense stimulation would abolish the self-sustaining activity and produce pain relief.