Sensory-processing dysfunctions, deficit states, and the combinations of seemingly disparate behavioral symptoms of schizophrenia are addressed with regard to a common thread--the possibility of dysfunctional processing in the thalamus. Recent views of the connectional neuroanatomy and electrical activity of thalamus are examined. A hypothesis is presented in which disturbances in the timing and phasic neuronal activity of the thalamus and, especially, its connections with other brain regions may result in many of the behavioral manifestations of schizophrenia. It is suggested that neurotransmitter or other chemical imbalances might produce such thalamic disturbances. Experimental findings of enhanced dopamine content in the thalami of schizophrenic patients are reported. Several varieties of distributional patterns of this elevated dopamine are shown and evaluated.