Spontaneous and associated hyperkinetic facial movements and contracture which follow injury to the seventh cranial nerve (postparalytic hemifacial spasm) or arise without known previous injury (cryptogenic hemifacial spasm) are pathological motor phenomena not found in the distribution of other cranial or somatic motor nerves. The commonly expressed hypotheses of pathogenesis--aberrant regeneration and fiber excitation by false synapse formation (ephapses) at the site of injury--cannot account for all aspects of these phenomena or for the uniqueness of such movements to the distribution of the seventh nerve. The suggestion is made that the existing diversity of facial motor behavior, which encompasses voluntary, emotional, and especially automatic, associated, and reflexive movements, is based on a unique central organization that sets it apart from other motor groups. I hypothesize that because of this organization, the changes following axonal injury--which include selective deafferentation, glial response, axonal sprouting, functional reconnection, and hyperexcitability from dendritic spike generation--can unmask and augment automatic, associated, and reflexive movements already present in the facial neuronal network to result in facial hyperkinesia.