Blink rate is determined by many factors, including local eye irritation, the state of the corneal tear film, factors related to general visual function, the amount of general facial movement, cognitive variables, and the level of arousal. These factors appear to be mediated by several neuroanatomic structures (Table 2). The timing and the nature of the interrelationship between neuroanatomic structures during blinking remains to be determined. Dopamine is the neurotransmitter that is most strongly linked to blinking, exerting its effect on blinking primarily through the D2 receptor. The reduced rate in Parkinson's disease seems to implicate the nigrostriatal system. Perhaps efferents of the nigrostriatal system, such as those to the superior colliculus, are primarily involved, as suggested by the reduced blinking in PSP. Changes in blinking produced in the sylvian aqueduct syndrome further suggest involvement of the periaqueductal structures. At best, however, these conclusions are tentative, as the biochemical neuroanatomy will probably prove more complicated than suggested by the initial studies using the dopaminergic paradigm. Nevertheless, insofar as blink rate represents a noninvasive probe of CNS dopamine activity, the failure to associate dyskinesias (except levodopa-induced dyskinesia) with increased blinking, indicates that the pathophysiology of these conditions may not involve hyperactivity of CNS dopamine systems. Fittingly, the current clinical potential of blink rate seems maximal in parkinsonism, both to follow the severity of the illness and to monitor side effects of dopamine agonist treatment.