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This review is organized according to the two most easily recognizable phases in the evolution of facial paralysis: (1) Just after presentation of facial palsy, patients may exhibit an increase in their spontaneous blinking rate as well as a sustained low\u2010level contraction of the muscles of the nonparalyzed side, occasionally leading to blepharospasm\u2010like muscle activity. This finding may be due to an increase in the excitability of facial motoneurons and brainstem interneurons mediating trigeminofacial reflexes. (2) If axonal damage has occurred, axonal regeneration beginning at approximately 3 months after the lesion leads inevitably to clinically evident or subclinical hyperactivity of the previously paralyzed hemifacial muscles. The full\u2010blown postparalytic facial syndrome consists of synkinesis, myokymia, and unwanted hemifacial mass contractions accompanying normal facial movements. The syndrome has probably multiple pathophysiological mechanisms, including abnormal axonal branching after aberrant axonal regeneration and enhanced facial motoneuronal excitability. Although the syndrome is relieved with local injections of botulinum toxin, fear of such uncomfortable contractions may lead the patients to avoid certain facial movements, with the implications that this behavior might have on their emotional expressions. \u00a9 2003 Movement Disorder Society<\/jats:p>","DOI":"10.1002\/mds.10605","type":"journal-article","created":{"date-parts":[[2003,12,10]],"date-time":"2003-12-10T05:00:27Z","timestamp":1071032427000},"page":"1424-1435","source":"Crossref","is-referenced-by-count":83,"title":["Movement disorders in patients with peripheral facial 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