PURPOSE Various patterns of synkinesis have been observed following both congenital and acquired III nerve palsies. Aberrant regeneration is the most widely accepted mechanism which explains this synkinesis. Two models of aberrant regeneration have been proposed, namely central collateral axon sprouting, and misdirection of regenerating neurones at the site of nerve injury. We have studied the clinical patterns of III nerve recovery and synkinesis following III nerve palsies and relate the findings to the proposed models of synkinesis. MATERIALS AND METHODS Twelve patients with acquired and two with early onset III nerve synkinesis were reviewed. The type, rate and pattern of recovery of III nerve palsy was established from case notes. Observations and measurements of ocular motility, pupil movements, eyelid position and intraocular pressure changes were performed on each patient. Signs of contralateral synkinetic movements were also sought. RESULTS Upper lid retraction on attempted down gaze and in adduction was the most frequent synkinetic movement recorded. Observation of pupil size revealed evidence of pupillary-extraocular muscle synkinesis in all gaze positions except abduction. Similarly, intraocular pressure changes and signs of globe retraction showed widespread extraocular muscle co-contraction. Synkinetic levator innervation of extraocular muscles [i.e., LPS to MR, IR, SR] was also observed, a finding not previously reported in III nerve palsy but predicted by our model of misdirection of regenerating neurones at the site of nerve injury. There was no evidence of contralateral aberrant innervation. CONCLUSION Evidence of III nerve synkinesis in patients with III nerve palsy is widespread and the patterns of synkinesis observed were broadly similar for all patients irrespective of the aetiology. Random aberrant III nerve regeneration at the site of nerve injury best explains the patterns of synkinesis observed. Central collateral axon sprouting does not seem to play a major part in the synkinetic movements observed in acquired III nerve lesions.