A 64-year-old man developed bilateral exotropia in the primary position after a stroke. CT revealed bilateral thalamic infarction. The saggital view of MRI disclosed that the lesion extended from the thalamus toward the rostral portion of the mesencephalon, in the territory of the paramedian thalamic arteries.
Occlusion of these arteries may cause bilateral paramedian thalamic infarction, because these arteries arise from a common trunk of the basilar communicating artery which then bifurcates. Clinically, bilateral paramedian thalamic infarction is characterized as the following triad; hypersomnolent apathy, amnestic syndrome, and vertical gaze paresis.
This patient, however, was awake and had no memory disturbances. He was unable to adduct both eyes in lateral gaze, although adduction palsy could be overcome by covering the contralateral eye. Upward gaze was completely impaired, while downward gaze was limited in both eyes. Vertical oculocephalic maneuver elicited vertical eye movement and Bell's phenomenon was preserved. Convergence was absent.
These combined supranuclear horizontal and vertical gaze palsies were attributed to the rostral mesencephalic lesion, including the rostral interstitial nucleus of the MLF, posterior commissures and interruption of cortico-pontine pathways to the paramedian pontine reticular formation (PPRF).