Divergence Paresis: A Nonlocalizing Cause of Diplopia

OBJECTIVESTo determine the causes, clinical characteristics, and localizing value of divergence paresis, which is characterized by acquired and uncrossed diplopia when viewing distant targets, fusion when viewing near targets, and no limitation of ocular ductions. Controversy persists regarding the diseases underlying divergence paresis and the existence of a divergence “center.” MATERIALS AND METHODSThe charts of 15 patients with divergence paresis examined between 1983 and 1998 were reviewed. All patients underwent neuroimaging and detailed ocular motility testing, with measurement of esotropia in prism diopters in 14 patients. RESULTSDivergence paresis in 15 patients was idiopathic in three patients, was associated with central nervous system microangiopathy or infarct in seven patients, and clivus lymphoma, chronic lymphocytic leukemia with sinusitis, Wernicke ophthalmoplegia, Parkinson disease, myasthenia gravis, cryptic cerebellar vascular malformation, and childhood esotropia in one patient each (two patients had two diagnoses). The mean maximum esotropia was 10.4 prism diopters, and there was no significant correlation (Fisher exact test) between the magnitude of esotropia and vasculopathic etiology or posterior fossa lesion site. Although six patients had posterior fossa disease, neuroimaging showed no common circumscribed lesion site or evidence of increased intracranial pressure. CONCLUSIONSDivergence paresis is an uncommon cause of acquired diplopia. Divergence paresis is associated with diverse central nervous system diseases and can be mimicked by myasthenia. The absence of a single consistent lesion in our study, which is the largest reported series, suggests that divergence paresis is a nonlocalizing cause of horizontal diplopia and that multiple or diffusely distributed neural structures may govern divergence. Alternatively, elusive divergence “centers” may not exist, and divergence paresis may arise from impaired inhibition or from defective passive antagonism of orbital structures to convergence.