esotropia/oxidase

To explore the structural basis for visuomotor deficits in infantile esotropia, we examined binocular connections and metabolic activity in the primary visual cortex of two strabismic macaque monkeys. The animals were documented to have onset of natural esotropia in early infancy. Behavioral testing

To describe the structural basis for lack of binocular fusion in strabismic primates, we investigated intrinsic horizontal connections within striate cortex (area V1) of normal and strabismic, adult macaque monkeys. The strabismic animals had early-onset natural esotropia (the visual axes deviated

Previous experiments in animals have shown that early unilateral eyelid suture, a model of amblyopia induced by cataract, causes shrinkage of ocular dominance columns serving the deprived eye in the striate cortex. It is unknown whether the ocular dominance columns are affected in amblyopia produced

BACKGROUND Suppression is a major sensorial abnormality in humans and monkeys with infantile strabismus. We previously reported evidence of metabolic suppression in the visual cortex of strabismic macaques, using the mitochondrial enzyme cytochrome oxidase as an anatomic label. The purpose of this

Leigh syndrome is an inherited, progressive neurodegenerative disorder of infancy and childhood. Mutations in the nuclear SURF-1 gene are specifically associated with cytochrome C oxidase-deficient Leigh syndrome. This report describes two patients with similar facial features. One of them was a

BACKGROUND To investigate the structural basis for functional deficits in infantile strabismus we used a neuroanatomic tracer and a histochemical label to examine the primary visual cortex (area V1) of adult esotropic macaque monkeys. METHODS The animals had developed natural esotropia in the first