When the eyes are aligned they are called conjugate, and when they are not aligned they are called dysconjugate. Dysconjugate eyes may cause the symptom of diplopia (double vision). Gaze refers to movement of both eyes, and gaze paresis refers to inability to fully move both eyes in some direction. Ophthalmoparesis is a more general term that refers to eye movement weakness, which could include one or more direction of gaze paresis, or limited movement of only one eye in one or more direction. Tropia is a fixed dysconjugacy, and phoria is an intermittent dysconjugacy. These can be further specified as: exotropia/phoria (deviation of an eye laterally), esotropia/phoria (deviation of an eye medially), hypertropia/phoria (deviation of an eye superiorly), or hypotropia/phoria (deviation of an eye inferiorly). Skew refers to a vertical dysconjugacy without specifying which eye is abnormal.
The pathway controlling horizontal gaze involves multiple structures. The abducens nucleus in the lower brainstem controls eye abduction by the lateral rectus muscle, and the oculomotor nucleus in the upper brainstem controls eye adduction by the medial rectus muscle. For right gaze, the frontal eye field on the left frontal lobe somehow communicates with a nucleus in the right lower brainstem, called either the horizontal gaze center or the pontine paramedian reticular formation. The anatomy of this pathway is unclear, because corticobulbar tract lesions between the frontal eye field and the horizontal gaze center usually do not cause gaze abnormalities. Neurons in the horizontal gaze center project to the nearby right abducens nucleus to synapse on lower motor neurons that project through the right abducens nerve causing right lateral rectus muscle contraction, so that the right eye abducts. Another neuron in either the right horizontal gaze center or the right abducens nucleus (there appears to be disagreement on this point, but they are physically so close that it does not really matter) sends an axon that decussates and then ascends the left brainstem in a tract called the medial longitudinal fasciculus. This axon will synapse in the left oculomotor nucleus, on lower motor neurons that project through the left oculomotor nerve causing left medial rectus muscle contraction, so that the left eye adducts. This pathway, and its pair for left gaze, controls conjugate horizontal gaze.
Because both frontal eye fields cause contralateral gaze, the eyes usually rest in primary position (straight ahead), but unilateral frontal eye field dysfunction may cause ipsilateral gaze preference, where the eyes rest in the direction ipsilateral to the lesion, and contralateral gaze paresis, where the eyes are unable to fully move in the direction contralateral to the lesion.
The pathways controlling vertical gaze are less clear, but involve a vertical gaze center in the upper brainstem, composed of several nuclei near the oculomotor nucleus. This area appears to receive axons from multiple areas of the cerebral cortex, and projects to the oculomotor and trochlear nuclei to cause conjugate vertical gaze. This area, or an adjacent area, also appears to mediate convergence (bilateral eye adduction) for visual fixation on near objects. Convergence is the only normal dysconjugate eye movement.
All of the nuclei involved in eye movements also receive axons from the vestibular nuclei via the medial longitudinal fasciculus. These connections are involved in reflexive eye movements in response to head movements, which is called the vestibulocular reflex. This reflex allows the eyes to remain fixed on an object of interest when the head is moving, such as during walking. Dysfunction of this reflex is probably the cause of nystagmus with abnormalities of vestibular pathways.