Vergence eye movements slowly drive the eyes in opposite directions to maintain the image of an object on the fovea of both eyes as the object moves toward or away from the observer. Vergence stimuli include tonic vergence, fusional vergence, accommodative vergence, and voluntary vergence. Without innervation, the anatomy of the orbits creates a divergent misalignment of the eyes (as occurs during sleep or anesthesia). Thus, a baseline amount of tonic vergence is required to align the eyes in alert humans. Fusional vergence is driven by a disparity in the relative location of images on the retinas and realigns the lines of sight to achieve single binocular vision. Accommodative vergence is driven by retinal blur. As an object approaches the eye, retinal blur stimulates the near triad, which consists of accommodation, convergence, and pupillary constriction. Humans are also able to voluntarily stimulate the near triad (voluntary vergence). Clinically, the most important stimuli for vergence consist of retinal disparity (fusional vergence) and retinal blur (accommodative convergence, as part of the near triad).
The cerebral structures controlling vergence movements in primates are not well understood. Binocularly driven cortical cells in the occipital lobe as well as regions of the frontal, parietal, and temporal lobes innervate brainstem neurons located in the mesencephalic reticular formation just dorsal to the CN III nuclei (both directly and via the cerebellum). The mesencephalic reticular formation in turn innervates the medial rectus subnucleus of each CN III nucleus, resulting in convergence.
Convergence is tested with an accommodative target that has enough detail to require an effort to see it clearly (a penlight or finger is not adequate). Fusional and accommodative convergences are simultaneously evaluated by determining the near point of convergence (NPC). The patient fixates on a small accommodative target that is slowly brought toward the nose. The NPC is the distance at which fusion is not maintained and a divergent movement occurs. A normal NPC is approximately 3–5 cm from the nose.
Accommodative convergence is measured by the accommodative convergence/ accommodation ratio (AC/A ratio), using the lens gradient method or the heterophoria method. The lens gradient method entails performing the prism and alternate cover test to measure the ocular deviation with distance fixation. The test is repeated with a –2.00 D lens placed in front of each eye. The change in the ocular deviation after lens placement (in prism diopters) is divided by 2 to determine the AC/A ratio. A normal AC/A ratio is 3–5 Δ/D. The heterophoria method determines the AC/A ratio by the following formula:
AC/A = pupillary distance (in centimeters) + (deviation near − deviation distance)/3.
Although vergence disorders are common, they can be challenging to diagnose because convergence depends strongly on patient effort. These disorders are frequently classified as convergence insufficiency, accommodative esotropia, convergence spasm, or divergence insufficiency. Unlike other supranuclear disorders, vergence disorders usually result in diplopic symptoms.
Convergence insufficiency (CI) consists of an exodeviation that is greater at near fixation than at distance fixation. It is a common cause of eye strain, headache, blurred vision, and intermittent diplopia during near-point tasks. Patients with CI have decreased convergence amplitudes and a remote NPC, often greater than 10 cm. This condition often occurs as an isolated finding; in the absence of other neurologic symptoms, further workup is not needed. Nonetheless, many neurologic conditions are associated with CI, most notably closed head trauma and extrapyramidal disorders such as Parkinson disease and PSP. Lesions of the pretectal area may also be associated with CI; however, such lesions are typically accompanied by other features of dorsal midbrain syndrome (see the section Gaze Preference, Gaze Palsy, and Tonic Deviations). In rare instances, lesions of the midbrain (within the mesencephalic reticular formation and just dorsal to the CN III nuclei) may cause CI with normal CN III function. Treatment options include monocular occlusion, convergence exercises, prism glasses, and, in rare cases, strabismus surgery.
Excessive convergence tone is typically observed in younger patients who have an inborn convergence abnormality that manifests as an early-onset esotropia—that is, a high AC/A ratio, which produces an excessive amount of convergence for a given amount of accommodation (see BCSC Section 6, Pediatric Ophthalmology and Strabismus).
Spasm of the near reflex (convergence spasm)
Spasm of the near reflex consists of intermittent episodes of excess convergence, accommodation, and pupillary constriction. Isolated spasm of the near reflex is almost never related to organic disease. However, when convergence spasm is associated with other abnormalities, especially convergence-retraction nystagmus and reduced conjugate upgaze (as in dorsal midbrain syndrome), organic neurologic impairment is present. Acquired convergence spasm may also be observed in patients with lesions at the junction of the diencephalon and mesencephalon, thalamus, lower brainstem, and cerebellum, in association with other signs and symptoms related to lesion location (eg, thalamic esotropia due to thalamic hemorrhage, Wernicke encephalopathy, Arnold-Chiari malformation, multiple sclerosis, midbrain stroke, and phenytoin intoxication).
Divergence insufficiency (DI) is an acquired ocular misalignment defined by an esodeviation that is greater at distance than near fixation, without lateral incomitance and without abduction deficits. This disorder is usually benign and not related to neurologic dysfunction. In older patients, DI often results from involution of the connective tissue band between the superior rectus and lateral rectus muscles, causing inferior displacement of the lateral rectus muscles (ie, sagging eye syndrome). The malpositioned lateral rectus muscles have reduced abduction force, resulting in DI pattern esotropia. Rarely, DI may be caused by neurological disorders such as increased intracranial pressure, midbrain tumors, Miller Fisher syndrome, head trauma, intracranial hypotension, Arnold-Chiari malformation, and cerebellar degeneration (often with other signs of these disorders). In addition, DI can be confused with bilateral CN VI palsies, incipient unilateral CN VI palsy, or resolving CN VI palsy. Unlike DI, CN VI palsy is associated with slow abduction saccades and abduction deficits. When present as an isolated neurologic finding, DI does not require further workup, although patients should be observed for development of other neurologic signs. Treatment options include monocular occlusion, prism glasses, and strabismus surgery.
Chaudhuri Z, Demer JL. Sagging eye syndrome: connective tissue involution as a cause of horizontal and vertical strabismus in older patients. JAMA Ophthalmol. 2013;131(5): 619–625.
Jacobson DM. Divergence insufficiency revisited: natural history of idiopathic cases and neurologic associations. Arch Ophthalmol. 2000;118(9):1237–1241.
Excerpted from BCSC 2020-2021 series: Section 5 - Neuro-Ophthalmology. For more information and to purchase the entire series, please visit https://www.aao.org/bcsc.