CLINICAL ABNORALITIES OF CONVERGENCE
Timothy C. Hain, MD Page last modified:
February 26, 2017
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Common disorders of vergence include convergence insufficiency, convergence excess, divergence insufficiency, and divergence excess. In these conditions the terms "excess" and "insufficiency" refer to high and low AC/A ratios, respectively, and convergence and divergence to the viewing distance (near or far) at which the largest phoria exists. These terms all refer to horizontal vergence -- clinical disorders due to abnormalities of vertical vergence or cyclovergence are less well characterized.
Convergence insufficiency (CI)
CI accompanied by asthenopia or diplopia at near is a common disorder among teenagers and college students. It is found as well as in individuals after head trauma (Krohel et al, 1986). Some patients are able to make the necessary eye movements to align two images but cannot blend or "lock" them. This condition is ascribed to central abnormalities in "sensory fusion" (Pratt-Johnson and Tillson, 1979). More commonly however, convergence weakness can be demonstrated by decreased fusional amplitudes and is associated with a similar degree of accommodative dysfunction. A complete convergence paralysis causes exotropia in the near position, which becomes progressively less with increasing distance.
Convergence insufficiency is not an inevitable consequence of aging and no statistical difference can be found between convergence amplitudes in healthy elderly subjects vs. younger individuals (Mellick, 1949). It must be remembered however that accommodation insufficiency does accompany increasing age, and one must take care to assess vergence using stimuli that do not require accommodation such as large targets that do not require a fine visual discrimination or the patient's own finger. In patients who can accommodate, the maximum vergence effort can usually be elicited by a near card as in this case one combines disparity, blur, and sense of nearness cues.
Many acquired neurologic disorders cause disturbances of vergence, often associated with abnormalities of vertical gaze, as was originally pointed out by Parinaud (1883). In progressive supranuclear palsy, vergence is impaired or absent. In Parkinson's disease, vergence is often poor. Presumably these disorders affect descending vergence pathways from higher centers to premotor vergence neurons.
Convergence insufficiency can also result from ocular muscle weakness due to external ophthalmoplegia, dysthyroid ophthalmopathy, myasthenia gravis, and orbital blowout fractures. Patients with congenital strabismus frequently have diminished fusional amplitudes. This may be in part due to maldevelopment of binocular fusional mechanisms, or related to an underlying disorder which caused the strabismus. Convergence insufficiency can also be induced by a variety of medications. Tranquilizers such as diazepam and anticholinergics such as atropine, tricyclic anti-depressants, anti-parkinsonian agents, and medications used to decrease bowel irritability often weaken accommodation. Treatment includes orthoptic exercises and prisms (Kroehel et al, 1986). Bilateral medial rectus resection surgery has been employed in intractable cases (Hermann, 1981)
Convergence spasm may be either a sign of organic lesions or a functional disorder.
The functional syndrome, spasm of the near triad is more common than organic convergence excess. Spasm of the near triad, is caused by voluntary convergence in hysterical patients. Its features are illustrated in the following case history given by Leigh and Zee (1983).
"A 20-year old woman presented to the emergency room complaining of headache and diplopia. Her headache had come on suddenly the previous evening. It had been getting worse, and on direct questioning, she agreed that it was "the worse headache of my life". Despite her pain, she remained alert and oriented. Her vital signs were normal. In the emergency room, she developed a "noticeable esotropia....her eye movements are full, but not conjugate." The patient's neck was supple and her neurologic examination was otherwise normal.
She was thought to have had a subarachnoid hemorrhage, so computed tomography and a spinal tap were performed; both were normal. Her headache persisted and the nursing staff noted that she was "unable to focus her eyes well".
When seen in consultation, she was emotionally upset. Her corrected near visual acuity was 20/30 when each eye was tested separately. Ocular ductions (movements with one eye viewing) were full. With both eyes viewing (versions) there was a characteristic limitation in movement of the abducting eye: as it crossed the midline there were shimmering, small to-and-fro movements associated with varying constriction of the pupils.
It eventually emerged that the patient had been summarily dismissed from her job the afternoon before admission."
Comment: This case history illustrates features typical of spasm of the near reflex. It is frequently misdiagnosed as bilateral 6th nerve palsy. Careful examination of the eye movements allows the diagnosis to be made. There is often a full range of movements with only one eye viewing. When both eyes are viewing, the patient limits abduction by imposing a strong convergence command ("voluntary vergence") that causes accommodation, and miosis. On lateral gaze there may be dissociated nystagmus greatest in the abducting eye. The convergence spasms typically come and go, but some patients can sustain them for long periods. They may cause the complaint of ocular pain. Rapid passive head-turns (the "dolls-head" maneuver) elicit a full range of eye movements. Treatment is best directed toward the underlying psychologic factors.
Organic causes include thalamic hemorrhage or infarcts (Fisher, 1959; Gomez et al, 1988), pituitary tumor (Dagi et al, 1987), encephalitis (Cogan, 1956), Wernicke-Korsakoff syndrome (Thompson and Lynde, 1969), occipitoatlantal instability with vertebrobasilar ischemia (Coria et al, 1982), in patients with the Chiari malformation or downbeat nystagmus (Cogan, 1955; Dagi et al, 1987), and phenytoin intoxication (Guiloff et al, 1980). In convergence excess syndromes, bilateral adduction can occur without the usually associated pupillary constriction and increased accommodation that constitutes the near triad.
There are examples of convergence excess related to sensory, central, and motor dysfunction. Convergence exess due to an abnormal sensory input can occur in hyperopia where there is increased demand for accommodation. Hyperopia causes blurred vision at near which the patient can clear by accommodating, but in consequence develops esotropia. Correction of the hyperopia by appropriate spectacles is the treatment.
Vergence excess due to an abnormal central input-output relationship is typified by patients with inappropriately large convergence for a given accommodation (high AC/A ratio). In these patients, esotropia becomes manifest only at near when accommodation is maximal. Bifocals to decrease accommodative demand or surgery are used in these patients. Anticholinergics combined with reading glasses are also used (Cogan, 1956; Dagi et al, 1987).
It is doubtful that many patients exist with convergence excess due to increased central vergence tone because in normal individuals resting ocular alignment can be readjusted in minutes. This is called phoria adaptation (Henson and North, 1980). The anatomic substrate of phoria adaptation is unknown. Whether some patients with convergence excess are unable to phoria adapt, or do adapt but to an inappropriate set point is unknown. Prisms might be the best approach to patients who cannot phoria adapt.
The last category of vergence excess is an inappropriate motor response to a normal premotor vergence signal. Accordingly, bilateral lateral rectus weakness or medial rectus restriction, divergence paresis, and decompensated strabismus must be distinguished from convergence excess. This is not vergence excess in the sense of the previous syndromes as although the eyes are converged, in these patients pupillary responses and accommodation remains normal. Examination of saccades and ocular range usually suffices to identify peripheral syndromes. Divergence paresis will be discussed subsequently. Decompensated strabismus may be diagnosed if there is a history of strabismus or other clinical signs of strabismus.
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This page is based on a a review article by Hain and Zee (1989)
February 26, 2017
, Timothy C. Hain, M.D.
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