Timothy C. Hain, MD Page last modified: May 12, 2018
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This page is written to provide a background for the individual who is might have visual vertigo. It mainly discusses how the eyes work together, but also attempts to discuss interaction with the inner ear. It is based on a Hain and Zee (1989), with updates.
Vergence moves the eyes in opposite directions to enable binocular fixation of a single object. It permits stereopsis and prevents diplopia. Horizontal vergence movements must be incorporated into virtually all binocular ocular motor activity.
Maddox originally postulated that there were four input stimuli to the horizontal vergence system including retinal disparity, blur, awareness of nearness (proximal vergence), and vergence tone (1893). Recent workers have suggested that other cues such as change in size or "looming" (Erkelens and Regan, 1986). The relative importance of these input stimuli for normal activity is still debated. Maddox believed that accommodation was the primary stimulus to vergence. Recently awareness of nearness has been proposed to be the primary input (Wick and Bedell, 1989). However, others have argued convincingly that disparity is the most important stimulus to ocular alignment (Miles et al, 1987, Schor et al, 1986, Judge and Miles, 1985). In any case, under normal circumstances these inputs interact to elicit the appropriate vergence movement.
Vergence is one part of a group of linked motor responses called the near triad. A second component of the near triad is accommodation which is a change in the shape of the lens of the eye. When the lens is focused for infinity, the lens is stretched by its attachments. To focus on close objects, the ciliary muscle contracts to reduce the tension on the suspensory ligaments of the lens. The lens then becomes more spherical and is accommodated for near vision. Accommodation is measured in sphere diopters (D) that are calculated by taking 1/fixation distance in meters. Vergence is quantified in units of prism diopters which is the angle which corresponds to an apparent displacement of 1 cm at 1 meter distance.
The third component of the near triad is pupillary constriction. Although it probably plays only a minor role in focusing near objects, pupillary contraction is a useful clinical sign.
(Figure 1; From Hain and Zee, 1989).
Figure 1 shows a schematic for the horizontal vergence system. It is formulated as containing the 4 sensory inputs mentioned above, a central crosslink matrix which combines the sensory inputs and generates premotor innervation, and a set of motor outflow pathways implementing the near triad. The diagram is similar to a model proposed by Semmlow and Hung (1983). It does not contain the nonlinearities or dynamic elements needed to simulate the near response with precision, but can be used to attempt an understanding on a systems level.
The vergence system contains two closed loops which control retinal disparity and lens power. These pathways contain integrators (denoted as 1/s), so that accomodation or eye position will be held constant, even after the original stimulus that provoked a near response vanishes when the near response takes effect. Because proximity or "sense of nearness" is unaffected by vergence, it affects overall vergence control in an open-loop fashion. Tone is affected by disparity and accomodation but in a less clear-cut way and over a more prolonged time course.
As the vergence system has both multiple inputs and multiple inputs there is the possibility of cross-linking between inputs or outputs. The cross-links are represented in figure 1 in a general way by a matrix. Of the 12 possibile crosslinks that are made explicit by this formulation, two are particularly well studied. Accommodative vergence (AC) is the name given to the change in ocular alignment that occurs for a near stimulus when one eye is covered. In this situation one combines blur and proximity as an input, and measures vergence as the output. Fusional vergence is the name given to the change in alignment that occurs when a prism is placed before one eye. In this instance one holds proximity and blur constant, but alters disparity. Abnormalities in the ratio of accommodative vergence to accommodation (A) of the lens can be expressed as a ratio (AC/A) and used to infer the presence of convergence excess or insufficiency. A/CA corresponds approximately to matrix element V31 in figure 1.
The CA/C ratio similarly expresses the ratio of convergence induced accommodation to convergence. It corresponds approximately to matrix element V14 in figure 1. It is obvious from this type of a formulation that the measures of vergence that are available to clinicians probably only reflect a small subset of the internal paramaters relevant to the neural control of vergence.
Horizontal vergence movements unaccompanied by versions are characteristically slow, taking as long as one second for completion. The waveform of such movements is a decreasing velocity exponential with a time constant of about 200 msec. This observation was used to suggest that the command signal for vergence is a step change in innervation to the extraocular movements (Robinson, 1966).
However, it is peculiar that it should take so long for us to focus on a near target and other workers have observed that most vergence movements to targets that require both version and vergence can be much faster. In this instance most of the vergence is accomplished by unequal saccades rather than by slow drifts as described above (Enright, 1984). Also, recent workers have described "vergence burst neurons", which may assist in mediation of these faster changes in vergence (Mays, Porter et al, 1986).
Vertical and torsional disjunctive movements are also possible but their properties differ from those of the horizontal system. Vertical fusional movements are much slower than their horizontal equivalents taking as long as 8 seconds for completion, and are usually not evenly distributed between the two eyes (Houtman et al, 1981; Kertesz, 1983). Vertical fusion cannot usually overcome disparities of more than a degree and even then part of the fusion response (about 20%) is accomplished by sensory not motor processes. In some patients with a vertical muscle imbalance, however, and especially those with fourth nerve palsies acquired early in life, the vertical fusional range may be increased. Cyclodisparities also elicit cyclotorsional fusional movements but like vertical vergence these also are slow and of limited range though the amount of motor response is evenly distributed between the two eyes. In addition there is a strong sensory component to cyclofusion which is greatest for small disparities (Kertesz, 1983)
It is surmised that the midbrain is the final common pathway for vergence as midbrain lesions can abolish vergence and premotor neurons carrying vergence signals are found near the oculomotor nucleus complex. However the details of how information indicating that a change in vergence is required is transmitted to the midbrain are unclear. As the contraction of the medial recti that occurs during convergence is accompanied by relaxation of the lateral recti, vergence signals must also reach the abducens nuclei. However, whether these reciprocal changes in activity are mediated by oculomotor interneurons or are a direct consequence of descending information from higher centers is uncertain.
With regard to the source of vergence commands, there is evidence that striate, parietal, median temporal, and frontal cortex may all participate to some extent in either detecting disparity or formulating a vergence command. Multiple areas of cerebral cortex respond to disparity. In the striate cortex of the awake monkey, cells have been identified that are sensitive to retinal disparity (Poggio and Fisher, 1977; Poggio and Talbot, 1981). Some cells show a binocular response over a narrow depth range about the fixation point and might participate in fine tuning of vergence. Other cells respond to binocular stimulation farther away from fixation and might participate in coarser sensory input to the fusional vergence system. However, even dissimilar stimuli presented to the eye independently can initiate vergence movements (Westheimer and Mitchell, 1956). Neurons with similar properties to those in striate cortex have been reported in the middle temporal area (MT) of monkeys (Maunsell and Van Essen, 1983). Neurons that are activated during visual tracking of objects in the sagittal plane are found in the parietal lobe (Motter and Mountcastle, 1981; Sakata et al, 1983).
Attempts to elicit convergence via electrical stimulation of the cortex have largely been performed in anesthetized animals. This makes it difficult to be sure that the results apply to normal awake activity because low levels of anesthetic can change stimulation-induced saccades into slow or disjunctive eye movements (Robinson and Fuchs, 1969). Nevertheless, electrical stimulation of Brodman areas 19 and 22 in the occipital cortex of monkeys produces combinations of the near triad (Jampel, 1960). In addition, stimulation of the "frontal and occipital eye fields" produced convergence movements, sometimes associated with versional movements (Jampel, 1960).
The precise route by which vergence commands reach the brainstem is unknown. The striate cortical cells which respond to disparity are most commonly encountered in layers V and VI, which project to the superior colliculus, pulvinar, and lateral geniculate (Poggio and Fischer, 1977). There is no evidence to date that the colliculus participates in the control of vergence movement and these pathways may actually influence vergence via their ascending projections to the pretectum (Benevento et al, 1977). Since lesions of the median longitudinal fasciculus often spare vergence, the major vergence inputs must pass directly to the oculomotor nucleus and not via the projections from abducens internuclear neurons that mediate adducting versional eye movements.
It appears likely that vergence commands from higher centers go first to a set of premotor neurons in the midbrain and then are distributed to the oculomotor nuclei. Figure 2 shows the neurons involved in vergence found in the monkey. They lie in two regions: one group is found in the mesencephalic reticular formation, 1-2 mm dorsal and dorsolateral to the oculomotor nucleus (Mays, 1984; Judge and Cumming, 1986), and a second group is found more dorsally, near the pretectum (Mays et al, 1986). Most of these cells discharge directly in relation to the convergence angle but are unaffected by the direction of conjugate gaze. They change their firing rate 10-30 msec before any detectable eye movements. There are also a smaller number of cells with firing rates that decrease with convergence and increase with divergence. Further studies have shown that some of the cells that appear to discharge with vergence actually discharge primarily in relation to accommodation (Judge and Cumming, 1986). The cells that do discharge specifically with vergence, however, do so equally well whether the sensory stimulus is blur or retinal disparity, suggesting that these cells are related to the motor output of the vergence system rather than to a sensory signal.
In addition to cells that discharge in relation to vergence angle there are other cells that exhibit a burst of activity, before and during convergence, that is linearly related to the velocity of the vergence movement (Mays, Porter et al., 1986). For most of these cells the number of spikes within each burst, i.e. the integral of the rate of discharge, is correlated with the amplitude of the movement. These cells have been called vergence burst neurons, analogous to saccadic burst neurons which discharge in relation to saccade velocity. Another class of cells in this region, termed vergence burst-tonic cells, combine vergence position and vergence velocity information in their output - the burst is related to vergence velocity, the tonic firing rate to vergence angle. These cells are located dorsolateral to the oculomotor nucleus.
To summarize, the premotor staging areas for vergence commands contain three types of neurons, those that discharge in relation to vergence angle, to vergence velocity, and to both. Unfortunately, there are many unanswered questions about vergence pathways. Where do higher level voluntary and proximal vergence inputs come from? How is the processing of open-loop input signals such as proximity different from closed-loop input signals such as disparity ? How do vergence commands reach both the abducens and the oculomotor neurons? (Recall that convergence requires simultaneous excitation of the medial recti and inhibition of the lateral recti, divergence the opposite.) What role do abducens and oculomotor interneurons (each of which has projections to the other nucleus) play in generating the vergence command?
The key information required to evaluate patients with potential abnormalities of vergence are measures of ocular alignment, near points of convergence and accommodation, fusional amplitude, and the AC/A ratio. With this data the clinician can attempt to separate disorders of vergence from other disorders of oculomotor alignment, disorders of convergence from disorders of divergence, and convergence or divergence excess from insufficiency syndromes.
Ocular alignment is assessed at the bedside using the cover tests or the Maddox rod. The objective is to separate comitant from noncomitant deviations , allowing for normal variants such as A and V pattern exophorias and esophorias. Noncomitant deviations are usually not due to disorders of vergence, but rather are usually due to muscle weakness.
The near point of convergence is measured with both eyes viewing using an accommodative target such as a near visual-acuity card. The nearest point at which a single image can be seen is noted in centimeters. The near point of accommodation, each eye tested separately, is also measured in centimeters, and represents the point at which a clear image begins to blur. Loss of accommodation occurs steadily throughout life.
Fusional amplitude is measured by noting the amount of prism that a subject can fuse. One method of measuring fusional amplitude is the following. The subject is seated and asked to fixate an accommodative target, at near or at distance. A rotary prism or prism bar is placed in front of one eye and base-out prism is added until the patient indicates diplopia. This is the "breakpoint". After a rest one can then measure the breakpoint for base-in prism. Von Noorden recommends measuring vertical vergence between the horizontal measurements (Von Noorden, 1980). The sum of the base-out and base-in prism that can be fused is the fusional amplitude. Convergence normally is always greater than divergence, and vertical vergence is smaller than either of the two. Horizontal vergences measured at distance are smaller than those obtained at near.
Convergence Divergence Vertical At 6 m 14.1 5.83 2.54 At 25 cm 38.2 16.47 2.57
Normal values in prism diopters from Berens et al (1927) are given above.
The AC/A ratio designates the ratio of accommodative convergence (AC) to accommodation (A). There are a number of methods available for measuring the AC/A ratio (Von Noorden, 1980). The simplest is to compare the phoria at distance and at near (33 cm). If the two measurements are approximately equal, the AC/A is said to be normal. A more precise method is the heterophoria method. One measures the deviation at distance and the deviation at 33 cm. The AC/A ratio is then determined from the equation:
AC/A = PD + -------------
where PD is the interpupillary distance in cm and dn and df refer to the deviations in prism diopters (d) at 33 cm and at distance, respectively. Note that esodeviations are conventionally taken to be positive and exodeviations to be negative. The term PD is needed to adjust for the fact that the phoria does not measure convergence, but rather is the difference between the actual convergence and the needed convergence. The denominator, is 3 sphere diopters (D) which reflects amount of accomodation needed at 33 cm.
The AC/A ratio is normally about 3.5. This means that the convergence induced by a purely accommodative stimulus is less than the 6 d/D required to fixate binocularly a near target. Hence, during binocular viewing of a close object, disparity driven vergence must also help to align the visual axes.
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 of sustained convergence 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.
Abnormalities of divergence,
Divergence insufficiency, divergence paralysis, and divergence excess, are uncommon and poorly understood entities. Divergence paralysis was first described as a clinical entity by Parinaud in 1883. Since then it has been reported with a variety of neurologic diseases, especially conditions raising the intracranial pressure such as tumor, pseudotumor, aqueductal stenosis, intracranial hematoma or head trauma (Hogg and Schoenberg, 1979; Rutkowski and Burian, 1972). Bielschowsky (1940) defined the diagnostic criteria. There is esotropia with uncrossed diplopia during attempted fixation of a distant object. Single vision is obtained during fixation of objects located at about ten to twenty inches; more proximal fixation may cause crossed diplopia (due to associated convergence insufficiency). Horizontal motion of the eyes may be normal; the diplopia is unchanged or may even disappear on lateral gaze.
Paresis of divergence must be differentiated from bilateral sixth nerve palsy, convergence spasm, and decompensated strabismus. Excluding bilateral lateral rectus palsies may be particularly difficult. Kirkham, Bird and Sanders (1972) demonstrated that saccadic velocities of the abducting eye were low in some patients with divergence paralysis, even though the range of motion was full. They hypothesized that "minimal interference of sixth nerve function by raised intracranial pressure may produce the features of divergence paralysis without other evidence of sixth nerve palsy". Whether divergence paralysis may occur in the absence of measurable saccadic slowing is uncertain.
Vergence and Nystagmus
Convergence-retraction nystagmus is the most common sort of vergence nystagmus.
This nystagmus generally does not occur spontaneously but is elicited by asking the patient to follow a hand-held drum or tape while the stripes are moving downward. Typically, slow downward following movements occur but upward quick phases are replaced by rapid convergent movements that may also retract the globe. Excessive convergence drives may appear during horizontal saccades: the abducting eye moves slower than the adducting eye. This has also been called "pseudo-abducens palsy" (Daroff and Hoyt, 1971) and often leads to an early complaint of patients with pretectal lesions: difficulty in reading caused by their slow refocussing while changing lines. A similar nystagmus was called "pretectal pseudobobbing" by Keane (1985). It differs from convergence-retraction nystagmus because it is spontaneous and convergence is accompanied by downward ocular movement.
Eye movement recordings and electromyographic studies of convergence retraction nystagmus have shown that the convergent movements are not normal vergence movements (Gay et al, 1963). In one well studied patient, they had the velocity-amplitude relationship of saccades (Ochs et al, 1979). Indeed, in many patients with convergence-retraction nystagmus, responses to conventional vergence stimuli are impaired or absent. Furthermore there is an apparent co-contraction of the extraocular muscles during the convergence-retraction jerk. Thus the normal reciprocal innervation of the agonist and antagonist has been disrupted.
Levi and associates (1988) found that normal subjects occasionally accomplish convergence with opposed adducting or abducting sacccades. In other words, there is a potential substrate for "convergence nystagmus" that can be found even in normal individuals. Convergence retraction nystagmus has been produced in the monkey by lesions of the posterior commissure (Pasik et al, 1969b). In some of these animals, voluntary vergence movements were also paralyzed (Pasik et al, 1969a).
Divergence nystagmus (i.e., nystagmus with divergent quick phases) may occur in patients with posterior fossa anomalies (e.g. Arnold-Chiari malformation) who also have downbeat nystagmus (Baloh and Spooner, 1981). Thus these patients have slow phases of nystagmus that are directed upward and inward. Divergent nystagmus has also been reported in a case of tumor involving the floor of the 4th ventricle (Cogan, 1959). Divergent nystagmus may be a manifestation of an inappropriate otolith response since normal individuals may show divergent nystagmus during forward acceleration of the head (Smith, 1985).
Repetitive divergence (nystagmus with divergent slow phases) has been reported in a patient comatose due to hepatic encephalopathy The eyes slowly diverged to extreme bilateral abduction and then rapidly returned to the primary position (Noda et al, 1987). A similar abnormality was reported in a neonate in association with abnormalities of the electroencephalogram, perhaps related to seizures (Nelson et al, 1986).
Pendular vergence nystagmus (i.e. nystagmus without out a fast phase) , mainly includes spasmus nutans, and certain forms of nystagmus seen in amblyopia and chiasmal gliomas
Some of these oscillations presumably derive from abnormalities of vergence but other anatomical substrates such as lesions close to the oculomotor nuclei or lesions in otolithic pathways may account for others.
We also do not discuss spasmus nutans or the disjunctive nystagmus associated with amblyopia or optic nerve glioma as it is unclear whether or not their disjunctive appearance derives from activation of vergence pathways. Nevertheless, given the multiple inputs and outputs of the vergence system with the potential for lesions disturbing the gain and timing of multiple signals, it is surprising that disjunctive oscillations are not more common.
Pendular vergence nystagmus occasionally occurs in association with contractions of the masticatory muscles. The entire complex is called ocular-masticatory myoarrythmia. This abnormality has only been reported in patients with Whipples' disease involving the central nervous system and may be pathognomonic for this disease (Schwartz et al, 1986). These patients also had a vertical gaze palsies in association with somnolence and intellectual deterioration. The ocular oscillations are characterized by smooth pendular convergence-divergence movements, first adducting the eyes, then turning them to the primary position, occurring at a frequency of 0.8-1.2 Hz.
Vertically disjunctive oscillations such as see-saw nystagmus and periodic skew are so commonly attributed to otolith pathway lesions. They are not reviewed here.
Finally, vergence can also interact with other forms of nystagmus.
Voluntary nystagmus, which is a saccadic nystagmus that occurs in normal individuals, can often be produced only in association with convergence (Shults et al, 1977).
Convergence usually dampens congenital nystagmus. In some instances, patients purposefully attempt to reduce their nystagmus by habitually converging creating the so-called "nystagmus blockage syndrome" (Von Noorden, 1980).
Convergence often increases downbeat nystagmus and can convert upbeat nystagmus into downbeat nystagmus. This interaction may be related to the known modulation of otolith-induced nystagmus by vergence (Viirre et al, 1986).
Rarely, acquired convergent-divergent pendular nystagmus may be induced by convergence, e.g. in multiple sclerosis (Daroff et al, 1968; Sharpe, Hoyt and Rosenberg, 1975).
Lid nystagmus may also be affected by convergence tone (Daroff et al, 1978; Sanders et al, 1968).