Hyperphoria is a potential deviation of one eye upwards which becomes an actual deviation when the two eyes are dissociated, and which recovers when the dissociating factors are removed. In hypophoria, the deviation is downwards and, as hypophoria of one eye may be regarded as the same as hyperphoria of the other, the term ‘hypophoria’ is not in general use. Right hyperphoria is the same as left hypophoria. Occasionally, vertical heterophoria occurs in one eye only which is usually found to be amblyopic.
Hyperphoria is often present as a secondary condition, and the first step is to treat the primary cause. Any residual hyperphoria can then be managed as discussed in the next section. First, the main causes of secondary hyperphoria are summarised.
High degrees of comitant esophoria or exophoria are often accompanied by a small vertical component. In these cases, the treatment will be that which is appropriate to the primary condition, but prism relief of the hyperphoria may help.
Paretic conditions involving the elevator or depressor muscles may begin as hyperphoria and develop later into strabismus. It is important that this early sign of pathology is detected. The sudden onset of intermittent vertical diplopia and/or other symptoms, and the incomitant nature of the deviation, are the main diagnostic features. The most common cyclovertical incomitancy is superior oblique underaction, so it is important to look carefully for cyclophoria in all cases of hyperphoria and skew deviation is another differential diagnosis ( Chapter 17 ). Congenital incomitant deviations are frequently accompanied by a vertical element, but symptoms are usually absent.
Unilateral High Myopia (Heavy Eye Syndrome)
Heavy eye syndrome involves anisometropia, usually with high myopia, and hyperphoria or hypertropia. The more myopic eye is hypotropic or hypophoric. The notion that the disorder results from a ‘heavy’ myopic eye is incorrect: the cause is an abnormally low muscle path of the lateral rectus in the involved eye ( Yanoff & Duker, 1999 ). The vertical deviation ranges from 2–25Δ, although there is no correlation between the amount of anisometropia and the amount of hypotropia. Elevation of the low eye may be limited. Frequently, the head tilts to the side of the hypotropic eye.
Tilted Spectacles, Unilateral Toric Contact Lenses, and Anisometropia
If spectacles are incorrectly fitted or the frame becomes bent, a vertical prism element may be introduced which initially shows as hyperphoria. Usually, the patient adapts quite quickly to this abnormal prism and the hyperphoria reduces. When this occurs, hyperphoria will be present when the glasses are removed, or the spectacle frame straightened. This will disappear after a few days.
Toric contact lenses, most commonly disposable soft lenses, often contain a vertical prism to aid lens orientation. The strength of prism ranges from 0.52Δ to 1.15Δ which, in patients who only require monocular correction of astigmatism, might cause symptoms in sensitive patients ( Sulley, Hawke, Lorenz, Toubouti, & Olivares, 2015 ).
Corrections for anisometropia may also produce hyperphoria when the eyes are not looking through the lens optical centres. Again, adaptation to this variable prismatic effect usually occurs after a few days of using the anisometropic correction, but difficulties can arise with a correction for marked anisometropia particularly where no glasses have been worn before ( Chapter 11 ). Similarly, problems may arise if a refractive correction has changed markedly (e.g., after a cataract extraction operation). A near hyperphoria can result when multifocal spectacles are prescribed to a patient with significant anisometropia ( Chapter 11 ).
A spectacle correction which has not been correctly balanced between the two eyes may also cause hyperphoria. The same applies to uncorrected anisometropia.
Primary hyperphoria is usually considered attributable to slight anatomical misalignments of the eyes and/or orbits or muscle insertions for which there is a physiological compensation. Usually, this type of hyperphoria is less than 3Δ, and it seldom causes symptoms. It has been shown that about 98% of symptom-free people will show some degree of hyperphoria after a period of prolonged occlusion of one eye, but this disappears after a few hours when the binocular vision is restored ( Duke-Elder, 1973 ). Vertical heterophoria is not associated with the convergence system in the way that applies to horizontal heterophoria, and this further suggests that anatomical factors play a larger part in its aetiology.
However, hyperphoria can decompensate due to stress on the visual system or on the general well-being of the patient ( Chapter 4 ).
A routine eye examination should be carried out. The following points may be particularly useful in hyperphoria:
Symptoms , which can sometimes be very marked in hyperphoria, even where the degree of the heterophoria is low. They seem to occur more frequently in middle age. Frontal headache and ocular discomfort or pain are the most common symptoms. Sometimes, there is an anomalous head position, and other patients may report that vision is more comfortable if one eye is closed or occluded. An association has been suggested between hyperphoria, lower back pain, and postural stability ( Matheron & Kapoula, 2011 ), although this requires further research with larger sample sizes.
History should include questions about the history of traumatic brain injury as hyperphoria is a common finding in such cases ( Doble et al., 2010 ).
Motility test for incomitancy. The test method is described in Chapter 2 and interpretation in Chapter 17 . If the clinical results suggest an incomitancy of recent onset, the patient should be referred.
Refraction , particularly attending to the binocular balance of the spherical error between the two eyes. An unbalanced correction can sometimes be the cause of hyperphoria.
Compensation assessment , as described in Chapter 4 . The cover test and fixation disparity tests are likely to be useful.
Removal of Cause of Decompensation
Care must be taken to explore the visual working conditions and any stress or ill health that may be the cause of the decompensation. These should receive attention before other aspects of management.
In some cases, the provision of a correction for previously uncorrected refractive error will alleviate the hyperphoria without any other treatment. Balancing the refractive correction is very important in hyperphoria.
In the case of marked anisometropia where no previous correction has been worn, a partial correction of the more hypermetropic eye may prevent disturbance by vertical prismatic effects when the patient is not looking through the optical centres of the lenses. The correction is reduced in the more hypermetropic eye until the vertical heterophoria is compensated when looking through the lenses a little above or below the optical centres. This can be judged by Turville’s ‘nodding test’. Traditionally the infinity balance septum is used, and the patient asked to raise and lower their head in a slight nodding motion until the reduced sphere does not create a change of level in the two letters. Nowadays, it is more common to carry out a version of this test with the patient slowly nodding whilst viewing the vertical Mallett fixation disparity test. This correction may be increased to a fuller prescription with subsequent glasses (see also Chapter 11 ).
Eye exercises to improve the vertical fusional reserves very seldom prove successful, and do not seem to help in making the hyperphoria compensated. This is not surprising as vertical vergence may not be disparity driven ( Ygge, 2000 ) and, unlike horizontal vergence, is not influenced by emphasising the need for accuracy during vergence changes ( Stevenson, Lott, & Yang, 1997 ). However, one study (a non-controlled trial) indicated that it might be possible to change vertical fusional reserves with exercises ( Luu et al., 2000 ). When the hyperphoria is associated with horizontal heterophoria, exercises to increase the horizontal fusional reserves will often result in the vertical heterophoria becoming compensated ( Cooper, 1988a ).
Most primary hyperphoria can be readily relieved by weak vertical prisms, although randomised controlled trials are lacking ( Doble et al., 2010 ). As explained earlier, the smallest prism that will neutralise the fixation disparity with a Mallett unit can be prescribed. As noted in Chapter 8 , such vertical prism relief may also help any decompensated horizontal heterophoria ( Sheard, 1923 ; London and Wick, 1987 ).
Incomitant hyperphoria with intermittent diplopia of recent onset indicates the need for medical investigation. When there is a high degree of hyperphoria and congenital incomitancy which gives rise to intolerable symptoms, surgical relief is sometimes considered. Medical advice should be sought.
Dissociated Vertical Deviation (DVD)
This is a comparatively unusual anomaly which is also known as ‘alternating sursumduction’. Although it could be mistaken for hyperphoria, the clinical appearance is not the same. It is usually seen during the cover test. When one eye is covered with an occluder or a dark filter it slowly deviates upwards, possibly by as much as 40Δ. This differs from hyperphoria in that, whichever eye is covered, there is an upward movement of the eye behind the cover. When the cover is removed, the eye slowly recovers to the fixation position. The upward movement is not always equal in the two eyes, and sometimes it can be absent in one eye, giving the appearance of a ‘unilateral hyperphoria’. In all cases, if a neutral density filter bar is placed before the uncovered eye and the density of the filter increased, the eye under the cover will slowly move down. When the density of filter is reduced, the covered eye moves slowly up again. This is called the Bielschowsky phenomenon.
DVD is usually associated with a history of infantile esotropia syndrome (p. 227). There is sometimes a cyclorotation of the occluded eye ( Burian & von Noorden, 1974 ). Various surgical approaches have been used for DVD, but the evidence-base for these is weak ( Hatt, Wang, & Holmes, 2015 ).
When DVD exists without any other deviation or anomaly, there are usually no symptoms and no independent treatment is required. If it exists with other conditions, treatment appropriate to the primary condition can be considered. Occasionally, patients with DVD complain that one eye deviates spontaneously and this is noticed by other people. The condition rarely produces symptoms ( Mallett, 1988a ), but if the condition is cosmetically unacceptable surgery is indicated ( Kanski, 1994 ).
Many patients with long-standing cyclodeviations are asymptomatic because of sensory adaptations (Von Noorden, 1996 ). Dissociation tests reveal that it is normal to have a small degree of excyclophoria, typically 0.7–1.5 degrees ( Flodin, Pansell, Rydberg, & Andersson Grönlund, 2019 ). Clinically, cyclophoria can be readily detected with the Maddox wing test.
In heterophoric patients, a double Maddox rod test (p. 259), which dissociates the eyes, will reveal more cyclodeviation than an associated test (e.g., Mallett fixation disparity test or double Bagolini lenses; p. 259). Patients with cyclodeviations that had an onset in the first 6 years of life may develop torsional harmonious anomalous retinal correspondence (HARC) ( Chapter 12 ), and it has been suggested that this might prevent subjective torsion from being detectable even on dissociation tests, like the double Maddox rod test ( Phillips & Hunter, 1999 ).
However, the double Maddox rod test is generally accepted as the most thorough way of assessing cyclodeviations. The example shown in Fig. 9.1 indicates 10 degrees incyclophoria in the left eye. The patient is viewing (in darkness, not as shown) a spotlight and sees two horizontal red lines. If the lines are not separated (i.e., there is no hyperdeviation) a vertical prism is introduced. When the Maddox rods are both orientated at 90 degrees (not as shown), this patient reports the line seen by the left eye as tilted. The left Maddox rod had to be rotated, top inwards (in the opposite direction to the apparent tilt), to make the left eye’s image parallel with that of the right. The angle of the left rod, as seen on the trial frame axis (100 degrees), indicates the dissociated position of the left eye is 10 degrees intorted (i.e., 10 degrees incyclodeviation). As with all dissociation tests, this test gives little indication of compensation, but this can be determined with the Mallett fixation disparity test ( Chapter 4 ).