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DVD remains a moving target!
Editorial DVD Remains a Moving Target! Michael C. Brodsky, MD
D
issociated vertical divergence (DVD) is an ocularmotor phenomenon that is observed in early-onset strabismus and that, until recently, has remained inexplicable. I have proposed that DVD is a dorsal light reflex that emerges in humans when early-onset strabismus precludes the development of normal binocular vision.1 This hypothesis is based on physiologic studies that show that unequal light input to the 2 eyes of a vertically restrained fish produces a vertical divergence of the eyes, with depression of the eye that has greater visual input and elevation of the eye that has lesser visual input.2 In unrestrained fish, unequal visual input induces a body tilt in the roll (frontal) plane toward the side with greater input (ie, a dorsal light reflex).3 Land-based animals cannot tilt in space without falling; therefore, a body tilt in aquatic animals is supplanted by a head tilt in humans. Because humans have frontally placed eyes, ocular rotation in the roll plane corresponds to a cyclovertical movement in which the eye with lesser visual input elevates and the eye with greater visual input is used for fixation.1 Three-dimensional scleral search coil recordings have shown that DVD consists of a cyclovertical vergence movement of both eyes, followed by a vertical movement of both eyes that reestablishes fixation with the lowest eye.4,5 These prominent torsional movements implicate the oblique muscles as the primary activators of DVD,4-5 as predicted long ago by Guyton and Kirkham.6 For example, in DVD with hyperdeviation of the left eye, simultaneous innervation to the right superior oblique and the left inferior oblique muscles create a cyclovertical divergence of the eyes. When this occurs, vertical stabilization of the lower right eye necessitates upward fixational innervation to counteract the infraducting action of the superior oblique muscle. This conjugate fixational innervation to the superior rectus and inferior oblique muscles of both eyes stabilizes the right eye and actively drives the hyperdeviation in the left eye. Because both eyes are innervated simultaneously to produce this dissociated movement, one should not refer to the elevating eye as the “affected eye” or “the eye with DVD.”
From the University of Arkansas for Medical Sciences, Little Rock, Arkansas. Supported in part by a grant from Research to Prevent Blindness, Inc. Reprint requests: Michael C. Brodsky, MD, Arkansas Children’s Hospital, 800 Marshall, Little Rock, AR 72202. J AAPOS 1999;3:325-7. Copyright © 1999 by the American Journal for Pediatric Ophthalmology and Strabismus. 1091-8531/99 $8.00 + 0 75/1/99183
Journal of AAPOS
The superimposition of DVD on the static and dynamic innervational derangements associated with congenital esotropia expands its clinical expression to produce the following signs: 1. Variable torsional component. The variable torsional component of DVD can be explained by considering the baseline torsional position of the eyes. von Noorden7 has observed that when DVD is accompanied by “true” inferior oblique muscle overaction, the dynamic intorsion of the deviated eye is absent as it returns to primary position. Conversely, I have observed that patients with DVD and superior oblique muscle overaction often have a prominent torsional component that may exceed the vertical component of the deviation.8 These observations suggest that the torsional amplitude of DVD is defined by the disparity between the extorsional position of the hyperdeviated eye during inferior oblique muscle activation, and the baseline torsional position of the globe. When the baseline position is one of extorsion (as occurs with inferior oblique muscle overaction),9 this torsional disparity is minimal and the corresponding torsional movement is small as the extorted eye ascends and descends to an extorted position. When the baseline position of the globes is one of intorsion (as occurs with superior oblique muscle overaction), there is a large torsional disparity that is manifested as a prominent torsional movement as the eye ascends and descends. 2. Pseudoinferior oblique muscle overaction. DVD can manifest in adduction and thereby simulate inferior oblique muscle overaction. This finding is classically attributed to occlusion of the adducting eye by the nose.7,10 However, the notion that the child’s nose acts as an occluder is dubious, because young children have a poorly formed nasal bridge. Furthermore, alternate cover testing in lateral gaze (which can only be obtained when no occlusion is present) confirms that the adducting eye is elevated when the abducting eye is fixating in DVD. It has been my observation that spontaneous hyperdeviation of the adducting eye in DVD begins as the eye rotates into the vertical field of action of the inferior oblique muscle, suggesting that paroxysmal activation of the inferior oblique muscle can excessively elevate the adducted eye. As the eye moves into adduction, the increasing vertical action of the inferior oblique muscle explains how
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326 Brodsky DVD can manifest primarily in adduction in the absence of true inferior oblique muscle overaction (ie, without hypotropia of the abducting eye, a V pattern, or fundus extorsion).10,11 3. Additivity with oblique muscle overaction. In children with early-onset esotropia, DVD often coexists with oblique muscle overaction.7,10-12 Whereas DVD is caused by paroxysmal activation of the oblique muscles (with secondary fixational activation of the vertical rectus muscles), oblique muscle overaction is generally caused by sensory torsion of the globes that leads to tight oblique muscles.5,9 When both conditions are present, their additive effects determine the observed vertical deviation in lateral gaze.10,11 Although some believe that DVD is neither created nor abated by surgical weakening of the oblique muscles, the relative effects of oblique muscle surgery on the torsional and vertical components of DVD in different positions of gaze have not been measured. 4. Association with torticollis. DVD is often associated with an anomalous head tilt that may be directed toward or away from the side of the hyperdeviated eye.13-18 In some patients, head tilting may be a compensatory means of controlling the hyperdeviation. Jampolsky15,16 has characterized the head tilt pattern in DVD in which a hyperdeviation of either eye increases or becomes manifest when the head is tilted to the opposite side. This observation is now understandable (and indeed predictable) on the basis of the torsional kinematics of DVD. For example, DVD with hyperdeviation of the left eye occurs when the right superior oblique and left inferior oblique muscles receive simultaneous innervation and a secondary fixational innervation is recruited to maintain monocular fixation with the lower (and visually preferred) right eye.5 A head tilt to the right activates otolithic innervation to the right superior oblique and the left inferior oblique muscles and thereby increases the left hyperdeviation, whereas a head tilt to the left would recruit otolithic innervation to neutralize this cyclovertical divergence.19 This reasoning suggests that a head tilt to the side of the hyperdeviating eye can serve as a compensatory means of recruiting otolithic innervation to control the hyperdeviation. Other patients with DVD have a head tilt pattern characterized by a hyperdeviation that becomes manifest or increases when the head is tilted to the same side.15-18 According to Jampolsky,16 when fixation with 1 eye predominates in DVD, tonic fixational innervation to the contralateral superior rectus muscle can eventually lead to a contracture. If this contracture occurs, it can alter the head tilt response to one characteristic of superior rectus muscle contracture, with an increase in the vertical deviation on head tilt to the side of the hyperdeviating eye.16-18 When superior
Journal of AAPOS Volume 3 Number 6 December 1999
rectus muscle contracture develops, a compensatory head tilt to the opposite side is presumably used to minimize otolithic innervation to the tight superior rectus muscle, and a head tilt to the side of the higher eye will make manifest or increase a hyperdeviation.16-18 In this setting, surgical recession of a tight superior rectus muscle can reduce or eliminate the compensatory head tilt.18 Some head tilts in children with DVD are accompanied by a manifest hyperdeviation.13,14 A dorsal light reflex in humans would produce a head tilt away from the side of the hyperdeviating eye. Such a tilt would reflect a central vision-dependent tonus asymmetry19 and would potentiate the DVD. This head tilt does not exist to realign the eyes, and surgical treatment of the associated hyperdeviation should not eliminate it. 5. Relationship to latent nystagmus. Most children with congenital esotropia and DVD also have latent nystagmus.5,7,12,14,20 Guyton et al5 have proposed that DVD is a compensatory movement that damps the cyclovertical component of latent nystagmus. von Noorden has argued that this variable damping of latent nystagmus could be an effect rather than the cause of DVD.5 Pritchard21 recently found DVD in 47% of patients with intermittent exotropia, most of whom had no latent nystagmus. Latent nystagmus, like DVD, is linked to unequal visual input to the extent that occlusion, suppression, or amblyopia makes it manifest and alternate occlusion reverses its direction. In describing DVD, Bielschowsky22 noted that “. . . while this eye maintains constant fixation, the other eye, which is deviated upward behind the screen, will make at irregular intervals vertical movements of different extent. . . .” This observation correlates with eye movement recordings that show that DVD can be associated with a vertical latent nystagmus in the hyperdeviating eye.23,24 If latent nystagmus occurs because asymmetric visual input resets central vestibular tone in the yaw plane (ie, plane of rotation about an earth-vertical axis), then DVD might incorporate a similar oscillation. Alternatively, the cyclovertical divergence that occurs in DVD could translate a component of the latent nystagmus into the vertical plane, which could reduce the horizontal component and cause it to appear on eye movement recording as a vertical latent nystagmus. Ironically, these complex ocular kinematics ultimately raise basic diagnostic questions. Although the torsional component of DVD is not cosmetically problematic, what is its significance for the patient? When does it begin? Is it synonymous with the torsional nystagmus seen in uncorrected congenital esotropia? Is it associated with a shift in the subjective visual vertical? When DVD improves spontaneously, does it merely revert to a torsional component that is subclinical?
Journal of AAPOS Volume 3 Number 6 December 1999
Our fundamental treatment goals for DVD are also called into question. Is the goal of strabismus surgery simply to eliminate the vertical component of DVD? Does oblique muscle weakening selectively alter the torsional component? Can vertical rectus muscle surgery selectively reduce the vertical component of DVD at the expense of worsening the torsional component? Answers to these questions will inevitably redirect our approach to surgical treatment of DVD. In its essence, DVD is a balancing movement that uses binocular visual input to calibrate ocular motor and postural tone in the roll plane. As we undertake to recognize its subjective correlates and define its adaptational functions, we are reminded that DVD remains a moving target. References 1. Brodsky MC. Dissociated vertical divergence: a righting reflex gone wrong. Arch Ophthalmol. 1999;117:1216-22. 2. Holst E von. Über den Lichtrückenreflex bei Fische. Pubbl Staz Zool (Napoli) 1935:15:143-8. 3. Graf W, Meyer DL. Central mechanisms counteract visually induced tonus asymmetries: a study of ocular responses to unilateral illumination in goldfish. J Comp Physiol 1983;150:473-81. 4. Van Rijn LJ, Collewijn H. Eye torsion associated with disparityinduced vertical vergence in humans. Vision Res 1994;17:2307-16. 5. Guyton DL, Cheeseman EW, Ellis FJ, Straumann D, Zee DS. Dissociated vertical deviation: an exaggerated normal eye movement used to damp cyclovertical latent nystagmus. Trans Am Ophthalmol Soc 1998;96:389-429. 6. Guyton JS, Kirkham N. Ocular movement, I: mechanics, pathogenesis, and surgical treatment of alternating hypertropia (dissociated vertical divergence, double hypertropia) and some related phenomena. Am J Ophthalmol 1956;41:438-75. 7. von Noorden GK. Binocular vision and ocular motility: theory and management of strabismus, 4th ed. St Louis: Mosby–Year Book; 1990. p. 341-5.
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8. Brodsky MC. Dissociated torsional deviation. Binoc Vis Q 1999;14:6. 9. Guyton DL, Weingarten PE. Sensory torsion as the cause of primary oblique muscle overaction/underaction and A- and V-pattern strabismus. Binoc Vis Q 1994;9:209-36. 10. Wilson ME, Parks MM. Primary inferior oblique overaction in congenital esotropia, accomodative esotropia, and intermittent exotropia. Ophthalmology 1989;96:950-7. 11. McCall LC, Rosenbaum AL. Incomitant dissociated vertical divergence and superior oblique overaction. Ophthalmology 1991;98:911-8. 12. Helveston EM. Dissociated vertical deviation: a clinical and laboratory study. Trans Am Ophthalmol Soc 1980;78:734-79. 13. Lang J. Congenital convergent strabismus. Int Ophthalmol Clin 1972;4:88-92. 14. Crone RA. Alternating hyperphoria. Br J Ophthalmol 1954;38:591-604. 15. Jampolsky A. Management of vertical strabismus. In: Pediatric ophthalmology and strabismus, transactions of the New Orleans Academy of Ophthalmology. New York: Raven Press; 1986. p. 157-64. 16. Jampolsky A. A new look at the head tilt test. In Fuchs AF, Brandt TH, Büttner U, Zee DS, editors. Contemporary ocular motor and vestibular research: a tribute to David A. Robinson. Stuttgart: Springer Verlag; 1994. p. 432-9. 17. Betchel RT, Kushner BJ, Morton GV. The relationship between dissociated vertical divergence (DVD) and head tilts. J Pediatr Ophthalmol Strabismus 1996;33:303-6. 18. Santiago AP, Rosenbaum AL. Dissociated vertical deviation and head tilts. J AAPOS 1998;2:5-11. 19. Brodsky MC. Vision-dependent tonus mechanisms of torticollis: an evolutionary perspective. Am Orthop J. 1999;49:156-60. 20. Anderson JR. Latent nystagmus and occlusion hyperphoria. Am J Ophthalmol 1954;38:217-31. 21. Pritchard C. Incidence of dissociated vertical divergence in intermittent exotropia. Am Orthop J 1998;48:90-3. 22. Bielschowsky A. Disturbances of the vertical motor muscles of the eyes. Arch Ophthalmol 1938;20:175-200. 23. Irving EL, Goltz HC, Steinbach MJ, Kraft SP. Objective video eye movement recording: a useful tool in diagnosis of dissociated vertical deviation. Binoc Vis Q 1997;12:181-90. 24. Irving EL, Goltz HC, Steinbach MJ, Kraft SP. Vertical latent nystagmus component and vertical saccadic asymmetry in subjects with dissociated vertical deviation. J AAPOS 1998;2:344-50.
D
issociated vertical divergence (DVD) is an ocularmotor phenomenon that is observed in early-onset strabismus and that, until recently, has remained inexplicable. I have proposed that DVD is a dorsal light reflex that emerges in humans when early-onset strabismus precludes the development of normal binocular vision.1 This hypothesis is based on physiologic studies that show that unequal light input to the 2 eyes of a vertically restrained fish produces a vertical divergence of the eyes, with depression of the eye that has greater visual input and elevation of the eye that has lesser visual input.2 In unrestrained fish, unequal visual input induces a body tilt in the roll (frontal) plane toward the side with greater input (ie, a dorsal light reflex).3 Land-based animals cannot tilt in space without falling; therefore, a body tilt in aquatic animals is supplanted by a head tilt in humans. Because humans have frontally placed eyes, ocular rotation in the roll plane corresponds to a cyclovertical movement in which the eye with lesser visual input elevates and the eye with greater visual input is used for fixation.1 Three-dimensional scleral search coil recordings have shown that DVD consists of a cyclovertical vergence movement of both eyes, followed by a vertical movement of both eyes that reestablishes fixation with the lowest eye.4,5 These prominent torsional movements implicate the oblique muscles as the primary activators of DVD,4-5 as predicted long ago by Guyton and Kirkham.6 For example, in DVD with hyperdeviation of the left eye, simultaneous innervation to the right superior oblique and the left inferior oblique muscles create a cyclovertical divergence of the eyes. When this occurs, vertical stabilization of the lower right eye necessitates upward fixational innervation to counteract the infraducting action of the superior oblique muscle. This conjugate fixational innervation to the superior rectus and inferior oblique muscles of both eyes stabilizes the right eye and actively drives the hyperdeviation in the left eye. Because both eyes are innervated simultaneously to produce this dissociated movement, one should not refer to the elevating eye as the “affected eye” or “the eye with DVD.”
From the University of Arkansas for Medical Sciences, Little Rock, Arkansas. Supported in part by a grant from Research to Prevent Blindness, Inc. Reprint requests: Michael C. Brodsky, MD, Arkansas Children’s Hospital, 800 Marshall, Little Rock, AR 72202. J AAPOS 1999;3:325-7. Copyright © 1999 by the American Journal for Pediatric Ophthalmology and Strabismus. 1091-8531/99 $8.00 + 0 75/1/99183
Journal of AAPOS
The superimposition of DVD on the static and dynamic innervational derangements associated with congenital esotropia expands its clinical expression to produce the following signs: 1. Variable torsional component. The variable torsional component of DVD can be explained by considering the baseline torsional position of the eyes. von Noorden7 has observed that when DVD is accompanied by “true” inferior oblique muscle overaction, the dynamic intorsion of the deviated eye is absent as it returns to primary position. Conversely, I have observed that patients with DVD and superior oblique muscle overaction often have a prominent torsional component that may exceed the vertical component of the deviation.8 These observations suggest that the torsional amplitude of DVD is defined by the disparity between the extorsional position of the hyperdeviated eye during inferior oblique muscle activation, and the baseline torsional position of the globe. When the baseline position is one of extorsion (as occurs with inferior oblique muscle overaction),9 this torsional disparity is minimal and the corresponding torsional movement is small as the extorted eye ascends and descends to an extorted position. When the baseline position of the globes is one of intorsion (as occurs with superior oblique muscle overaction), there is a large torsional disparity that is manifested as a prominent torsional movement as the eye ascends and descends. 2. Pseudoinferior oblique muscle overaction. DVD can manifest in adduction and thereby simulate inferior oblique muscle overaction. This finding is classically attributed to occlusion of the adducting eye by the nose.7,10 However, the notion that the child’s nose acts as an occluder is dubious, because young children have a poorly formed nasal bridge. Furthermore, alternate cover testing in lateral gaze (which can only be obtained when no occlusion is present) confirms that the adducting eye is elevated when the abducting eye is fixating in DVD. It has been my observation that spontaneous hyperdeviation of the adducting eye in DVD begins as the eye rotates into the vertical field of action of the inferior oblique muscle, suggesting that paroxysmal activation of the inferior oblique muscle can excessively elevate the adducted eye. As the eye moves into adduction, the increasing vertical action of the inferior oblique muscle explains how
December 1999
325
326 Brodsky DVD can manifest primarily in adduction in the absence of true inferior oblique muscle overaction (ie, without hypotropia of the abducting eye, a V pattern, or fundus extorsion).10,11 3. Additivity with oblique muscle overaction. In children with early-onset esotropia, DVD often coexists with oblique muscle overaction.7,10-12 Whereas DVD is caused by paroxysmal activation of the oblique muscles (with secondary fixational activation of the vertical rectus muscles), oblique muscle overaction is generally caused by sensory torsion of the globes that leads to tight oblique muscles.5,9 When both conditions are present, their additive effects determine the observed vertical deviation in lateral gaze.10,11 Although some believe that DVD is neither created nor abated by surgical weakening of the oblique muscles, the relative effects of oblique muscle surgery on the torsional and vertical components of DVD in different positions of gaze have not been measured. 4. Association with torticollis. DVD is often associated with an anomalous head tilt that may be directed toward or away from the side of the hyperdeviated eye.13-18 In some patients, head tilting may be a compensatory means of controlling the hyperdeviation. Jampolsky15,16 has characterized the head tilt pattern in DVD in which a hyperdeviation of either eye increases or becomes manifest when the head is tilted to the opposite side. This observation is now understandable (and indeed predictable) on the basis of the torsional kinematics of DVD. For example, DVD with hyperdeviation of the left eye occurs when the right superior oblique and left inferior oblique muscles receive simultaneous innervation and a secondary fixational innervation is recruited to maintain monocular fixation with the lower (and visually preferred) right eye.5 A head tilt to the right activates otolithic innervation to the right superior oblique and the left inferior oblique muscles and thereby increases the left hyperdeviation, whereas a head tilt to the left would recruit otolithic innervation to neutralize this cyclovertical divergence.19 This reasoning suggests that a head tilt to the side of the hyperdeviating eye can serve as a compensatory means of recruiting otolithic innervation to control the hyperdeviation. Other patients with DVD have a head tilt pattern characterized by a hyperdeviation that becomes manifest or increases when the head is tilted to the same side.15-18 According to Jampolsky,16 when fixation with 1 eye predominates in DVD, tonic fixational innervation to the contralateral superior rectus muscle can eventually lead to a contracture. If this contracture occurs, it can alter the head tilt response to one characteristic of superior rectus muscle contracture, with an increase in the vertical deviation on head tilt to the side of the hyperdeviating eye.16-18 When superior
Journal of AAPOS Volume 3 Number 6 December 1999
rectus muscle contracture develops, a compensatory head tilt to the opposite side is presumably used to minimize otolithic innervation to the tight superior rectus muscle, and a head tilt to the side of the higher eye will make manifest or increase a hyperdeviation.16-18 In this setting, surgical recession of a tight superior rectus muscle can reduce or eliminate the compensatory head tilt.18 Some head tilts in children with DVD are accompanied by a manifest hyperdeviation.13,14 A dorsal light reflex in humans would produce a head tilt away from the side of the hyperdeviating eye. Such a tilt would reflect a central vision-dependent tonus asymmetry19 and would potentiate the DVD. This head tilt does not exist to realign the eyes, and surgical treatment of the associated hyperdeviation should not eliminate it. 5. Relationship to latent nystagmus. Most children with congenital esotropia and DVD also have latent nystagmus.5,7,12,14,20 Guyton et al5 have proposed that DVD is a compensatory movement that damps the cyclovertical component of latent nystagmus. von Noorden has argued that this variable damping of latent nystagmus could be an effect rather than the cause of DVD.5 Pritchard21 recently found DVD in 47% of patients with intermittent exotropia, most of whom had no latent nystagmus. Latent nystagmus, like DVD, is linked to unequal visual input to the extent that occlusion, suppression, or amblyopia makes it manifest and alternate occlusion reverses its direction. In describing DVD, Bielschowsky22 noted that “. . . while this eye maintains constant fixation, the other eye, which is deviated upward behind the screen, will make at irregular intervals vertical movements of different extent. . . .” This observation correlates with eye movement recordings that show that DVD can be associated with a vertical latent nystagmus in the hyperdeviating eye.23,24 If latent nystagmus occurs because asymmetric visual input resets central vestibular tone in the yaw plane (ie, plane of rotation about an earth-vertical axis), then DVD might incorporate a similar oscillation. Alternatively, the cyclovertical divergence that occurs in DVD could translate a component of the latent nystagmus into the vertical plane, which could reduce the horizontal component and cause it to appear on eye movement recording as a vertical latent nystagmus. Ironically, these complex ocular kinematics ultimately raise basic diagnostic questions. Although the torsional component of DVD is not cosmetically problematic, what is its significance for the patient? When does it begin? Is it synonymous with the torsional nystagmus seen in uncorrected congenital esotropia? Is it associated with a shift in the subjective visual vertical? When DVD improves spontaneously, does it merely revert to a torsional component that is subclinical?
Journal of AAPOS Volume 3 Number 6 December 1999
Our fundamental treatment goals for DVD are also called into question. Is the goal of strabismus surgery simply to eliminate the vertical component of DVD? Does oblique muscle weakening selectively alter the torsional component? Can vertical rectus muscle surgery selectively reduce the vertical component of DVD at the expense of worsening the torsional component? Answers to these questions will inevitably redirect our approach to surgical treatment of DVD. In its essence, DVD is a balancing movement that uses binocular visual input to calibrate ocular motor and postural tone in the roll plane. As we undertake to recognize its subjective correlates and define its adaptational functions, we are reminded that DVD remains a moving target. References 1. Brodsky MC. Dissociated vertical divergence: a righting reflex gone wrong. Arch Ophthalmol. 1999;117:1216-22. 2. Holst E von. Über den Lichtrückenreflex bei Fische. Pubbl Staz Zool (Napoli) 1935:15:143-8. 3. Graf W, Meyer DL. Central mechanisms counteract visually induced tonus asymmetries: a study of ocular responses to unilateral illumination in goldfish. J Comp Physiol 1983;150:473-81. 4. Van Rijn LJ, Collewijn H. Eye torsion associated with disparityinduced vertical vergence in humans. Vision Res 1994;17:2307-16. 5. Guyton DL, Cheeseman EW, Ellis FJ, Straumann D, Zee DS. Dissociated vertical deviation: an exaggerated normal eye movement used to damp cyclovertical latent nystagmus. Trans Am Ophthalmol Soc 1998;96:389-429. 6. Guyton JS, Kirkham N. Ocular movement, I: mechanics, pathogenesis, and surgical treatment of alternating hypertropia (dissociated vertical divergence, double hypertropia) and some related phenomena. Am J Ophthalmol 1956;41:438-75. 7. von Noorden GK. Binocular vision and ocular motility: theory and management of strabismus, 4th ed. St Louis: Mosby–Year Book; 1990. p. 341-5.
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8. Brodsky MC. Dissociated torsional deviation. Binoc Vis Q 1999;14:6. 9. Guyton DL, Weingarten PE. Sensory torsion as the cause of primary oblique muscle overaction/underaction and A- and V-pattern strabismus. Binoc Vis Q 1994;9:209-36. 10. Wilson ME, Parks MM. Primary inferior oblique overaction in congenital esotropia, accomodative esotropia, and intermittent exotropia. Ophthalmology 1989;96:950-7. 11. McCall LC, Rosenbaum AL. Incomitant dissociated vertical divergence and superior oblique overaction. Ophthalmology 1991;98:911-8. 12. Helveston EM. Dissociated vertical deviation: a clinical and laboratory study. Trans Am Ophthalmol Soc 1980;78:734-79. 13. Lang J. Congenital convergent strabismus. Int Ophthalmol Clin 1972;4:88-92. 14. Crone RA. Alternating hyperphoria. Br J Ophthalmol 1954;38:591-604. 15. Jampolsky A. Management of vertical strabismus. In: Pediatric ophthalmology and strabismus, transactions of the New Orleans Academy of Ophthalmology. New York: Raven Press; 1986. p. 157-64. 16. Jampolsky A. A new look at the head tilt test. In Fuchs AF, Brandt TH, Büttner U, Zee DS, editors. Contemporary ocular motor and vestibular research: a tribute to David A. Robinson. Stuttgart: Springer Verlag; 1994. p. 432-9. 17. Betchel RT, Kushner BJ, Morton GV. The relationship between dissociated vertical divergence (DVD) and head tilts. J Pediatr Ophthalmol Strabismus 1996;33:303-6. 18. Santiago AP, Rosenbaum AL. Dissociated vertical deviation and head tilts. J AAPOS 1998;2:5-11. 19. Brodsky MC. Vision-dependent tonus mechanisms of torticollis: an evolutionary perspective. Am Orthop J. 1999;49:156-60. 20. Anderson JR. Latent nystagmus and occlusion hyperphoria. Am J Ophthalmol 1954;38:217-31. 21. Pritchard C. Incidence of dissociated vertical divergence in intermittent exotropia. Am Orthop J 1998;48:90-3. 22. Bielschowsky A. Disturbances of the vertical motor muscles of the eyes. Arch Ophthalmol 1938;20:175-200. 23. Irving EL, Goltz HC, Steinbach MJ, Kraft SP. Objective video eye movement recording: a useful tool in diagnosis of dissociated vertical deviation. Binoc Vis Q 1997;12:181-90. 24. Irving EL, Goltz HC, Steinbach MJ, Kraft SP. Vertical latent nystagmus component and vertical saccadic asymmetry in subjects with dissociated vertical deviation. J AAPOS 1998;2:344-50.