- •Foreword
- •Preface
- •Contributors
- •Contents
- •1. Epidemiology of Pediatric Strabismus
- •1.1 Introduction
- •1.2 Forms of Pediatric Strabismus
- •1.2.1 Esodeviations
- •1.2.1.1 Congenital Esotropia
- •1.2.1.2 Accommodative Esotropia
- •1.2.1.3 Acquired Nonaccommodative Esotropia
- •1.2.1.4 Abnormal Central Nervous System Esotropia
- •1.2.1.5 Sensory Esotropia
- •1.2.2 Exodeviations
- •1.2.2.1 Intermittent Exotropia
- •1.2.2.2 Congenital Exotropia
- •1.2.2.4 Abnormal Central Nervous System Exotropia
- •1.2.2.5 Sensory Exotropia
- •1.2.3 Hyperdeviations
- •1.3 Strabismus and Associated Conditions
- •1.4.1 Changes in Strabismus Prevalence
- •1.4.2 Changes in Strabismus Surgery Rates
- •1.5 Worldwide Incidence and Prevalence of Childhood Strabismus
- •1.6 Incidence of Adult Strabismus
- •References
- •2.1 Binocular Alignment System
- •2.1.2 Vergence Adaptation
- •2.1.3 Muscle Length Adaptation
- •2.2 Modeling the Binocular Alignment Control System
- •2.2.1 Breakdown of the Binocular Alignment Control System
- •2.2.4 Changes in Basic Muscle Length
- •2.2.6 Evidence Against the “Final Common Pathway”
- •2.3 Changes in Strabismus
- •2.3.1 Diagnostic Occlusion: And the Hazard of Prolonged Occlusion
- •2.3.2.1 Supporting Evidence for Bilateral Feedback Control of Muscle Lengths
- •2.4 Applications of Bilateral Feedback Control to Clinical Practice and to Future Research
- •References
- •3.1 Dissociated Eye Movements
- •3.2 Tonus and its relationship to infantile esotropia
- •3.5 Pathogenetic Role of Dissociated Eye Movements in Infantile Esotropia
- •References
- •4.1 Introduction
- •4.2.1 Binocular Correspondence: Anomalous, Normal, or Both?
- •4.3 MFS with Manifest Strabismus
- •4.3.1 Esotropia is the Most Common Form of MFS
- •4.3.2 Esotropia Allows for Better Binocular Vision
- •4.3.3 Esotropia is the Most Stable Form
- •4.4 Repairing and Producing MFS
- •4.4.1 Animal Models for the Study of MFS
- •References
- •5.1 Esotropia as the Major Type of Developmental Strabismus
- •5.1.2 Early Cerebral Damage as the Major Risk Factor
- •5.1.3 Cytotoxic Insults to Cerebral Fibers
- •5.1.5 Development of Binocular Visuomotor Behavior in Normal Infants
- •5.1.6 Development of Sensorial Fusion and Stereopsis
- •5.1.7 Development of Fusional Vergence and an Innate Convergence Bias
- •5.1.8 Development of Motion Sensitivity and Conjugate Eye Tracking (Pursuit/OKN)
- •5.1.9 Development and Maldevelopment of Cortical Binocular Connections
- •5.1.10 Binocular Connections Join Monocular Compartments Within Area V1 (Striate Cortex)
- •5.1.11 Too Few Cortical Binocular Connections in Strabismic Primate
- •5.1.12 Projections from Striate Cortex (Area V1) to Extrastriate Cortex (Areas MT/MST)
- •5.1.15 Persistent Nasalward Visuomotor Biases in Strabismic Primate
- •5.1.16 Repair of Strabismic Human Infants: The Historical Controversy
- •5.1.18 Timely Restoraion of Correlated Binocular Input: The Key to Repair
- •References
- •6. Neuroanatomical Strabismus
- •6.1 General Etiologies of Strabismus
- •6.2 Extraocular Myopathy
- •6.2.1 Primary EOM Myopathy
- •6.2.2 Immune Myopathy
- •6.2.4 Neoplastic Myositis
- •6.2.5 Traumatic Myopathy
- •6.3 Congenital Pulley Heterotopy
- •6.4 Acquired Pulley Heterotopy
- •6.5 “Divergence Paralysis” Esotropia
- •6.5.1 Vertical Strabismus Due to Sagging Eye Syndrome
- •6.5.2 Postsurgical and Traumatic Pulley Heterotopy
- •6.5.3 Axial High Myopia
- •6.6 Congenital Peripheral Neuropathy: The Congenital Cranial Dysinnervation Disorders (CCDDs)
- •6.6.1 Congenital Oculomotor (CN3) Palsy
- •6.6.3 Congenital Trochlear (CN4) Palsy
- •6.6.4 Duane’s Retraction Syndrome (DRS)
- •6.6.5 Moebius Syndrome
- •6.7 Acquired Motor Neuropathy
- •6.7.1 Oculomotor Palsy
- •6.7.2 Trochlear Palsy
- •6.7.3 Abducens Palsy
- •6.7.4 Inferior Oblique (IO) Palsy
- •6.8 Central Abnormalities of Vergence and Gaze
- •6.8.1 Developmental Esotropia and Exotropia
- •6.8.2 Cerebellar Disease
- •6.8.3 Horizontal Gaze Palsy and Progressive Scoliosis
- •References
- •7.1 Congenital Cranial Dysinnervation Disorders: Facts About Ocular Motility Disorders
- •7.1.1 The Concept of CCDDs: Ocular Motility Disorders as Neurodevelopmental Defects
- •7.1.1.1 Brainstem and Cranial Nerve Development
- •7.1.1.2 Single Disorders Representing CCDDs
- •7.1.1.3 Disorders Understood as CCDDs
- •7.2 Congenital Cranial Dysinnervation Disorders: Perspectives to Understand Ocular Motility Disorders
- •7.2.1.1 Brown Syndrome
- •Motility Findings
- •Saccadic Eye Movements
- •Comorbidity
- •Epidemiologic Features
- •Laterality
- •Sex Distribution
- •Incidence
- •Heredity
- •Potential Induction of the Syndrome
- •Radiologic Findings
- •Natural Course in Brown Syndrome
- •Intra-and Postoperative Findings
- •References
- •8.1 Amblyopia
- •8.2 What Is Screening?
- •8.2.1 Screening for Amblyopia, Strabismus, and/or Refractive Errors
- •8.2.1.1 Screening for Amblyopia
- •8.2.1.2 Screening for Strabismus
- •8.2.1.3 Screening for Refractive Error
- •8.2.1.4 Screening for Other Ocular Conditions
- •8.3 Screening Tests for Amblyopia, Strabismus, and/or Refractive Error
- •8.3.1 Vision Tests
- •8.3.3 Stereoacuity
- •8.3.4 Photoscreening and/or Autorefraction
- •8.3.6 Who Should Administer the Screening Program?
- •8.4 Treatment of Amblyopia
- •8.4.1 Type of Treatment
- •8.4.2 Refractive Adaptation
- •8.4.3 Conventional Occlusion
- •8.4.4 Pharmacological Occlusion
- •8.4.5 Optical Penalization
- •8.4.7 Treatment Compliance
- •8.4.8 Other Treatment Options for Amblyopia
- •8.4.9 Recurrence of Amblyopia Following Therapy
- •8.5 Quality of Life
- •8.5.1 The Impact of Amblyopia Upon HRQoL
- •8.5.3 Reading Speed and Reading Ability in Children with Amblyopia
- •8.5.4 Impact of Amblyopia Upon Education
- •8.5.6 The Impact of Strabismus Upon HRQoL
- •8.5.7 Critique of HRQoL Issues in Amblyopia
- •8.5.8 The Impact of the Condition or the Impact of Treatment?
- •References
- •9. The Brückner Test Revisited
- •9.1 Amblyopia and Amblyogenic Disorders
- •9.1.1 Early Detection of Amblyopia
- •9.1.2 Brückner’s Original Description
- •9.2.1 Physiology
- •9.2.2 Performance
- •9.2.3 Shortcomings and Pitfalls
- •9.3.1 Physiology
- •9.3.2 Performance
- •9.3.3 Possibilities and Limitations
- •9.4.1 Physiology
- •9.4.2 Performance
- •9.4.3 Possibilities and Limitations
- •9.5 Eye Movements with Alternating Illumination of the Pupils
- •References
- •10. Amblyopia Treatment 2009
- •10.1 Amblyopia Treatment 2009
- •10.1.1 Introduction
- •10.1.2 Epidemiology
- •10.1.3 Clinical Features of Amblyopia
- •10.1.4 Diagnosis of Amblyopia
- •10.1.5 Natural History
- •10.2 Amblyopia Management
- •10.2.1 Refractive Correction
- •10.2.2 Occlusion by Patching
- •10.2.3 Pharmacological Treatment with Atropine
- •10.2.4 Pharmacological Therapy Combined with a Plano Lens
- •10.3 Other Treatment Issues
- •10.3.1 Bilateral Refractive Amblyopia
- •10.3.3 Maintenance Therapy
- •10.4 Other Treatments
- •10.4.1 Filters
- •10.4.2 Levodopa/Carbidopa Adjunctive Therapy
- •10.5 Controversy
- •10.5.1 Optic Neuropathy Rather than Amblyopia
- •References
- •11.1 Introduction
- •11.1.2 Sensory or Motor Etiology
- •11.1.4 History
- •11.1.5 Outcome Parameters
- •11.2 Outcome of Surgery in the ELISSS
- •11.2.1 Reasons for the ELISSS
- •11.2.2 Summarized Methods of the ELISSS
- •11.2.3 Summarized Results of the ELISSS
- •11.2.4 Binocular Vision at Age Six
- •11.2.5 Horizontal Angle of Strabismus at Age Six
- •11.2.6 Alignment is Associated with Binocular Vision
- •11.3 Number of Operations and Spontaneous Reduction into Microstrabismus Without Surgery
- •11.3.1 The Number of Operations Per Child and the Reoperation Rate in the ELISSS
- •11.3.2 Reported Reoperation Rates
- •11.3.3 Test-Retest Reliability Studies
- •11.3.6 Spontaneous Reduction of the Angle
- •11.3.7 Predictors of Spontaneous Reduction into Microstrabismus
- •Appendix
- •References
- •12.1 Overview
- •12.1.2 Manifest Latent Nystagmus (MLN)
- •12.1.2.1 Clinical Characteristics of Manifest Latent Nystagmus (MLN)
- •12.1.3 Congenital Periodic Alternating Nystagmus (PAN)
- •12.1.3.1 Clinical characteristics of congenital periodic alternating nystagmus
- •12.2 Compensatory Mechanisms
- •12.2.1 Dampening by Versions
- •12.2.2 Dampening by Vergence
- •12.2.3 Anomalous Head Posture (AHP)
- •12.2.3.4 Measurement of AHP
- •12.2.3.6 Testing AHP at Near
- •12.3 Treatment
- •12.3.1 Optical Treatment
- •12.3.1.1 Refractive Correction
- •12.3.1.2 Spectacles and Contact Lenses (CL)
- •12.3.1.3 Prisms
- •12.3.1.4 Low Visual Aids
- •12.3.2 Medication
- •12.3.3 Acupuncture
- •12.3.4 Biofeedback
- •12.3.6 Surgical Treatment of Congenital Nystagmus
- •12.3.6.1 Management of Horizontal AHP
- •12.3.6.2 Management of Vertical AHP
- •12.3.6.3 Management of Head Tilt
- •Retro-Equatorial Recession of Horizontal Rectus Muscles
- •The Tenotomy Procedure
- •References
- •13.1 Dissociated Deviations
- •13.2 Surgical Alternatives to Treat Patients with DVD
- •13.2.1 Symmetric DVD with Good Bilateral Visual Acuity, with No Oblique Muscles Dysfunction
- •13.2.2 Bilateral DVD with Deep Unilateral Amblyopia
- •13.2.3 DVD with Inferior Oblique Overaction (IOOA) and V Pattern
- •13.2.4 DVD with Superior Oblique Overaction (SOOA) and A Pattern
- •13.2.5 Symmetric vs. Asymmetric Surgeries for DVD
- •13.3 Dissociated Horizontal Deviation
- •13.4 Dissociated Torsional Deviation. Head tilts in patients with Dissociated Strabismus
- •13.5 Conclusions
- •References
- •14.1 Introduction
- •14.2 Clinical and Theoretical Investigations
- •References
- •15.1 General Principles of Surgical Treatment in Paralytic Strabismus
- •15.1.1 Aims of Treatment
- •15.1.2 Timing of Surgery
- •15.1.3 Preoperative Assessment
- •15.1.4 Methods of Surgical Treatment
- •15.2 Third Nerve Palsy
- •15.2.1 Complete Third Nerve Palsy
- •15.2.2 Incomplete Third Nerve Palsy
- •15.3 Fourth Nerve Palsy
- •15.4 Sixth Nerve Palsy
- •References
- •16.1 Graves Orbitopathy (GO): Pathogenesis and Clinical Signs
- •16.1.1 Graves Orbitopathy is Part of a Systemic Disease: Graves Disease (GD)
- •16.1.2 Graves Orbitopathy−Clinical Signs
- •16.1.2.1 Clinical Changes Result in Typical Symptoms
- •16.1.3 Clinical Examination of GO
- •16.1.3.1 Signs of Activity
- •16.1.3.2 Assessing Severity of GO
- •16.1.3.3 Imaging
- •16.2 Natural History
- •16.3 Treatment of GO
- •16.3.1.1 Glucocorticoid Treatment
- •16.3.1.2 Orbital Radiotherapy
- •16.3.1.3 Combined Therapy: Glucocorticoids and Orbital Radiotherapy
- •16.3.1.4 Other Immunosuppressive Treatments and New Developments
- •16.3.2 Inactive Disease Stages
- •16.3.2.1 Orbital Decompression
- •16.3.2.2 Extraocular Muscle Surgery
- •16.3.2.3 Lid Surgery
- •16.4 Thyroid Dysfunction and GO
- •16.5.1 Relationship Between Cigarette Smoking and Graves Orbitopathy
- •16.5.2 Genetic Susceptibility
- •16.6 Special Situations
- •16.6.1 Euthyroid GO
- •16.6.2 Childhood GO
- •16.6.3 GO and Diabetes
- •References
13.2 Surgical Alternatives to Treat Patients with DVD |
175 |
Summary for the clinician
■DD have three components: vertical (DVD), horizontal (DHD), and torsional (DTD) movements.
■Surgical plan requires taking into account the three components and must be tailored to treat each particular case.
13.2Surgical Alternatives to Treat Patients with DVD
Patients with DVD are usually asymptomatic, but in those cases where significant hypertropia is manifested spontaneously, or those associated with horizontal misalignment, surgical treatment should be considered knowing that the problem will not always be completely solved. DVD neither disappears nor improves over time [15]. Treatment is focused on obtaining a latent vertical deviation, only present with occlusion and to a lesser amount.
Multiple techniques have been developed for DVD treatment; the most successful ones are those that limit elevation to a greater degree.
To choose the surgical procedure, the following should be taken into account: (1) visual acuity (VA) (2) degree of non-DVD incomitance (3) oblique muscles dysfunction with A or V pattern (4) Degree of DVD symmetry.
13.2.1Symmetric DVD with Good Bilateral Visual Acuity, with No Oblique Muscles Dysfunction
The following are the most used procedures in these cases:
1.Bilaterallargesuperiorrectus(SR)recession(7–12 mm) [16–20]
2.Bilateral retro-equatorial myopexy (posterior fixation) of the SR combined with or without recession of these muscles [18, 21–24]
3.Four oblique muscles weakening procedure (superior oblique (SO) recession or tenectomy and inferior oblique (IO) recession or anterior transposition (IOAT) ) [25–28]
4.Bilateral inferior rectus (IR) resection [16, 29–32]
Large SR recession with hang-loose technique is one of the mostly used in these cases. Extensive dissection is required to clean attachments o the SR to avoid
retraction and lid fissure asymmetry. This technique may limit elevation, especially in abduction (Pseudo inferior oblique over action (IOOA) ). It should be noted that weakening of SR modifies horizontal deviation in PP, causing a 6 PD exodeviation, which should be taken into account when planning surgery.
Conventional recession (3–5 mm) of SR together with retroequatorial myopexy (12–15 mm of original insertion) is used by several author successfully [64]. The posterior fixation suture must be placed at least 20 mm, and preferably 23–25 mm from the limbus, which often is technically troublesome.
The four oblique weakening procedures proved to be an e ective technique to treat these cases. This procedure is especially useful in cases that underwent surgery on two horizontal rectus muscles in each eye and in those where operating on the SR implies a risk of anterior segment ischemia.
IR resection: Although this technique has been proposed as a primary procedure, we believe that it should be reserved for reoperation in the case of failure of SR recession. It creates a marked restriction of elevation and in some cases alterations in the lid fissures. Its additional horizontal e ect, ET on PP, should also be considered.
13.2.2Bilateral DVD with Deep Unilateral Amblyopia
DVD cases with deep monocular amblyopia are usually characterized by great asymmetry in vertical deviation, even simulating monocular DVD.
Monocular surgery is possible in patients with a deviating eye with no possibilities of becoming fixating eye due to deep amblyopia.
There are four procedures that may be used in these cases:
1.Unilateral SR recession [16, 33].
2.Unilateral inferior oblique anterior transposition (IOAT) [34, 35].
3.Unilateral IR resection or tucking [36].
4.Unilateral SR retroequatorial myopexy (posterior fixation) combined with or without recession of this muscle [18].
When unilateral SR recess is decided, the amount of such must be moderate (5–7 mm) to avoid postoperative hypotropia. This technique is chosen in cases showing comitant vertical deviation in lateroversions.
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13 Surgical Management of Dissociated Deviations |
Many authors express concern that unilateral SR recession might also result in an unacceptable postoperative hypotropia in the operated eye or in a large hypertropia in the contralateral eye, if the patient were to switch
13 fixation [20].For this reason,unilateral surgery is reserved for patients with dense amblyopia, who would have little or no chance of changing fixation after surgery. In Schwartz and Scott’s paper [33], postoperative hypotropia developed in the operated eye in 12 patients (21%). Nine of these patients had deviations less than 10 PD. In Helveston’s study [3], only 5 out of 33 patients undergoing unilateral surgical correction of DVD developed a significant deviation in the unoperated eye. Duncan and von Noorden [21] demonstrated the development of contralateral DVD postoperatively in 8/35 cases.
In those cases manifesting incomitance in lateroversions: greater hypertropia in adduction, unilateral IOAT is chosen.
Bothun and Summers [34] proved that unilateral IOAT is an e ective treatment for unilateral or markedly asymmetric DVD in patients with a strong, contralateral fixation preference. This surgery reduces IOOA, but may also cause an ipsilateral hypotropia. Ipsilateral DVD in PP decreased from a mean of 20.2 to 3.7 PD in their series. Ninety percent of the patients had an excellent postoperative result.
Goldchmit et al. [35] found that the unilateral IOAT produces a mean correction of 18.1 PD (range, 4–33) in PP, directly proportional to the size of the hypertropia before surgery.
13.2.3DVD with Inferior Oblique Overaction (IOOA) and V Pattern
When DVD is associated with IOOA, the hypertropia is greater in adduction and a V pattern may be observed. In extreme adduction, a true hypertropia may be seen in addition to the DVD.
1.Bilateral IOAT has become a popular surgical treatment for DVD with IOOA.
2.The second alternative is to perform a bilateral SR recession added to bilateral IO recession [37].
The IOAT reduces the hypertropia to an acceptable amount, and eliminates the IOOA and the V pattern with a low incidence of recurrence. However, this surgical procedure has yielded poor results in patients with asymmetric DVD and IOOA [38].
Nine out of 20 consecutive patients in our series with DVD and IOOA who underwent bilateral and symmetric
IOAT remained with postoperative vertical deviation. 10/20 of such cases had preoperative asymmetric DVD.
Although late development of a postoperative A pattern strabismus does not appear to be a problem even in patients with modest preoperative V patterns, the true incidence of the development of A pattern have not been addressed to date.
Bradley Black [39] reported that after the operation,50% of his patients had experienced neither A nor V pattern. Thirty-three percent had a V pattern averaging 4 PD (2–8 PD). Seventeen percent had a postoperative A pattern.
In our series, 4/20 patients with bilateral IOAT had postoperative A pattern (20%) over 36-month follow-up on average.
When there is a remaining postoperative vertical deviation after the IOAT, a unilateral SR recession can be performed according to the amount of vertical deviation in PP. This procedure proved e ective in obtaining good vertical alignment and has apparently given a predictable and stable result with low incidence of postoperative complications.
Several studies have attempted to obtain better surgical outcomes in asymmetric DVD with IOOA by performing asymmetric procedures. There are several surgical alternatives:
■Combined unilateral IO resection and bilateral IOAT.
■Graded bilateral IOAT (1, 2, or 3 mm anterior to the IR muscle insertion).
■Graded bilateral IOAT (1, 2, or 3 mm posterior to the IR muscle insertion).
■Symmetric and bilateral IOAT + SR recession of the most hypertropic eye.
Burke et al. [40] suggested a graded procedure to e ectively treat coexisting DVD and IOOA. It has significantly reduced the mean DVD from 13.4 PD to 6.7 PD. In cases of asymmetric DVD, unequal transpositions were performed: IOAT in the eye with the larger DVD can be placed up to 2 mm anterior to the temporal pole of the IR. The DVD remained controlled in 86% of their cases after a 2-year follow-up. The best results were obtained in those patients with a preoperative DVD of less than 15 PD.
Mims and Wood [41] also performed bilateral graded displacement of the IO tendon, attaching the muscle at a point 2–4 mm anterior to the lateral end of the IR insertion. These authors reported low residual IOOA in 11/61 patients. Only one patient required reoperation for manifest DVD.
Kratz et al. [42] compared two groups of patients with DVD who underwent standard or graded IOAT. In the graded group, the IO tendon was placed in one of the
13.2 Surgical Alternatives to Treat Patients with DVD |
177 |
three stations: 1 mm posterior or 1 mm anterior to the IR insertion or at the level of the IR insertion. In the standard group, the IO tendon was positioned 1 mm anterior to the IR insertion for all degrees of DVD. The residual postoperative DVD was 1.15 PD in the graded group compared with 2.44 PD in the standard group. This difference was statistically significant.
Finally, Snir et al. [43], to improve the postoperative outcome in patients with asymmetric DVD with IOOA, augmented the functional change in the IO induced by IOAT by resecting the IO muscle in the eye with greater vertical deviation before displacing it anterior to the IR insertion. The IO resection was graded according to the di erence in the preoperative vertical deviation between the eyes: 3 mm for a di erence of up to 10 PD and 5 mm for a di erence of 11–20 PD. These authors compared the postoperative outcomes of six consecutive patients who underwent combined graded monocular resection and bilateral ATIO with six consecutive historical control patients who underwent equal IOAT. The mean di erence of the asymmetric DVD in the primary position was reduced from 13.3 to 2.2 PD in the study group and from 13.3 to 10.2 PD in the control group (P = 0.004).
In conclusion, for patients with asymmetric DVD and coexisting IOOA and V pattern, we recommend bilateral IOAT combined with monocular graded IO resection in the eye with greater DVD or bilateral but graded IOAT to prevent the postoperative vertical deviation.
The weakening of both elevators (IO and SR) always results in an elevation deficiency, that could be acceptable in cases with large hypertropia, but it could induce a noticeable and undesirable chin-up head position.
13.2.4DVD with Superior Oblique Overaction (SOOA) and A Pattern
In these cases, DVD is greater in abduction of the nonfixating eye than in PP. The SOOA causes incomitance in DVD and A pattern [14, 44, 45] (Fig. 13.2).
In this group, when A pattern anisotropia is small not over 14 PD
1.Bilateral SR improves DVD and controls A pattern [46].
If the A pattern is larger, undercorrection is obtained; therefore, other alternatives should be used.
2.Bilateral SR recession + bilateral SO posterior tenectomy or [44, 47, 48].
3.Four oblique weakening procedure [27, 28].
Simultaneous weakening of SO and SR may cause an inversion of vertical incomitance, transforming the A pattern into V pattern. Thus, it is beneficial to carry out the four oblique weakening procedure in these patients [28, 44].
Fig. 13.2 Dissociated vertical deviation (DVD) with SOOA and A pattern: DVD is greater in abduction of the nonfixating eye
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13 Surgical Management of Dissociated Deviations |
It may be a quite complex and lengthy procedure for nonexperienced surgeons; it produces a symmetric outcome and so it is not the preferred option in a markedly asymmetrical case. It could also produce a vertical devi-
13 ation. When this complication occurs, a simple SR recession of the hypertropic eye can be performed according to the hypertropia amount in PP, thus solving the problem.
There are several surgical alternatives to treat asymmetric cases with A pattern. A graded bilateral IOAT or a SR recession of the most hypertropic eye can be added to the usual SO weakening.
The size of the A pattern and the presence of asymmetry are important when deciding the technique to be employed.
13.2.5Symmetric vs. Asymmetric Surgeries for DVD
tropia, or it can remain aligned when the DVD is of a similar magnitude to that of the vertical tropia. This situation may be erroneously interpreted as monocular DVD.
Asymmetric DVD will often appear to be unilateral. However, by performing the proper maneuvers, the bilaterality of most cases can be detected. The objective eye movement recording clearly demonstrates that DVD is bilateral in almost all cases.
Bilateral symmetric procedures are performed for cases of bilaterally symmetric DVD (within ± 7 PD), but asymmetric DVD is more common, and larger DVD can be found in the nonfixating eye or even in the fixating eye.
Determining the di erence in the amount of SR recession in these asymmetric cases remains challenging. The maximum di erence allowed to obtain a good outcome remains controversial.
DVD is often perceived as a bilateral condition; however, many cases are markedly asymmetric. These cases are usually found associated with unilateral deep amblyopia.
Just as oblique muscle dysfunction makes DVD incomitant in di erent gaze positions, the presence of a true vertical deviation (hypo or hypertropia) makes it asymmetric.
The nondissociated vertical tropia can be lesser or larger than the amplitude of the DVD.
When the nondissociated hypertropia is larger than the magnitude of the DVD, the hypotropic eye is never the higher eye.
Despite the fact that the greater amplitude of DVD is usually seen in the nonfixating eye, cases with greater DVD in the fixating eye do exist and may show hypotropia of the fellow eye in binocular conditions. When the cover test is performed, this hypotropic eye can either become hypertropic if DVD is larger than the vertical
13.2.6DVD with Hypotropia of the Nonfixating Eye
DVD usually manifests as an intermittent hypertropia, but there are certain cases with hypotropia of the nonfixating eye. Although rare, these cases are identified in different reports under the labels of Dissociated hypotropia [49, 50], Hypotropic DVD, Hypotropic Dissociated Deviation [51], or Inverse DVD (Fig. 13.3).
Yet, we are not going to refer to patients with this condition, but to those with DVD and a hypotropic nonfixating eye. We can distinguish two groups:
1.Consecutive cases: cases secondary to surgical overcorrection (previous vertical acting muscles surgery).
2.Primitive cases: patients with asymmetric DVD (greater in the fixating eye), with associated nondissociated vertical tropia or with unilateral deep amblyopia.
Fig. 13.3 Bilateral DVD with left hypotropia in primary position
