- •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
Chapter 15 |
|
Pearls and Pitfalls in Surgical |
15 |
Management of Paralytic Strabismus |
Seyhan B. Özkan
Core Messages
■Careful preoperative assessment and a correct diagnosis of the problem are the essential factors for a successful outcome of surgical treatment.
■The pearl to go through the correct route in surgical management of paralytic strabismus is to know the questions that need to be answered during the preoperative assessment. The correct answers for these questions clarify the method of appropriate surgical treatment.
■During the preoperative assessment, the potential for fusion must be carefully evaluated. Acquired loss of fusion or, in other words, central fusion disruption may coexist in acquired paralytic ocular motility problems. In such cases, restoration of the ocular alignment may make the symptoms worse because of the increased awareness of diplopia with two overlapping images.
■The aims of surgical treatment are primarily to obtain a diplopia-free field, to achieve symmetric ocular motility and a good looking eye that will allow eye contact, and to correct the abnormal head posture, if any.
■The major pitfall in paralytic strabismus is the coexistence of a restrictive element. The secondary restrictions may mask the partial functional recovery in a paretic extraocular muscle (EOM), and sometimes they may become a more prominent problem than the paralytic condition itself.
■The restoration of ocular alignment should be planned to create a new balance in both eyes. Paralytic strabismus is a binocular problem even in cases with unilateral involvement. There should be no hesitation to operate the sound eye where necessary.
■The methods of surgical treatment primarily aim to weaken the unopposed overaction of the antagonist, then to strengthen the paretic muscle where possible or to create a mechanical e ect by transposition, and finally to weaken the yoke muscle in the sound eye. In certain cases like complete third nerve palsy, creating a restriction with surgery may be required to keep the eye in primary position.
15.1General Principles of Surgical Treatment in Paralytic Strabismus
Paralytic strabismus is one of the most challenging areas in strabismus practice. In other types of strabismus, the ophthalmic surgeon considers to operate six muscles for each eye to restore the ocular alignment. However, in paralytic strabismus, the ocular alignment needs to be restored with limited number of muscles, sometimes even with only one functioning extraocular muscle (EOM). In this chapter, the general principles of surgical treatment will be reviewed first and then the treatment strategies in third, fourth, and sixth cranial nerves will be evaluated.
15.1.1 Aims of Treatment
The major aims of treatment are enlargement of diplopiafree field, restoration of ocular alignment, and restoration of the appearance of the patient, to correct abnormal head posture,and to improve the ductions.The last one is the concern of the strabismus surgeon, and the patients usually do not complain of limited ductions and are mostly not even aware of the limitation of their ductions if it is not very severe.
15.1.2 Timing of Surgery
In all types of paralytic strabismus, the stability of the deviation must be observed before considering any surgical
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15 Pearls and Pitfalls in Surgical Management of Paralytic Strabismus |
intervention. The time period that the spontaneous recovery occurs is usually accepted as 6 months; however, this period may last longer, especially in third nerve palsies. A waiting period of 12 months is recommended for third nerve palsies
15 and spontaneous recovery may occur even in a longer period of time in some cases [1]. As a general rule, one must consider that if the deviation is still unstable following consecutive examinations after 6 months,surgical treatment must be postponed till the deviation becomes stable.
15.1.3Preoperative Assessment
Prior to any treatment, one must be sure about the diagnosis. Restrictive motility problems may simulate paralytic conditions and sometimes both restrictive and paralytic problems occur at the same time making the clinical picture more complicated. The combination of restrictive and paralytic problems mostly occurs in orbital blow-out fractures and in long-standing paralytic problems. The combination of restrictive element has a negative e ect on the predictability of surgical results, so the presence of any restrictive factors must be carefully evaluated in all cases with paralytic strabismus.
For a correct surgical planning, the following questions need to be answered preoperatively in cases with paralytic strabismus:
1.Is the problem partial (paresis) or total (paralysis)?
2.Are there any restrictive factors?
3.Is the problem congenital or acquired?
4.Is there “acquired loss of fusion” or in other words “central fusion disruption?”
The answers for the first two questions will be discussed together.
■Is the paralytic problem partial or total?
■Are there any restrictive factors?
If there are no restrictive forces, it is not di cult to assess whether the paralytic condition is partial or total. These factors may be primary as it is the case in blow-out fracture or secondary as the contracture of the antagonist muscle(s) in long-standing paralytic problems.
For a correct evaluation of the role of accompanying restrictive factors and the residual function of the paretic EOM, the following tests may be used:
■Measurement of the deviation in nine positions of gaze
■Assessment of the ocular rotations
■Traction test
■Active forced generation test
■Electromyography (EMG)
■Increase of intraocular pressure with positions of gaze
■Measurement of saccadic eye movements
■Botulinum toxin A (BTXA) injection into the antagonist EOM
Among those methods, the saccadic eye movement recordings provide very reliable information. However, in most of the clinics, saccadic eye movement recording is not available as a routine clinical method.
BTXA may also be used as a diagnostic tool in paralytic strabismus [2]. The secondary unopposed contracture of the antagonist EOM may not allow the eye to move toward the direction of the a ected muscle despite some spontaneous recovery. For diagnostic purpose, BTXA is injected into the antagonist EOM.An improvement of the movement toward the functional area of the paretic muscle indicates that there is some residual function of the paretic muscle [3] (Figs. 15.1 and 15.2). However, it must be kept in mind that in presence of severe contracture with fibrosis BTXA injection does not give reliable results, as BTXA cannot eliminate the fibrotic tissue e ect.
Despite the numerous methods for preoperative assessment of the restrictive forces, the surgeon may have to change the surgical plan depending upon the traction test results under general anesthesia. In long-standing paralytic strabismus, the contracture and fibrosis may not only a ect the EOMs but also the fascial structures and EOM pulleys and an orbital fibrosis develops [4, 5]. In such cases, the traction test will be found positive despite the disinsertion of the EOM. These cases represent the most challenging paralytic ocular motility problems.
■ Is the problem congenital or acquired?
In congenital paralytic disorders, there may be some developmental abnormalities like the tendon abnormalities in congenital superior oblique palsy, EOM fibrosis, or orbital fibrosis. Most of the congenital cases do not complain of diplopia. The exception of this is decompensated congenital fourth nerve palsy presenting with vertical diplopia.
■Is there “acquired loss of fusion (central fusion disruption)?”
Acquired loss of fusion or central fusion disruption may occur in paralytic strabismus cases especially the posttraumatic ones. In these cases, because of the involvement of the fusional areas which are supposed to be located in the midbrain, the previously healthy fusional ability is lost causing intractable diplopia. When the
15.1 General Principles of Surgical Treatment in Paralytic Strabismus |
197 |
Fig. 15.1 Use of botulinum toxin A (BTXA) for assessment of the function of the paretic muscle. If the paretic muscle has some residual function the eye moves toward the functional area of the paretic extraocular muscle (EOM) following injection of BTXA into the antagonist muscle [3]
Paretic EOM
Partially recovered |
Contracture of |
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paretic EOM |
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the antagonist |
Paralysis of the |
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antagonist with BTXA |
a
b
Fig. 15.2 In a patient with left sixth nerve palsy (a) the improvement of abduction of the left eye after injection of BTXA into the medial rectus muscle is shown (b) [3]
deviation is neutralized by prisms or synoptophor, these patients typically describes a vertical sliding of the images when the two images were overlapped and were just about to appear single. The diagnosis of this challenging problem preoperatively is very important. If the patient has an acquired loss of fusion and intractable diplopia, the deviation should better be corrected temporarily by prisms or BTXA to allow the assessment of the tolerance of diplopia [2, 6]. In some cases during this period, the fusional ability may be regained and in those ones surgery may be performed safely. Our preferred method is BTXA injection in such cases to provide a temporary period of orthophoria under real-life conditions. The decreased contrast sensitivity and the loss of image quality related to Fresnel prisms may have a negative e ect on recovery of fusion. If the patient cannot overcome or tolerate diplopia with the use of BTXA or prisms, surgical correction of the deviation may cause an increase of the complaint of diplopia. Orthophoria in a patient with intractable diplopia is much more bothersome compared with the diplopia with a large deviation. The overlapping
two close images cannot be tolerated and cause more symptoms compared with the two far away images in a patient with a large deviation.
15.1.4Methods of Surgical Treatment
■Decreasing the strength of the antagonist: Recession or disinsertion of the antagonist is the preferred method. If it will be combined with full tendon transposition, BTXA injection instead of surgical recession should be preferred for the risk of anterior segment ischemia.
■Strengthening the paretic EOM: Resection or tendon tuck could be performed. For strengthening procedures, the paretic muscle is preferred to have some residual function. The exception of this is superior oblique palsy. Because of the tendon length and the anatomical characteristics, superior oblique tendon tuck may be performed in a superior oblique muscle with no residual function.
