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10. Levy Y, Kremer I, Shavit S, Korczyn AD. The pupillary effects of retrobulbar injection of botulinum toxin A (oculinum) in albino rats. Invest Ophthalmol Vis Sci 1991;32:122-5. 11. Thompson HS. Adie’s syndrome: some new observations. Trans Am Ophthalmol Soc 1977;75:587-626.
Foveal hypoplasia in autosomal recessive spastic ataxia of Charlevoix-Saguenay Christopher T. Shah, MD,a Tyson S. Ward, MD,a Julie A. Matsumoto, MD, FACR,b and Yevgeniy Shildkrot, MDa A 14-year-old boy presented with a presumed diagnosis of autosomal recessive spastic ataxia of Charlevoix-Saguenay (ARSACS). The neurological examination, nerve conduction study, and brain imaging results were all consistent with the diagnosis. The ophthalmologic examination was notable for a prominent myelinated nerve fiber layer extending from the disk along the major temporal arcades in both eyes. Loss of foveal depression was noted clinically and on spectral domain optical coherence tomography. This case highlights a novel finding that may aid in the diagnosis of ARSACS.
A
utosomal recessive spastic ataxia of CharlevoixSaguenay (ARSACS) was first described in 1978 as a cause of early-onset cerebellar ataxia in the eponymous region of Canada and has since been confirmed in France, Turkey, Italy, Spain, Tunisia, Holland, and Japan.1 Various mutations in the SACS gene located on chromosome 13q12 have since been found to be responsible for ARSACS.1 The clinical phenotype is characterized by early-onset cerebellar ataxia, lower limb spasticity, and peripheral neuropathy.1 Electromyography shows signs of severe denervation in the distal muscles, and nerve conduction studies demonstrate signs of axonal neuropathy with associated demyelinating features.2 Magnetic resonance imaging (MRI) findings include atrophy of the superior vermis, cerebellar hemispheres and cervical cord, and linear hypointensities on T2- and T2/FLAIR-weighted images in the pons, thinning of the corpus callosum, and a rim of T2 hyperintensity around the thalami.3 Patients with ARSACS have been noted to have abnormal thickening or myelination of the peripapillary nerve fiber layer.1,4-7
Author affiliations: aDepartment of Ophthalmology, University of Virginia, Charlottesville, Virginia; bDepartment of Radiology and Medical Imaging, University of Virginia, Charlottesville, Virginia Submitted March 17, 2015. Revision accepted October 7, 2015. Correspondence: Yevgeniy Shildkrot, MD, Department of Ophthalmology, PO Box 800715, Charlottesville, VA 22908 (email: [email protected]). J AAPOS 2016;20:81-83. Copyright Ó 2016 by the American Association for Pediatric Ophthalmology and Strabismus. 1091-8531/$36.00 http://dx.doi.org/10.1016/j.jaapos.2015.10.007
Journal of AAPOS
FIG 1. A, Magnetic resonance imaging demonstrating atrophy of the superior vermis (long arrow), with enlarged posterior fossa subarachnoid space and thinning of the posterior body of the corpus callosum (short arrows). B, Characteristic bilateral paramedian T2/FLAIR-hypointense stripes in the basis pontis. C, Linear T2/FLAIR-hyperintense rims along the lateral thalami are also present.
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FIG 2. Fundus photograph of the right eye (A) and left eye (B) demonstrating prominent, myelinated nerve fiber layer surrounding the optic disk and extending along the major temporal arcades; the foveal pigment is normal.
FIG 3. Spectral domain optical coherence tomography images of the right eye (A) and left eye (B) through the macula and optic nerve, with corresponding infrared reflectance images. Bilaterally there is preserved lengthening of the outer segments with resulting bowing in of the ellipsoid zone (black-center arrows) and widening of the outer plexiform layer (white brackets and white-center arrows). The foveal pits and extrusion of inner retinal layers are absent bilaterally (dotted white ovals). There is thickening of the optic disk tissue, and the retinal nerve fiber layer does not extend to the fovea (white boxes).
Case Report A 14-year-old boy presented to the Retina Service of the University of Virginia, Charlottesville, having been referred from the Neurology Clinic, for evaluation of presumed ARSACS. He had initially presented to the Neurology Clinic 9 months earlier with gait and balance problems. Neurological examination was notable for length-dependent sensory changes in his legs, with reduced sensation to light touch and vibration. He had a diminished Achilles reflex, with bilateral upgoing toes, ataxia, and intention tremor with finger-nosefinger testing and ataxia with heel-to-shin, wide-based gait, and inability to walk in tandem. MRI demonstrated atrophy of the superior cerebellar vermis, thinning of the corpus callosum, characteristic bilateral paramedian T2/FLAIR-weighted hypointense stripes in the basis pontis and T2-hyperintense rims around the lateral thalami (Figure 1). Nerve conduction study and electromyography showed evidence of a large-fiber, predominantly axonal, sensorimotor polyneuropathy. Genetic testing had been declined by the patient’s mother. Ophthalmologic examination showed best-corrected visual acuity of 20/20 in each eye, with 0.50 D spherical correction in each eye. Extraocular movements were full with a subtle left-beating nystagmus on right gaze. No overshoot of saccades was observed. Anterior segment examination was unremarkable. Dilated fundus examination revealed prominent,
myelinated nerve fiber layer emanating from the disk, with obscuration of disk margin and associated opacification of the retinal nerve fiber layer (RNFL) layer along the arcades. The macula was flat, with preserved foveal hyperpigmentation but no foveal reflex. The periphery had normal coloration, with no evidence of pigmentary retinopathy (Figure 2). Spectral domain optical coherence tomography (SD-OCT) of the macula (Figure 3) demonstrated loss of central foveal depression and no extrusion of the inner retinal layers, with preserved lengthening of outer segments, intact ellipsoid zone, and widening of the outer nuclear layer in the area corresponding to the foveal center. There was notable elevation of the optic disk tissue and surrounding RNFL, without extension into the fovea.
Discussion We describe a novel finding of grade 2 foveal hypoplasia in a case of presumed ARSACS. The OCT features of adults with ARSACS have been studied by multiple groups since the description of myelinated nerve fibers in this condition. No studies to date have reported the SD-OCT findings in a child, and none have focused on foveal hypoplasia as an independent feature of ARSACS. Myelinated fibers radiating from the optic disk were thought previously to be a minor criterion for ARSACS diagnosis. However, the presence of myelination is not universal in non-Quebecois patients.2,8
Journal of AAPOS
Volume 20 Number 1 / February 2016 Nerve fiber layer may be thickened on OCT even without clinical appearance of opacified RNFL.1,4,5 This has led some to focus on peripapillary retinal fiber layer thickening rather than myelinated fiber appearance alone in the work-up of ARSACS.1,5 Both the RNFL thickening on OCT and clinical appearance of myelinated RNFL were present in our patient, strengthening the diagnosis of ARSACS along with the classic MRI and neurologic findings. Foveal hypoplasia has not been explicitly reported in patients with ARSACS. Recent work by Thomas and colleagues8 attempted to grade foveal hypoplasia on a scale from 1 (mildest) to 4 (most severe) based on SDOCT findings, with apparent correlation to visual function. Our patient had grade 2 foveal hypoplasia, which may explain his good visual acuity. Blunted foveal pit and increased overall macular thickness was previously noted by Desserre and colleagues,1 who examined OCT findings in 2 adults (33 and 40 years of age) with ARSACS and attributed the filling in of foveal depression to “thickening of the retinal optical fibers.” Our review of their OCT images, however, demonstrated that the RNLFL did not extend to the foveal pit; instead, grade 2 foveal hypoplasia similar to that seen in our case was present. Vingolo and colleagues4 compared earlier generation OCT findings in 5 adults (26-46 years of age) with ARSACS to 5 patients with congenital myelinated RNFL, demonstrating increased overall macular thickness in only the patients with ARSACS. No comment was made on the status of the fovea. More recently, Garcia-Martin and colleauges9 attempted automated retinal segmentation by SD-OCT in 10 adults (39-58 years of age) with ARSACS compared to healthy controls and found statistically significant thickening of the inner glial limiting membrane, nerve fiber layer, and ganglion cell layer in ARSACS patients only, although there may be questions about the accuracy of the segmentation protocol based on representative images included in the published report. Attenuated foveal depression is present on those OCT images as well. Earlier reports suggest that the apparent loss of foveal depression is secondary to the thickened RNFL.1,4,9 However, the review of OCT images in our case (Figure 3) and those in the aforementioned reports demonstrate that RNFL thickening does not extend to the foveal center. In fact, as seen with foveal hypoplasia of other causes, there is an apparent failure of extrusion of the inner retinal layers leading to blunted or lost foveal pit, suggesting an abnormality in the development of the foveal center. Great variability exists in the degree of visual impairment associated with foveal hypoplasia and lack of foveal pit.10 In conclusion, the finding of grade 2 foveal hypoplasia in our patient and in previously published, albeit unrecognized, cases suggests an interruption of normal foveal development occurring in parallel to abnormal myelination of prelaminar nerve fibers. Spectral domain OCT examina-
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tion of macula as well as of the optic nerve can aid in the often elusive diagnosis of ARSACS. References 1. Desserre J, Devos D, Sautiere BG, et al. Thickening of peripapillar retinal fibers for the diagnosis of autosomal recessive spastic ataxia of Charlevoix-Saguenay. Cerebellum 2011;10:758-62. 2. Bouhlal Y, Amouri R, El Euch-Fayeche G, Hentati F. Autosomal recessive spastic ataxia of Charlevoix-Saguenay: an overview. Parkinsonism Relat Disord 2011;17:418-22. 3. Martin MH, Bouchard JP, Sylvain M, St-Onge O, Truchon S. Autosomal recessive spastics ataxia of Charlevoix-Saguenay: a report of MR imaging in 5 Patients. AJNR Am J Neuroradiol 2007;28:1606-8. 4. Vingolo EM, Di Fabio R, Salvatore S, et al. Myelinated retinal fibers in autosomal recessive spastic ataxia of Charlevoix-Saguenay. Eur J Neurol 2011;18:1187-90. 5. Pablo LE, Garcia-Martin E, Gazulla J, et al. Retinal nerve fiber hypertrophy in ataxia of Charlevoix-Saguenay patients. Mol Vis 2011;17: 1871-6. 6. Garcia Martin E, Pablo LE, Gazulla J, et al. Retinal nerve fibre layer thickness in ARSACS: myelination or hypertrophy? Br J Ophthalmol 2013;97:238-41. 7. Yu-Wai-Man P, Pyle A, Griffin H, et al. Abnormal thickening is a common feature among patients with ARSACS-related phenotype. Br J Ophthalmol 2014;98:712-4. 8. Thomas MG, Kumar A, Mohammad S, et al. Structural grading of foveal hypoplasia using spectral-domain optical coherence tomography a predictor of visual acuity? Ophthalmology 2011;118: 1653-60. 9. Garcia-Martin E, Pablo LE, Gazulla J, et al. Retinal segmentation as noninvasive technique to demonstrate hyperplasia in ataxia of Charlevoix-Saguenay. Invest Ophthalmol Vis Sci 2013;54:7137-42. 10. Marmor MF, Choi SS, Zawadzki RJ, Werner JS. Visual insignificance of the foveal pit: reassessment of foveal hypoplasia as fovea plana. Arch Ophthalmol 2008;126:907-13.
Convergent strabismus fixus without high myopia Teena M. Mendonca, MS,a Shailja Tiberwala, MS,a Virender Sachdeva, MS,b and Ramesh Kekunnaya, MD, FRCSa A 37-year-old woman presented with progressive large-angle esotropia (>140D) since childhood. Her best-corrected visual acuity was 20/80 in right eye and unrecordable in the left eye because of severe esotropia and limitation of abduction. Computed tomography Author affiliations: aJasti V Ramanamma Children’s Eye Care Centre, L V Prasad Eye Institute, Hyderabad, India, bNimmagada Prasad Children’s Eye Care Centre, L V Prasad Eye Institute, Visakhapatnam, India Submitted March 23, 2015. Revision accepted October 16, 2015. Correspondence: Ramesh Kekunnaya, MD, FRCS, Head and Consultant, Pediatric Ophthalmology & Strabismus, Jasti V Ramanamma Chidlren’s Eye Care Center, L V Prasad Eye Institue, Road No 2, Banjara Hills, L V Prasad Marg, Hyderabad, 500034 India (email: [email protected], [email protected]). J AAPOS 2016;20:83-85. Copyright Ó 2016 by the American Association for Pediatric Ophthalmology and Strabismus. 1091-8531/$36.00 http://dx.doi.org/10.1016/j.jaapos.2015.10.015
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10. Levy Y, Kremer I, Shavit S, Korczyn AD. The pupillary effects of retrobulbar injection of botulinum toxin A (oculinum) in albino rats. Invest Ophthalmol Vis Sci 1991;32:122-5. 11. Thompson HS. Adie’s syndrome: some new observations. Trans Am Ophthalmol Soc 1977;75:587-626.
Foveal hypoplasia in autosomal recessive spastic ataxia of Charlevoix-Saguenay Christopher T. Shah, MD,a Tyson S. Ward, MD,a Julie A. Matsumoto, MD, FACR,b and Yevgeniy Shildkrot, MDa A 14-year-old boy presented with a presumed diagnosis of autosomal recessive spastic ataxia of Charlevoix-Saguenay (ARSACS). The neurological examination, nerve conduction study, and brain imaging results were all consistent with the diagnosis. The ophthalmologic examination was notable for a prominent myelinated nerve fiber layer extending from the disk along the major temporal arcades in both eyes. Loss of foveal depression was noted clinically and on spectral domain optical coherence tomography. This case highlights a novel finding that may aid in the diagnosis of ARSACS.
A
utosomal recessive spastic ataxia of CharlevoixSaguenay (ARSACS) was first described in 1978 as a cause of early-onset cerebellar ataxia in the eponymous region of Canada and has since been confirmed in France, Turkey, Italy, Spain, Tunisia, Holland, and Japan.1 Various mutations in the SACS gene located on chromosome 13q12 have since been found to be responsible for ARSACS.1 The clinical phenotype is characterized by early-onset cerebellar ataxia, lower limb spasticity, and peripheral neuropathy.1 Electromyography shows signs of severe denervation in the distal muscles, and nerve conduction studies demonstrate signs of axonal neuropathy with associated demyelinating features.2 Magnetic resonance imaging (MRI) findings include atrophy of the superior vermis, cerebellar hemispheres and cervical cord, and linear hypointensities on T2- and T2/FLAIR-weighted images in the pons, thinning of the corpus callosum, and a rim of T2 hyperintensity around the thalami.3 Patients with ARSACS have been noted to have abnormal thickening or myelination of the peripapillary nerve fiber layer.1,4-7
Author affiliations: aDepartment of Ophthalmology, University of Virginia, Charlottesville, Virginia; bDepartment of Radiology and Medical Imaging, University of Virginia, Charlottesville, Virginia Submitted March 17, 2015. Revision accepted October 7, 2015. Correspondence: Yevgeniy Shildkrot, MD, Department of Ophthalmology, PO Box 800715, Charlottesville, VA 22908 (email: [email protected]). J AAPOS 2016;20:81-83. Copyright Ó 2016 by the American Association for Pediatric Ophthalmology and Strabismus. 1091-8531/$36.00 http://dx.doi.org/10.1016/j.jaapos.2015.10.007
Journal of AAPOS
FIG 1. A, Magnetic resonance imaging demonstrating atrophy of the superior vermis (long arrow), with enlarged posterior fossa subarachnoid space and thinning of the posterior body of the corpus callosum (short arrows). B, Characteristic bilateral paramedian T2/FLAIR-hypointense stripes in the basis pontis. C, Linear T2/FLAIR-hyperintense rims along the lateral thalami are also present.
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FIG 2. Fundus photograph of the right eye (A) and left eye (B) demonstrating prominent, myelinated nerve fiber layer surrounding the optic disk and extending along the major temporal arcades; the foveal pigment is normal.
FIG 3. Spectral domain optical coherence tomography images of the right eye (A) and left eye (B) through the macula and optic nerve, with corresponding infrared reflectance images. Bilaterally there is preserved lengthening of the outer segments with resulting bowing in of the ellipsoid zone (black-center arrows) and widening of the outer plexiform layer (white brackets and white-center arrows). The foveal pits and extrusion of inner retinal layers are absent bilaterally (dotted white ovals). There is thickening of the optic disk tissue, and the retinal nerve fiber layer does not extend to the fovea (white boxes).
Case Report A 14-year-old boy presented to the Retina Service of the University of Virginia, Charlottesville, having been referred from the Neurology Clinic, for evaluation of presumed ARSACS. He had initially presented to the Neurology Clinic 9 months earlier with gait and balance problems. Neurological examination was notable for length-dependent sensory changes in his legs, with reduced sensation to light touch and vibration. He had a diminished Achilles reflex, with bilateral upgoing toes, ataxia, and intention tremor with finger-nosefinger testing and ataxia with heel-to-shin, wide-based gait, and inability to walk in tandem. MRI demonstrated atrophy of the superior cerebellar vermis, thinning of the corpus callosum, characteristic bilateral paramedian T2/FLAIR-weighted hypointense stripes in the basis pontis and T2-hyperintense rims around the lateral thalami (Figure 1). Nerve conduction study and electromyography showed evidence of a large-fiber, predominantly axonal, sensorimotor polyneuropathy. Genetic testing had been declined by the patient’s mother. Ophthalmologic examination showed best-corrected visual acuity of 20/20 in each eye, with 0.50 D spherical correction in each eye. Extraocular movements were full with a subtle left-beating nystagmus on right gaze. No overshoot of saccades was observed. Anterior segment examination was unremarkable. Dilated fundus examination revealed prominent,
myelinated nerve fiber layer emanating from the disk, with obscuration of disk margin and associated opacification of the retinal nerve fiber layer (RNFL) layer along the arcades. The macula was flat, with preserved foveal hyperpigmentation but no foveal reflex. The periphery had normal coloration, with no evidence of pigmentary retinopathy (Figure 2). Spectral domain optical coherence tomography (SD-OCT) of the macula (Figure 3) demonstrated loss of central foveal depression and no extrusion of the inner retinal layers, with preserved lengthening of outer segments, intact ellipsoid zone, and widening of the outer nuclear layer in the area corresponding to the foveal center. There was notable elevation of the optic disk tissue and surrounding RNFL, without extension into the fovea.
Discussion We describe a novel finding of grade 2 foveal hypoplasia in a case of presumed ARSACS. The OCT features of adults with ARSACS have been studied by multiple groups since the description of myelinated nerve fibers in this condition. No studies to date have reported the SD-OCT findings in a child, and none have focused on foveal hypoplasia as an independent feature of ARSACS. Myelinated fibers radiating from the optic disk were thought previously to be a minor criterion for ARSACS diagnosis. However, the presence of myelination is not universal in non-Quebecois patients.2,8
Journal of AAPOS
Volume 20 Number 1 / February 2016 Nerve fiber layer may be thickened on OCT even without clinical appearance of opacified RNFL.1,4,5 This has led some to focus on peripapillary retinal fiber layer thickening rather than myelinated fiber appearance alone in the work-up of ARSACS.1,5 Both the RNFL thickening on OCT and clinical appearance of myelinated RNFL were present in our patient, strengthening the diagnosis of ARSACS along with the classic MRI and neurologic findings. Foveal hypoplasia has not been explicitly reported in patients with ARSACS. Recent work by Thomas and colleagues8 attempted to grade foveal hypoplasia on a scale from 1 (mildest) to 4 (most severe) based on SDOCT findings, with apparent correlation to visual function. Our patient had grade 2 foveal hypoplasia, which may explain his good visual acuity. Blunted foveal pit and increased overall macular thickness was previously noted by Desserre and colleagues,1 who examined OCT findings in 2 adults (33 and 40 years of age) with ARSACS and attributed the filling in of foveal depression to “thickening of the retinal optical fibers.” Our review of their OCT images, however, demonstrated that the RNLFL did not extend to the foveal pit; instead, grade 2 foveal hypoplasia similar to that seen in our case was present. Vingolo and colleagues4 compared earlier generation OCT findings in 5 adults (26-46 years of age) with ARSACS to 5 patients with congenital myelinated RNFL, demonstrating increased overall macular thickness in only the patients with ARSACS. No comment was made on the status of the fovea. More recently, Garcia-Martin and colleauges9 attempted automated retinal segmentation by SD-OCT in 10 adults (39-58 years of age) with ARSACS compared to healthy controls and found statistically significant thickening of the inner glial limiting membrane, nerve fiber layer, and ganglion cell layer in ARSACS patients only, although there may be questions about the accuracy of the segmentation protocol based on representative images included in the published report. Attenuated foveal depression is present on those OCT images as well. Earlier reports suggest that the apparent loss of foveal depression is secondary to the thickened RNFL.1,4,9 However, the review of OCT images in our case (Figure 3) and those in the aforementioned reports demonstrate that RNFL thickening does not extend to the foveal center. In fact, as seen with foveal hypoplasia of other causes, there is an apparent failure of extrusion of the inner retinal layers leading to blunted or lost foveal pit, suggesting an abnormality in the development of the foveal center. Great variability exists in the degree of visual impairment associated with foveal hypoplasia and lack of foveal pit.10 In conclusion, the finding of grade 2 foveal hypoplasia in our patient and in previously published, albeit unrecognized, cases suggests an interruption of normal foveal development occurring in parallel to abnormal myelination of prelaminar nerve fibers. Spectral domain OCT examina-
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tion of macula as well as of the optic nerve can aid in the often elusive diagnosis of ARSACS. References 1. Desserre J, Devos D, Sautiere BG, et al. Thickening of peripapillar retinal fibers for the diagnosis of autosomal recessive spastic ataxia of Charlevoix-Saguenay. Cerebellum 2011;10:758-62. 2. Bouhlal Y, Amouri R, El Euch-Fayeche G, Hentati F. Autosomal recessive spastic ataxia of Charlevoix-Saguenay: an overview. Parkinsonism Relat Disord 2011;17:418-22. 3. Martin MH, Bouchard JP, Sylvain M, St-Onge O, Truchon S. Autosomal recessive spastics ataxia of Charlevoix-Saguenay: a report of MR imaging in 5 Patients. AJNR Am J Neuroradiol 2007;28:1606-8. 4. Vingolo EM, Di Fabio R, Salvatore S, et al. Myelinated retinal fibers in autosomal recessive spastic ataxia of Charlevoix-Saguenay. Eur J Neurol 2011;18:1187-90. 5. Pablo LE, Garcia-Martin E, Gazulla J, et al. Retinal nerve fiber hypertrophy in ataxia of Charlevoix-Saguenay patients. Mol Vis 2011;17: 1871-6. 6. Garcia Martin E, Pablo LE, Gazulla J, et al. Retinal nerve fibre layer thickness in ARSACS: myelination or hypertrophy? Br J Ophthalmol 2013;97:238-41. 7. Yu-Wai-Man P, Pyle A, Griffin H, et al. Abnormal thickening is a common feature among patients with ARSACS-related phenotype. Br J Ophthalmol 2014;98:712-4. 8. Thomas MG, Kumar A, Mohammad S, et al. Structural grading of foveal hypoplasia using spectral-domain optical coherence tomography a predictor of visual acuity? Ophthalmology 2011;118: 1653-60. 9. Garcia-Martin E, Pablo LE, Gazulla J, et al. Retinal segmentation as noninvasive technique to demonstrate hyperplasia in ataxia of Charlevoix-Saguenay. Invest Ophthalmol Vis Sci 2013;54:7137-42. 10. Marmor MF, Choi SS, Zawadzki RJ, Werner JS. Visual insignificance of the foveal pit: reassessment of foveal hypoplasia as fovea plana. Arch Ophthalmol 2008;126:907-13.
Convergent strabismus fixus without high myopia Teena M. Mendonca, MS,a Shailja Tiberwala, MS,a Virender Sachdeva, MS,b and Ramesh Kekunnaya, MD, FRCSa A 37-year-old woman presented with progressive large-angle esotropia (>140D) since childhood. Her best-corrected visual acuity was 20/80 in right eye and unrecordable in the left eye because of severe esotropia and limitation of abduction. Computed tomography Author affiliations: aJasti V Ramanamma Children’s Eye Care Centre, L V Prasad Eye Institute, Hyderabad, India, bNimmagada Prasad Children’s Eye Care Centre, L V Prasad Eye Institute, Visakhapatnam, India Submitted March 23, 2015. Revision accepted October 16, 2015. Correspondence: Ramesh Kekunnaya, MD, FRCS, Head and Consultant, Pediatric Ophthalmology & Strabismus, Jasti V Ramanamma Chidlren’s Eye Care Center, L V Prasad Eye Institue, Road No 2, Banjara Hills, L V Prasad Marg, Hyderabad, 500034 India (email: [email protected], [email protected]). J AAPOS 2016;20:83-85. Copyright Ó 2016 by the American Association for Pediatric Ophthalmology and Strabismus. 1091-8531/$36.00 http://dx.doi.org/10.1016/j.jaapos.2015.10.015
