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BACKGROUND/AIMS: Measurement of visual acuity can be difficult in children with cerebral palsy (CP). The purpose of this study was to determine the probability of obtaining quantitative (logMAR) visual acuities in CP children with different severities of motor dysfunction. METHODS: An observational, cross-sectional design study was conducted in 76 children (mean age 5.9 years) who had CP severity graded using the Gross Motor Function Classification Scale (GMFCS). Visual testing was performed using optotypes, spatial-sweep (SSVEP) or flash (FVEP) visually evoked potentials. RESULTS: LogMAR acuity was obtainable in 88% of CP children, using either optotypes or SSVEPs. The success rate decreased with increasing severity of GMFCS Levels 1-5; nevertheless, logMAR acuities were obtainable in more than one-half (56%) of children with the most severe disease: Level 5. Similar results were obtained for CP severity assessed using physiological-anatomical subtype (hemiplegic; diplegic; quadriplegic) rather than GMFCS. The mean logMAR acuity (0.37; 20/48) in the CP cohort as a whole was approximately 2 Snellen-equivalent lines worse than that recorded in age-matched, normal children (0.22; 20/33). CONCLUSION: Quantitative visual acuities can be obtained in the majority of CP children, including those with severe motor dysfunction. Difficulties in testing CP children lead often to the misconception that the children have immeasurably low vision.

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PURPOSE: Strabismus in human infants is linked strongly to nasotemporal asymmetries of smooth pursuit, but many features of this co-morbidity are unknown. The purpose of this study was to determine how the duration of early-onset strabismus (or timeliness of repair) affects the severity of pursuit asymmetries in a primate model. METHODS: Binocular image decorrelation was imposed on infant macaques by fitting them with prism goggles on day 1 of life. The goggles were removed after 3 weeks (n=2), 12 weeks (n=2) or 24 weeks (n=3), emulating surgical repair of strabismus in humans at 3, 12, and 24 months of age, respectively. Two control monkeys wore plano lenses. Several months after the goggles were removed, horizontal smooth pursuit was recorded using binocular search coils and a nasal-bias index (NBI) was calculated. RESULTS: Each animal in the 12- and 24-week groups developed a constant, alternating esotropic strabismus and a nasotemporal asymmetry of pursuit when viewing with either eye. Spatial vision was normal (no amblyopia). The 3-week duration monkeys were indistinguishable from control animals; they had normal eye alignment and symmetric pursuit. In the 12- and 24-week monkeys, the longer the duration of binocular decorrelation, the greater the pursuit asymmetry: for 15 degrees /s target motion, the NBI in the 12-week and 24-week animals was 16x and 22x greater respectively, than that in the 3-week animals (ANOVA, P=0.03). CONCLUSIONS: Binocular decorrelation in primates during an early period of fusion development causes permanent smooth pursuit asymmetries when the duration exceeds the equivalent of 3 months in human. These findings support the conclusion that early correction of infantile strabismus promotes normal development of cerebral gaze pathways.

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PURPOSE: To report longer term results of transscleral sutured intraocular lens (TSSIOL) implantation in a sizable cohort of aphakic children, who were not suitable for contact lens wear and lacked adequate capsular support for sulcus fixation of an intraocular lens. METHODS: Clinical outcome data were collated by retrospective review after surgery on 43 consecutive eyes in 32 aphakic children (mean age at implantation = 10 years; 33% < or = age 7 years). Outcome measures included visual acuity, postoperative refractive error, postoperative complications, and rate of reoperation. Follow-up averaged 37 months. RESULTS: Visual acuity improved after surgery in 70% (30) of operated eyes (in 69% or 22/32 children). Fifty-one percent (22/43 eyes) improved by two lines or more. No patient suffered a loss of acuity or exacerbation of preexisting amblyopia. Postoperative refraction was within +/-2.0 D of the predicted refraction in 93% (40/43) of eyes. Complications, with the exception of one eye (2%), were minor/transient and resolved in the first week after surgery. Complications included small hyphemas (7%, 3/43 eyes), vitreous hemorrhage (5%, 2/43 eyes), and ocular hypertension or hypotony (5%). Two eyes (5%) exhibited episodes of iris capture of the IOL optic, one of which (2%, 1/43) eventually necessitated reoperation for IOL exchange. No retinal detachments or other retinal complications were encountered. CONCLUSION: TSSIOL implantation appears to be a safe and effective method for correcting aphakia in pediatric eyes that lack adequate capsular support. Safety over a follow-up period longer than the average 3 years reported here remains to be determined. The surgery is more difficult to perform than capsular-bag or sulcus implantation and potentially carries greater risks.

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PURPOSE: To describe and evaluate alternate techniques for implanting intraocular lenses in children in the absence of adequate capsular support for traditional lens implantation. METHODS: Postoperative results of 18 eyes with posterior chamber intraocular lenses (PCIOLs) sutured to the ciliary sulcus and 10 eyes implanted with anterior chamber intraocular lenses (ACIOLs) were reviewed. Visual outcomes were divided into 2 groups: onset of aphakia during the critical period of visual development (< or = 9 years) and onset after the critical period (> 9 years). Visual outcomes and complications were recorded. RESULTS: Average follow-up was 10.3 months in the PCIOL group and 49.2 months in the ACIOL group. Eyes that became aphakic after the critical period of visual development achieved better overall final visual acuity than the eyes that became aphakic during the critical period; indeed, the eyes that became aphakic during the critical period did not achieve significantly improved vision. There were no complications in the PCIOL group. Complications in the ACIOL group included corectopia, haptic migration through the operative wound requiring removal, and pigment deposits on the lens. CONCLUSIONS: PCIOLs sutured to the ciliary sulcus offer a superior option to ACIOLs for correction of childhood aphakia in children lacking capsular support. ACIOLs had a high rate of serious complications (10%) in this small series. Secondary implantation with transsclerally sutured PCIOLs should be considered in complicated cases when more conservative options have been exhausted.

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PURPOSE: To determine the prevalence of retinal hemorrhages and their association with cerebral intraventricular hemorrhages (IVH) in low-birth-weight preterm neonates born at or before 32 weeks' gestation. METHODS: We prospectively studied a consecutive series of 22 neonates (24-30 weeks' gestation; mean gestational age, 27 weeks; mean weight, 1065 g) admitted to the neonatal intensive care unit. Anterior segment and indirect ophthalmoscopic examination, as well as cranial ultrasonographic examination, were performed on day 1 and day 10 of life. The prevalence of retinal and intraventricular hemorrhage was tested statistically for association with obstetric and neonatal clinical variables. RESULTS: The prevalence of retinal hemorrhage was 9% (2/22; 95% CI, 3%-21%) on day 1 and 2% (1/22) on day 10. The prevalence of IVH was 27% (6/22; 95% CI, 9%-46%): 14% (3/22) on day 1 and 23% (5/22) on day 10. Retinal hemorrhages occurred with greater frequency in neonates born to women who had intrauterine infection (chorioamnionitis, P =.043) and low umbilical cord pH levels (P =.027). No association was found between the presence of retinal hemorrhage and IVH (P = 1.000), mode of delivery (ie, vaginal vs cesarean section, P = 1.000), birth weight (P =.476), or gestational age (P = 1.000). The presence of subconjunctival hemorrhage was associated with IVH (P =.046). CONCLUSIONS: Retinal hemorrhages occur in less than 10% of low-birth-weight neonates, ie, a prevalence one half that observed in term neonates (22%). The hemorrhages tend to resolve without sequelae in the first 10 days of life and occur more commonly in infants born to women with uterine infection. Retinal hemorrhages in very premature neonates are not predictive of IVH-related brain damage.

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OBJECTIVE: To assess the interaction between versional and vergence eye movements in normal and strabismic monkeys. METHODS: Horizontal optokinetic nystagmus (OKN) and vergence were measured using the magnetic scleral search coil technique in a normal adult monkey and a strabismic monkey who had naturally occurring early-onset esotropia. Mean eye velocity and vergence angles were calculated during the slow phases of OKN. RESULTS: The strabismic monkey had a nasotemporal asymmetry of OKN favoring nasally directed motion in each eye. During monocular optokinetic stimulation, mean eye velocities were substantially greater for the adducting as compared to the abducting eye. The velocity of the abducting eye was between 55 and 80% of the velocity of the adducting eye (p < 0.01). As a consequence of the disjunctive movements, the eyes converged an average of 4 +/- 2.8 degrees during OKN. Saccadic analysis documented normal lateral rectus function in each eye. Neither an OKN asymmetry nor disjunctive OKN was observed in the normal monkey. CONCLUSION: Disjunctive OKN in the esotropic monkey suggests that the cerebral maldevelopment responsible for nasally biased OKN also contributes to nasal biases in vergence pathways.

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BACKGROUND: Anomalous retinal correspondence (ARC) is a neural adaptation to eye misalignment in which non-corresponding retinal points are linked in the visual cortex to provide binocular fusion. ARC within the striate cortex would require that horizontal neurons link right-eye and left-eye ocular dominance columns (ODCs) separated by a distance in the cortex proportional to the angle of strabismus. Two hypothetical mechanisms are possible: (1) The ODCs can be linked by axons of horizontal neurons that project monosynaptically from a right-eye to a left-eye ODC. The further apart the ODCs, the longer the axons; hence, axon length should be greater in subjects with strabismus than in healthy subjects (elongated axon, monosynaptic hypothesis). In this case, the clinical probability of developing ARC should be independent of the angle of strabismus, until an upper-limit angle of strabismus is reached equally to the maximal length of axons available to link nonadjacent ODCs, at which point an abrupt decline of ARC probability should be evident. (2) Alternatively, ODCs can be linked by a chain of horizontal neurons, the number of which increases as the distance among ODCs increases; axon length in subjects with strabismus would be expected to be the same as in healthy subjects (normal axon, polysynaptic hypothesis). In this case, the greater the angle of strabismus, the more horizontal neurons and synapses required for linkage, and the greater the probability of signal degradation. Thus, the clinical probability of developing ARC through a polysynaptic mechanism should be inversely proportional to the angle of strabismus. The purpose of this study was to test these 2 hypotheses neuroanatomically in primates and clinically in children. METHODS: For the neuroanatomic portion of the study, biotinylated dextran amine was injected into ODCs of area V1 to label individual neurons. The length of the horizontal axons from these neurons was then compared in strabismic and normal monkeys. In the clinical portion of the study, the medical records of 192 children with strabismus were reviewed retrospectively. The angle of strabismus (prism cover test) and the presence of ARC (Bagolini striated lenses, Worth/Polaroid 4-dot) were recorded. Plots of the presence of ARC as a function of the angle of strabismus were obtained. RESULTS: There was no significant difference in axon length between healthy (7. 02 +/- 0. 83 mm) and strabismic monkeys (6. 60 +/- 1. 07 mm) (P =.16). In children with strabismus, ARC decreased as the angle of strabismus increased (P <. 05). ARC was more prevalent in children who had primary or postsurgical deviations of

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PURPOSE: In humans, pathologic misalignment of the eyes (strabismus, or hetero-tropia) is readily detected using a clinical technique in which the visual axis of each eye is blocked briefly by a hand held occluder (i.e., the cover test, AKA the single cover test, or unilateral cover test). This manual technique is impractical for use in non-human primates. This paper reports the electronic hardware and computer software we have devised and adapted to perform an automated cover test in awake macaque monkeys (Macaca mulatta or rhesus, and Macaca nemistrina or pigtail) to facilitate the study of strabismus in this species. METHODS: Liquid crystal shutters (Displaytech LV2500OP-OEM) are mounted in aluminum spectacle frames which are positioned in front of the monkey's eyes by attaching the frame holder to an acrylic skull cap. The shutters are electrically actuated alternately to an "open" (transparent) or "closed" (opaque) state, occluding each eye in turn. The actuation signal (+/-5 volts) is generated by a single logic chip. The chip is driven by commercial data control and acquisition software (Spike 2, Cambridge Electronic Design) running on a Macintosh computer. Eye position and movement during this cover tests is monitored and recorded by the computer using surgically implanted scleral coils. Monkeys are rewarded for fixating small, moveable targets so that binocular misalignment can be measured with high precision at different or cardinal positions of horizontal and vertical gaze. RESULTS: The shutters produced occlusion of each eye as effective as that of an opaque plastic occluder used in previous experiments that required monocular viewing. Heterotropias were detected and recorded in monkeys and closely resembled those observed in human patients. It was also possible to detect heterophorias by actuating the shutters alternately. CONCLUSIONS: The shutters operated reliably, with negligible delay and transition times, providing automated, repeatable cover tests that are, in fact, in many respects superior to the standard clinical manual technique. In addition, their application to humans, using infrared electro-oculography instead of scleral coils to monitor eye position and movement, holds promise for future applications.

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BACKGROUND: The probability of visual recovery in tumor-related optic neuropathy usually correlates with the severity and duration of optic pathway compromise. Recovery of visual acuity to normal levels is unexpected after profound loss of vision extending for a period of weeks and months. METHODS: A 9-year-old girl who had neurosurgical resection of a craniopharyngioma compressing the optic chiasm and optic tract was followed up serially with neuroimaging and clinical examinations over a 6-year period. RESULTS: Within 3 months of the diagnosis of craniopharyngioma, the girl's vision was reduced to no-light-perception blindness when she viewed with the more involved eye. The blindness correlated with an amaurotic (i.e., >3.6 log unit) relative afferent pupillary defect and an absence of any response when tested with visual field perimetry. After more than a year of total blindness and cessation of all neurosurgical and radiation therapy, visual acuity recovered to a normal level (20/25), the afferent pupillary defect improved, and sensitivity in a portion of the temporal hemivisual field was restored. In the follow-up that has extended for 5 years from the time of recovery, stability of the restored vision has been documented. CONCLUSION: Children who have tumor-related loss of vision due to damage to the anterior visual pathways may be capable of recovery after intervals of blindness that would be considered irreversible in adults. The mechanism of the recovery in our patient may have been decompression-related restoration of axoplasmic flow, followed by gradual remyelination of visual fibers, which allowed reorganization of connections to the lateral geniculate nucleus to optimize synaptic transmission.

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We report a patient with pathologically proven idiopathic Parkinson's disease (IPD) who developed diplopia secondary to convergence insufficiency during his motor "off" periods. Diplopia resolved with onset of motor benefit from levodopa. Neuro-ophthalmologic examination demonstrated convergence insufficiency during motor "off" periods that was alleviated after onset of motor benefit from levodopa. This is the first reported case of convergence insufficiency in IPD responsive to levodopa.

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PURPOSE: To determine whether squirrel monkeys made artificially strabismic in infancy had ocular fixation abnormalities, directional asymmetries of horizontal optokinetic nystagmus (OKN) and asymmetries of motion visually evoked potentials (MVEPs) similar to those of humans with infantile strabismus. METHODS: Esotropia was produced in a newborn squirrel monkey by surgical tenotomy of both lateral rectus muscles. The alignment and eye rotations of the monkey were examined longitudinally and VEP testing was performed at the age of one year. Visual acuity was measured using spatial frequency sweep VEPs (SSVEP) in response to grating stimulation. OKN was tested under conditions of monocular viewing using full-visual-field, vertically oriented, moving stripes. MVEPs in response to horizontal motion were recorded with the animal sedated to reduce the possibility of eye movement artifact. RESULTS: The artificially strabismic squirrel monkey displayed a constant, committant esotropic strabismus accompanied by latent nystagmus. Monocular SSVEP acuity was subnormal in one eye, consistent with mild monocular strabismic amblyopia. The monkey demonstrated asymmetric OKN favoring nasally-directed stimulus motion when viewing with either eye. Monocular MVEPs were also characterized by a horizontal asymmetry with a directional bias inverted 180 degrees between the right and the left eyes. The eye movements and MVEP asymmetries were similar to those observed in strabismic macaque monkeys and humans with early-onset strabismus. Neither the OKN asymmetry nor the MVEP asymmetry was evident in a normal squirrel or normal macaque monkey. CONCLUSION: The artificially strabismic squirrel monkey is an appropriate eye movement and VEP model for the study of neural mechanisms in human infantile strabismus.

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BACKGROUND: Patients who have infantile strabismus exhibit a directional asymmetry of motion visually evoked potentials (MVEPs) recorded under conditions of monocular viewing. The majority of these patients also have latent nystagmus, raising the possibility that the MVEP asymmetry is an artifact of the nystagmus. To explore this issue, we correlated MVEPs and eye movements under conditions that eliminated or increased latent nystagmus. METHODS: MVEPs and eye movements were recorded under conditions of monocular viewing in three adults who had combined infantile-onset strabismus and latent nystagmus. The subjects viewed vertically oriented grating stimuli that oscillated horizontally at temporal frequencies of 6.6 to 11.0 Hz by use of spatial frequencies of 1 to 3 cycles/degree. Quantitative eye movement recordings of latent nystagmus and horizontal pursuit/optokinetic nystagmus were also obtained. RESULTS: Eye movement recordings showed that the latent nystagmus was absent or markedly diminished when the viewing eye was in a 45-degree adducted position, whereas nystagmus velocity increased 10 to 40 times (to 2.2 to 4.5 degrees/second) when the viewing eye was in an abducted position (p < 0.05). MVEPs were abnormal (asymmetry indices > 0.40) when the viewing eye was in an adducted or abducted position of gaze. No correlation was found between the MVEP asymmetry index and the velocity of latent nystagmus. CONCLUSIONS: MVEP asymmetries in infantile strabismus remain robust under conditions that eliminate or greatly reduce the oscillations of latent nystagmus. MVEP asymmetries and ocular motor abnormalities both characterize infantile strabismus, but the ocular motor defects do not cause the MVEP asymmetries. The nasotemporal asymmetry of MVEPs and the nasotemporal asymmetry of pursuit and latent nystagmus are likely caused by deficits in related but separate binocular visual cortical circuits.

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To quantify asymmetries of input from the two eyes into each cerebral hemisphere, we measured ocular dominance column (ODC) widths and areas in the striate visual cortex (area V1) of macaque monkeys. Ocular dominance stripes in layer 4C were labeled by using transneuronal transport of intraocularly injected wheat germ agglutinin-horseradish peroxidase (WGA-HRP) or cytochrome oxidase (CO) histochemistry, after deafferentation of one eye or even by leaving afferent input intact. In infant monkey aged 4 and 8 weeks, ocular dominance stripes labeled by WGA-HRP appeared adultlike with smooth, sharply defined borders. In normal infant and normal adult macaque, ocular dominance stripes driven by the nasal retina (i.e., contralateral eye) were consistently wider than stripes driven by the temporal retina (i.e., ipsilateral eye). Asymmetries in the percentage of area V1 driven by nasal vs. temporal ODCs showed a similar "nasal bias": in infant macaque, approximately 58% of ODCs in V1 were driven by nasal retina, and in adult macaque approximately 57%. The asymmetries tended to be slightly smaller in opercular V1 and greater in calcarine V1. "Spontaneous" ocular dominance stripes were revealed by CO staining of V1 in a naturally strabismic monkey and in a monkey made strabismic by early postnatal alternating monocular occlusion. In these animals, ocular dominance stripes and CO blobs corresponding to the nasal retina stained more intensely for CO in both the right and left V1. ODC spacing and the nasotemporal asymmetry in ODC width and area were similar in strabismic and normal monkeys. Our results in normal monkeys extend the observations of previous investigators and verify that nasotemporal inputs to opercular and calcarine V1 are unequal, with a consistent bias favoring inputs from the nasal retina. The CO results in strabismic macaque suggest that the nasal ODC bias promotes interocular suppression when activity in neighboring ODCs is decorrelated by abnormal binocular experience in infancy.

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BACKGROUND: Dacryocystitis in infants and older children is a serious complication of congenital or acquired nasolacrimal duct obstruction. To define the modes of presentation and treatment strategies of this disorder better, we reviewed the clinical courses of 54 children treated for dacryocystitis at St Louis Children's Hospital. METHODS: Clinical, neuroradiologic, and laboratory data were collated for all cases of dacryocystitis treated from 1990 to 1995. Average follow up of the children in this consecutive series was 1.75 years (range, 4 months to 5 years). RESULTS: Of the 54 patients, 36 (67%) had chronic low-grade dacryocystitis, which was treated with nasolacrimal duct probing on an outpatient basis. The remaining 18 patients (33%) had acute dacryocystitis, which was treated with a combined medical/surgical strategy. Medical treatment consisted of hospital admission for administration of intravenous antibiotics followed by inpatient surgery, which varied according to the age of the patient and the clinical history: 1) Acute dacryocystitis in neonates was treated surgically by nasolacrimal duct probing and nasal endoscopy for excision of intranasal duct cyst; 2) Acute dacryocystitis with periorbital cellulitis was treated surgically by nasolacrimal duct probing; 3) Acute dacryocystitis due to facial trauma was treated surgically by dacryocystorhinostomy and stent placement; and 4) Acute dacryocystitis complicated by orbital abscess was treated by inferior orbitotomy for orbital abscess drainage, simultaneous nasolacrimal duct probing, and stent placement. CONCLUSION: Dacryocystitis in the pediatric population may present in either chronic or acute forms. An effective and safe treatment for acute dacryocystitis is hospital admission, both for administering intravenous antibiotics and monitoring to rule out orbital cellulitis or abscess formation. Intravenous antibiotic therapy is followed within a day or two by surgery tailored to the clinical history. In the majority of both chronic and acute cases, nasolacrimal duct probing appears to be an effective treatment strategy.

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PURPOSE: To determine the prevalence and severity of uveitis in an outpatient pediatric arthritis clinic in the midwestern United States during the 1990s. METHODS: The prevalence and clinical characteristics of uveitis were studied retrospectively for all children diagnosed with arthritis at Shriner's Hospital for Crippled Children and followed by the pediatric rheumatology and ophthalmology units of the St Louis Children's Hospital between 1992 and 1995. RESULTS: Seven children (9%) developed uveitis in a population of 78 patients with juvenile arthritis. Six of the seven children were female, and all six females had anti-nuclear antibody (ANA)-positive, juvenile rheumatoid arthritis (JRA). The prevalence of anterior uveitis in females with ANA-positive, pauciarticular JRA was 20%, and in polyarticular JRA, 17%. One of the girls with uveitis had combined JRA and sarcoidosis; the boy with uveitis had juvenile spondylitis. Arthritis preceded the onset of uveitis in each child by 1 to 13 years (average, 6.4 years). Progression of the uveitis in three of the children resulted in band keratopathy and cataract, causing significant visual loss in two (i.e., in 29% of the children who developed uveitis). CONCLUSION: The prevalence and ocular morbidity of uveitis in juvenile arthritis appears to have remained relatively stable over the last 2 decades. Onset of the uveitis in several of the children in our study population occurred more than a decade after the diagnosis of arthritis. Girls with ANA-positive JRA and boys with juvenile spondylitis may need to be followed by periodic slit-lamp examination for longer periods than recommended previously.

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BACKGROUND: Congenital ocular motor apraxia (COMA) is characterized by the inability to generate volitional horizontal saccadic eye movements in the absence of other focal neurologic abnormalities. SUBJECTS: We report on two children (ages 5 months and 3 years) whose COMA did not adhere to these classic criteria. The children were followed up clinically with serial ocular motor examinations and neuroimaging over a period of 3 years. RESULTS: In the first child horizontal COMA was associated initially with neonatal communicating hydrocephalus. Two and one half years after the first signs of COMA, a fourth ventricle medulloblastoma appeared. The second child, who recovered from a periventricular hemorrhage caused by perinatal asphyxia, manifested vertical COMA and compensatory vertical head thrusts. CONCLUSIONS: COMA may be associated with hydrocephalus, pontocerebellar tumor, and periventricular hemorrhage. These rare variants of COMA emphasize that the eye movement deficits may arise from several locations, cerebral as well as pontocerebellar, in the neuronal pathways generating saccades.

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PURPOSE: To determine whether macaque monkeys who had onset of natural, alternating esotropia in early infancy have the eye movement abnormalities and motion visually evoked potential (VEP) abnormalities observed in human infantile esotropes. METHODS: Recordings were obtained of horizontal pursuit eye movements and fixation nystagmus under conditions of monocular viewing. Motion VEPs in response to horizontal motion were recorded with the animals sedated to reduce the possibility of eye movement artifact. RESULTS: The strabismic monkeys had a naso-temporal asymmetry of horizontal pursuit favoring nasally directed motion when viewing with either eye. When fixating stationary targets, latent nystagmus was apparent; the eyes drifted conjugately and the slow phase of the nystagmus was always nasally directed with respect to the fixating eye. Motion VEPs were characterized by a strong horizontal asymmetry with the directional bias inverted approximately 180 deg in the two eyes. These eye movement and motion VEP asymmetries were not observed in a normal macaque. CONCLUSIONS: Macaque monkeys who have infantile esotropia possess asymmetries of horizontal pursuit and motion VEPs like those documented in strabismic humans. Macaques with infantile esotropia appear to be an appropriate animal model for study of neural mechanisms in strabismus.

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