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Patients with amblyopia are known to have fixation instability, which arises from alteration of physiologic fixation eye movements (FEMs) and nystagmus. We assessed the effects of monocular, binocular, and dichoptic viewing on FEMs and eye alignment in patients with and without fusion maldevelopment nystagmus (FMN).Thirty-four patients with amblyopia and seven healthy controls were recruited for this study. Eye movements were recorded using infrared video-oculography during (1) fellow eye viewing (FEV), (2) amblyopic eye viewing (AEV), (3) both eye viewing (BEV), and (4) dichoptic viewing (DcV) at varying fellow eye (FE) contrasts. The patients were classified per the clinical type of amblyopia and FEM waveforms into those without nystagmus, those with nystagmus with and without FMN. Fixational saccades and intersaccadic drifts, quick and slow phases of nystagmus, and bivariate contour ellipse area were analyzed in the FE and amblyopic eye (AE).We found that FEMs are differentially affected with increased amplitude of quick phases of FMN observed during AEV than BEV and during DcV at lower FE contrasts. Increased fixation instability was seen in anisometropic patients at lower FE contrasts. Incomitance of eye misalignment was seen with the greatest increase during FEV. Strabismic/mixed amblyopia patients without FMN were more likely to demonstrate a fixation switch where the AE attends to the target during DcV than patients with FMN.Our findings suggest that FEM abnormalities modulate with different viewing conditions as used in various amblyopia therapies. Increased FEM abnormalities could affect the visual function deficits and may have treatment implications.

Pattern strabismus describes horizontal strabismus that is vertically incomitant. Historically, pattern strabismus is attributed to the oblique muscle dysfunction.1 Little is known about the etiology of isolated primary oblique overaction. Clinical observations have suggested that a torsional offset due to loss of fusion might alter the direction of the recti muscle action, hence causing the pattern strabismus.2,3 For example, excyclotorsion of the globe will result in medial rectus becoming a partial elevator leading to overelevation during adduction, and inferior rectus becoming a partial adductor and superior rectus a partial abductor causing a V-pattern. Correlation between the fundus torsion and static eye fixation in patients with pattern strabismus further supported the viewpoint emphasizing altered recti pull.4 Subsequent studies suggested that oblique overaction is a clinical description rather than an actual mechanism of the pattern strabismus.5 Static malposition or dynamic instability of the extraocular muscle pulleys in patients with craniofacial dysmorphism causes pattern strabismus.6 Neurophysiology experiments in nonhuman primates reared with alternate monocular occlusion suggested a neural basis for pattern strabismus.7–9 These animals had cross-axis eye movements; for example, intended horizontal saccades were associated with cross-axis vertical eye movement and vice versa. Neural recordings from ocular motor neurons have shown that horizontal cross-coupled movement corresponds to increased firing rate of horizontal motor neurons, whereas vertical cross-coupled movement corresponds to increased firing rate of vertical motor neurons. The presence of the neural correlate of cross-coupled movements in animal models suggested that abnormal central innervations might cause the pattern strabismus.7–9 These principles describing the pathophysiology of pattern strabismus are based on subjective clinical impression, orbital imaging, and neurophysiology in animal models. There is a paucity of investigations of objective eye movement assessments in human patients with pattern strabismus. We aimed to quantify eye movements and fundus torsion in patients with infantile and late onset pattern strabismus without craniofacial abnormalities. We hypothesized that overaction of the oblique muscles, as previously predicted in pattern strabismus, should be reflected in the static misalignment as well as dynamic disconjugacy of saccades. For example, inferior oblique overaction should cause an upward deviation of the adducting eye during a horizontal saccade, and the oblique upward saccade would have greater amplitude in the adducting than the abducting eye. It is unknown whether patients with pattern strabismus have cross-coupling of the eye movement, as described in the nonhuman primate model. If, indeed, animal models are analogous to the patients with pattern strabismus, we should also see cross-coupled eye movements in these patients. We quantitatively assessed the presence of cross-coupling of saccades in patients with pattern strabismus. There are several possible explanations for cross-coupled responses. Mechanical factors, such as an abnormal fundus torsion or inappropriate innervations, and consequent cross-talk between horizontal and vertical saccade generators, can result in cross-coupling. The torsion hypothesis predicts a correlation between the severity of cross-coupled saccades and the static fundus torsion. According to the torsion hypothesis, patients with greater static torsion will have larger cross-coupling of saccades. The absence of such a correlation would suggest that abnormal static torsion is not the exclusive cause of pattern strabismus.

PURPOSE Human brain generates miniature eye movements, such as microsaccades, to counteract image fading due to visual adaptation. Generation of microsaccade relies on the amount of retinal error or acuity demand for a desired visual task. The goal of this study was to assess the influence of visual blur, induced by uncorrected refractive error on microsaccades and saccades. METHODS Ten subjects with myopia held their gaze on a visual target during two experiment conditions: corrected refractive error and uncorrected refractive error. Eye movements were measured with high-resolution video oculography under binocular viewing conditions during both tasks. Gaze holding function, microsaccades, and visually guided saccades were analyzed and compared during both tasks. RESULTS We found an increase in the amplitude of microsaccades in the presence of uncorrected refractive error, but the microsaccade frequency and velocity remained unchanged. The microsaccade amplitude systematically increased with an increase in uncorrected refractive error. The main sequence relationship relating the saccade amplitude with respective peak velocity was not significantly different between two conditions. The onset latency, peak velocities, and accuracy of visually guided saccades also were unchanged between the two conditions. CONCLUSIONS These results suggest that visual blur, hence the precision of an image on the fovea, has an important role in calibrating the amplitude of fixational eye movements, such as microsaccades.

PURPOSE. Cerebral palsy (CP) is a permanent, nonprogressive disorder of movement and posture due to a lesion of the fetal or infant brain. The goal was to determine whether children with different severities of CP, as defined using the Gross Motor Function Classification System (GMFCS), had different degrees or types of visual dysfunction. METHODS. An observational, cross-sectional‐design study was conducted by using neurologic and masked ophthalmic measurements on a representative cohort of 50 children with CP. Mean age was 5.6 years (range, 2‐19.5 years); mean gestational age was 31 weeks. RESULTS. The likelihood of debilitating visual deficits was greater in children with higher GMFCS scores, independent of gestational age. Children with level 5 disease (most severe) were at greatest risk for high myopia, absence of binocular fusion, dyskinetic strabismus, severe gaze dysfunction, and optic neuropathy or cerebral visual impairment (CVI). These deficits were rare or absent in children with the mildest disease, level 1. When categorized by anatomic or physiologic CP subtype, diplegic and spastic children were more often hyperopic and esotropic, but had the highest prevalence of fusion and stereopsis. In contrast, children with quadriplegic and mixed CP (dyskinetic, athetoid, hypotonic, and ataxic) more often had high myopia, CVI, dyskinetic strabismus, and gaze dysfunction. CONCLUSIONS. Visual deficits differ in children who have mild versus severe CP. Children with GMFCS level 1 to 2 have sensorimotor deficits resembling those of neurologically normal children with strabismus and amblyopia; children at level 3 to 5 have more severe deficits, not observed in neurologically normal children. (Invest Ophthalmol Vis Sci. 2008;49: 572‐580) DOI:10.1167/iovs.07-0525