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Purpose Computerized static stabilometry is a clinical test in neurologic and muscular diseases to assess postural stability or body sway in a quantitative manner. The purpose of this study was to examine whether postural stability would change in the process of the prism adaptation test in patients with intermittent and constant exotropia. Methods Postural stability was measured before the prism adaptation test and immediately, 15 minutes, and 60 minutes after the prism adaptation test by computerized static stabilometry in 17 consecutive adult patients with exotropia, including 10 patients with intermittent exotropia and seven with constant exotropia. Stabilometric parameters were compared between patients with intermittent and those with constant exotropia for 60 minutes by repeated-measures analysis of variance as statistical analysis. Results The Romberg quotients for the root mean square areas of the sway path (cm(2)), the area in the condition of the patients' eyes open, divided by that in the condition of the patients' eyes closed, increased significantly in the time course of the prism adaptation test and returned to the pretest level in patients with intermittent exotropia and in patients with constant exotropia (P = 0.0173). No significant difference in the Romberg quotients was noted between the patients with intermittent exotropia and those with constant exotropia. Conclusions Postural instability became more pronounced by the prism adaptation test in the patients with exotropia. Binocular visual and motor perceptional changes induced by the prism adaptation test could lead to postural instability, with adaptation taking place 60 minutes after the start of the test.

PURPOSE. This study was designed to localize chromosomal susceptibility loci for comitant strabismus among Japanese families by genome-wide linkage analyses. METHODS. Fifty-five Japanese families, with at least two members with comitant strabismus (esotropia and/or exotropia), were subject to full ophthalmic examination, careful ocular history, and review of medical records. DNA was obtained and genotyping was performed with PCR amplification of 400 microsatellite markers. Parametric and nonparametric linkage (NPL) analyses scores were calculated. Linkage analysis was performed for the whole set of families (55 families), and then a second analysis was performed for two subgroups with the phenotypes, esotropia and exotropia. RESULTS. A multipoint parametric heterogeneity logarithm of the odds (HLOD) score of 3.62 was obtained at marker D4S1575 under a dominant model, with a NPL score of 2.68 (P = 0.001). Testing under different penetrances and disease allele frequencies revealed two other susceptibility loci at 7q31.2 under a recessive model (HLOD scores = 3.93 and 4.40 at 125.2 cM and 107.28 cM, respectively). Analysis of the subgroups revealed new susceptibility loci for esotropia; one locus at 8q24.21 is worthy of further investigation. CONCLUSIONS. This study suggests multiple susceptibility loci for comitant strabismus. The loci at chromosomes 4q28.3 and 7q31.2 show a significant evidence of linkage.

To study whether the variation in maximum oblique muscle size accounts for individual variation in the Bielschowsky head tilt phenomenon (BHTP) in clinically diagnosed superior oblique (SO) palsy.Seventeen subjects with clinically diagnosed early-onset or idiopathic SO palsy and 14 normal subjects were enrolled in the study. Magnetic resonance imaging (MRI) in coronal and sagittal planes was used for quantitative morphometry of inferior oblique (IO) and SO muscles. Maximum cross-sectional area of the SO and IO cross section at the mid-inferior rectus crossing were determined in central gaze and compared with paretic eye hypertropia on ipsilesional versus contralesional head tilt.Mean (+/-SD) maximum SO cross section was 18.1 +/- 3.2 mm(2) in normal subjects, 14.2 +/- 6.8 mm(2) ipsilesional to SO palsy, and 19.2 +/- 4.5 mm(2) contralesional to SO palsy. The ipsilesional SO cross section was significantly smaller than the contralesional (P = 0.004) and normal (P = 0.01) ones. The mean IO cross section was 18.3 +/- 3.5 mm(2) in normal subjects, 21.3 +/- 7.9 mm(2) ipsilesional to SO palsy (P = 0.43), and 22.0 +/- 6.7 mm(2) contralesional to SO palsy (P = 0.26). Hyperdeviation varied with head tilt by 20.1 +/- 5.5 degrees in subjects with SO atrophy, and 10.3 +/- 5.6 degrees in subjects without SO atrophy (P = 0.003). Although oblique muscle cross sections did not correlate with BHTP, subjects with clinically diagnosed SO palsy segregated into groups exhibiting normal versus atrophic SO size.SO size does not account for the variation in BHTP in clinically diagnosed SO palsy, supporting the proposition that the BHTP is nonspecific for SO function.