• Alexis Lion, Thierry Haumont, Gérome C Gauchard, Sylvette R Wiener-Vacher, Pierre Lascombes, and Philippe P Perrin.
• Balance Control & Motor Performance, University of Lorraine, UFR STAPS, Villers-lès-Nancy, France.
• Spine. 2013 Feb 1;38(3):238-44.

Study DesignCross-sectional study.ObjectiveTo determine whether adolescent idiopathic scoliosis (AIS) at onset is associated with oculomotor dysfunction and whether these oculomotor anomalies are correlated to the amplitude of the spine deformation.Summary Of Background DataAIS is related to abnormalities of postural control. To date, few studies have focused on visuo-oculomotor and vestibulo-ocular functions at early-stage AIS.MethodsFifty-three adolescent girls were diagnosed with AIS (mean age: 11.6 ± 2.1 yr) on clinical and radiological criteria (mean Cobb angle: 14.8° ± 5.0°). Visuo-oculomotor and vestibulo-ocular functions were studied with video-oculography, including saccades, smooth pursuit, caloric test, and pendular rotation, with visual vestibular ocular reflex and vestibulo-ocular reflex sequences. Two patient groups were defined according to the mean Cobb angle: group 1 included 29 patients with a Cobb angle from 5° to 14° and group 2 included 24 patients with a Cobb angle from 15° to 25°.ResultsThe group 2 showed different saccade characteristics than group 1: higher latencies for saccade sequences characterized by temporal uncertainty and predictive direction; lower velocity regardless of the type of the saccades. No difference was observed for saccadic accuracy and smooth-pursuit gain. For the visual vestibular ocular reflex, group 2 showed lower total maximal slow-phase velocity than group 1, whereas the vestibulo-ocular reflex (tested in dark) did not differ between groups. No difference was observed concerning the caloric vestibular test.ConclusionPatients with a Cobb angle of 15° or more presented normal vestibulo-ocular responses but altered visuo-oculomotor functions, especially for the saccadic latency and velocity. This could be the result of a dysfunction of oculomotor pathways at cerebellar and/or brainstem level. These central disorders may be incriminated in the development of AIS.

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