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Effect of diagnostic occlusion in acquired trochlear nerve palsy.

BACKGROUND: Monocular occlusion eliminates the stimulus for fusional vergence. Diagnostic occlusion may therefore be helpful in isolating the genuine profile of the fundamental ocular motility disorder, which may be an important finding regarding both differential diagnosis of strabismus and dosage of surgery. We investigated the effect of diagnostic occlusion on the motility pattern of acquired trochlear nerve palsy.

PATIENTS AND METHODS: Forty-eight patients aged between 6 and 78 years (median 49 years) with unilateral trochlear nerve palsy were first examined without patching, and then after 3 days of diagnostic occlusion. The onset of palsy was 1-35 years before (median 2 years). Squint angles localized with a dark red glass in front of the non-paretic eye were measured at a distance of 2.5 m, using the Harms tangent screen. Vertical and cyclotorsional angles in primary position (PP), 25 degrees abduction of the non-paretic eye (adduction of the paretic eye), and 25 degrees downgaze were measured.

RESULTS: The relation between hyperdeviation of the paretic eye and excyclodeviation (medians of the angles in degrees, ranges in brackets) before and after diagnostic occlusion was 5/5 and 4/6 (0;14/-1;10 and 0;19/2;13) in PP. In contralateral gaze, the relation was 8/5 and 8/6 (0;21/0;10 and 1;24/1;15), and in downgaze, 10/7 and 8/8 (0;21/1;14 and 0;23/3;18). The increase in excyclodeviation, though statistically significant (in PP, p = 0.0002) was small, with a median of 1 degree and large variability. The decrease in hyperdeviation was statistically significant in downgaze. The head-tilt phenomenon remained unchanged.

CONCLUSIONS: In patients with trochlear nerve palsy, diagnostic occlusion regularly causes an increase in excyclodeviation. In 25% of patients, this increase exceeds 3 degrees. The more variable change in vertical deviation, and the lack in change in the head-tilt phenomenon, can be explained by the fact that central gain-modulation causing an increase in both vertical deviation and the head-tilt phenomenon is not reversible within the relatively short time of 3 days. Diagnostic occlusion can eliminate compensatory innervation and may thereby release the genuine motility pattern, but the occlusion can also induce artificial squint angles.

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