PURPOSE. To investigate whether neuronal activity within the supraoculomotor area (SOA-monosynaptically connected to medial rectus motoneurons and encode vergence angle) of strabismic monkeys was correlated with the angle of horizontal misalignment and therefore helps to define the state of strabismus.METHODS. Single-cell neural activity was recorded from SOA neurons in two monkeys with exotropia as they performed eye movement tasks during monocular viewing.
RESULTS.Horizontal strabismus angle varied depending on eye of fixation (dissociated horizontal deviation) and the activity of SOA cells (n ¼ 35) varied in correlation with the angle of strabismus. Both near-response (cells that showed larger firing rates for smaller angles of exotropia) and far-response (cells that showed lower firing rates for smaller angles of exotropia) cells were identified. SOA cells showed no modulation of activity with changes in conjugate eye position as tested during smooth-pursuit, thereby verifying that the responses were related to binocular misalignment. SOA cell activity was also not correlated with change in horizontal misalignment due to A-patterns of strabismus. Comparison of SOA population activity in strabismic animals and normal monkeys (described in the literature) show that both neural thresholds and neural sensitivities are altered in the strabismic animals compared with the normal animals.CONCLUSIONS. SOA cell activity is important in determining the state of horizontal strabismus, possibly by altering vergence tone in extraocular muscle. The lack of correlated SOA activity with changes in misalignment due to A/V patterns suggest that circuits mediating horizontal strabismus angle and those that mediate A/V patterns are different. (Invest Ophthalmol Vis Sci. 2012;53:3858-3864) DOI:10.1167/iovs.11-9145 I nfantile forms of strabismus occur in as much as 5% of all children.1-3 The exact cause of strabismus is often unknown. 3-5 Many diverse factors, including refractive errors (anisometropia); visual acuity factors (congenital cataracts); genetic factors (congenital fibrosis of extraocular muscle, Marfan's syndrome); brainstem pathology (Duane's syndrome); and muscle pathology (dysthyroid opthalmopathy), likely trigger a cascade of events that result in misaligned eyes. [6][7][8][9][10][11][12][13][14] Despite the generally accepted notion that most strabismus must be a ''brain problem,'' not much is known about how different neural structures contribute to the development and maintenance of the strabismic state. An innervational source for strabismus can be triggered by specific genetic mutations causing structural changes in cranial nerves and thereby resulting in dysinnervation and atrophy of specific extraocular muscles (generally termed as congenital cranial dysinnervation disorders), but these tend to be relatively rare. 15 Pathologies that involve some sort of sensory insult during development, resulting in a cascading disruption in development of visual and oculomotor circuits and thereby misaligned eyes is more...