What is internuclear ophthalmoplegia (INO) in multiple sclerosis (MS)?

Updated: Feb 21, 2019
  • Author: Fiona Costello, MD, FRCP; Chief Editor: Hampton Roy, Sr, MD  more...
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INO is a disconnection syndrome characterized by impaired horizontal gaze. Affected individuals have slowed or limited adduction in the eye ipsilateral to the lesion, with associated abducting nystagmus in the contralateral eye. [40] Unilateral or bilateral INO(s) are caused by damage to the MLFs. [40] The MLFs support the rapid neural transmission necessary for abduction of one eye and adduction of the fellow eye to be synchronous in horizontal gaze. Unlike other myelinated tracts in which slight impairment may produce no clinical deficits, the system for coordinated horizontal saccades is extremely sensitive to transmission speeds, making INO a common manifestation observed and reported in MS. [40, 46]

Patients with INO may deny symptoms, particularly with chronicity. Symptomatic patients may describe experiencing blurred vision, oscillopsia, and diplopia. Patients with INO may note worsening symptoms with fatigue or increased body temperature (Uhthoff phenomenon). [40] The reported variability and fatigability may be mistaken for the “pseudo-INO” of myasthenia gravis.

On clinical examination, the adduction deficit in INO may manifest as slowing during the horizontal duction (adduction lag with a full excursion of the eye) or as incomplete adduction producing an incomitant exotropia The adduction lag in INO may be easily overlooked during smooth pursuit testing, and the clinician may need to provoke a quick horizontal saccade to unveil the disruption. Despite deficient adduction during horizontal saccades, medial rectus function is often intact in INO; this feature can be demonstrated with testing convergence, which is mediated by separate inputs to the medial rectus subnucleus that are distinct from the inputs arriving via the MLF. [40] Intact convergence has been interpreted to mean that MLF damage is relatively caudal in the brainstem whereas with more rostral involvement of the supranuclear input to the medial rectus or subnuclei may cause impaired convergence. [40] Because the MLF also contains fibers that mediate vertical eye movements (pursuit, vestibular, and otolithic pathways), vertical gaze deficits may be observed. Patients with bilateral INO may have impaired vertical gaze holding, resulting in primary-position or gaze-evoked vertical nystagmus. [40, 46]

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