Internuclear ophthalmoparesis (INO), also commonly referred to as intranuclear ophthalmoplegia, is a specific gaze abnormality characterized by impaired horizontal eye movements with weak adduction of the affected eye, and abduction nystagmus of the contralateral eye. It is one of the most localizing brainstem syndromes, resulting from a lesion in the medial longitudinal fasciculus (MLF) in the dorsomedial brainstem tegmentum of either the pons or the midbrain .
Foveation or visual targeting with binocular fusion and stereoscopy (depth perception) requires highly synchronous eye movements that place objects of visual interest on the corresponding points of both retinas. This process is dependent upon the precise coordination between cranial nerves III, IV, and VI, and their interneuronal pathways that project through the medial longitudinal fasciculus (MLF) (figure 1).
The paramedian pontine reticular formation (PPRF) is often referred to as the conjugate gaze center for horizontal eye movements. During horizontal eye movement, the PPRF burst cells innervate the abducens nucleus, which contains two distinctive sets of neurons. Axons from the abducens motorneurons directly innervate the ipsilateral lateral rectus muscle. Axons of the abducens interneurons cross the midline to become the MLF and subsequently innervate the medial rectus subnucleus of the oculomotor complex (cranial nerve nucleus III). This motorneuron innervates the medial rectus muscle.
The MLF exists as a pair of white matter fiber tracts that lie near the midline just under (or ventral to) the fourth ventricle and cerebral aqueduct and extend through the dorsomedial pontine and midbrain tegmentum. Because of their close physical proximity, bilateral injury is common.
An internuclear ophthalmoparesis (INO) results from injury to the MLF within the dorsomedial pontine or midbrain tegmentum. The side of the INO is named by the side of the adduction deficit, which is ipsilateral to the medial longitudinal fasciculus (MLF) lesion [2,3].