In contrast to horizontal gaze, which is generated by unilateral aggregates of cerebral and pontine neurons, vertical eye movements, with few exceptions, are under bilateral control of the cerebral cortex and upper brainstem. The groups of nerve cells and fibers that govern upward and downward gaze, as well as torsional saccades, are situated in the pretectal areas of the midbrain and involve three integrated structures—the riMLF, the INC, and the nucleus and fibers of the posterior commissure (Fig. 13-2).
The riMLF lies at the junction of the midbrain and thalamus, at the rostral end of the medial longitudinal fasciculus, just dorsomedial to the rostral pole of the red nucleus. It functions as the “premotor” nucleus with “burst cells” for the production of fast (saccadic) vertical versional and torsional movements. Input to the riMLF arises both from the PPRF and the vestibular nuclei. Each riMLF projects mainly ipsilaterally to the oculomotor and trochlear nuclei, but each riMLF is also connected to its counterpart by fibers that traverse the posterior commissure. Bilateral lesions of the riMLF or of their interconnections in the posterior commissure are more common than unilateral ones, and cause a loss either of downward saccades or of all vertical saccades.
The INC is a small collection of cells that lies just caudal to the riMLF on each side. Each nucleus projects to the motor neurons of the opposite elevator muscles (superior rectus and inferior oblique) by fibers that cross through the posterior commissure, and it projects ipsilaterally and directly to the depressor muscles (inferior rectus and superior oblique). The functional role of the INC appears to be in holding eccentric vertical gaze, especially after a saccade; it is also integral to the vestibuloocular reflex. Lesions of the INC produce a vertical gaze-evoked and torsional nystagmus, an ocular tilt reaction, and probably slow all conjugate eye movements, mainly vertical ones.
Lesions of the posterior commissure interrupt signals crossing to and from the INC and the riMLF. A lesion here characteristically produces a paralysis of upward gaze and of convergence, often associated with mild mydriasis, accommodative loss, convergence nystagmus, lid retraction (Collier “tucked lid” sign), and, less commonly, ptosis. This constellation is the Parinaud syndrome, also referred to as the pretectal, dorsal midbrain, or sylvian aqueduct syndrome (see “Vertical Gaze Palsy” further on). In some instances, only a restricted combination of these signs is seen. The same syndrome may be produced by unilateral lesions of the posterior commissure, presumably by interrupting bidirectional connections from the riMLF and INC. With acute lesions of the commissure, there is a tonic downward deviation of the eyes and lid retraction (“setting-sun sign”).
The MLF is the main conduit of signals that control vertical gaze from the vestibular nuclei in the medulla to the midbrain centers. For this reason, with internuclear ophthalmoplegia, along with the characteristic adductor paresis on the affected side, vertical pursuit and the VOR are impaired. This is most evident when bilateral internuclear ophthalmoplegia is present. Vertical deviation of the ipsilateral eye (skew) may be seen in cases of unilateral internuclear ophthalmoplegia, as discussed further on.