Syndrome of one and middle of the vertical look: possible clinical entity associated with percheron artery ischemia: semiological and neuroanatomic aspects

Context: The acute paralysis of the vertical gaze is usually caused by a mesencephalic lesion because the control of the vertical conjugated gaze is found there; there are three main structures: the rostral interstitial nucleus of the medial longitudinal fascicle (riFLM), the Cajal interstitial nucleus and the posterior commissure (CP). The riFLM, contains burst neurons responsible for the saccades, projecting to the subnuclei of the upper rectum and inferior oblique to look upwards and subnuclei of the lower rectum and superior oblique to look downwards. The projections for the elevators appear to be bilateral, with axons probably crossing within the oculomotor nuclear complex and apparently not via CP; depressors, on the other hand, are ipsilateral. Case report: Female, 78 years old, hypertensive and diabetic, suddenly started with vertical diplopia and vertigo. Examination: Bilateral hypoactive photomotor reflex, bilateral paralysis of the vertical gaze upward, monocular paralysis downward and torsional nystagmus in the left eye. Resonance with restriction the diffusion of water molecules in both thalamus and in the right rostral midbrain. Conclusions: riFLM is vascularized by the posterior thalamus-subthalamic paramedian artery. A single artery, Percheron’s, provides both riFLM in 20% of the population and allows bilateral lesions from a single infarction. Unilateral infarction can also cause saccadic paralysis of the bilateral vertical gaze. The disjunctive disorders of the vertical gaze have two variants of the one and a half syndrome. One consists of bilateral paralysis of the gaze upwards and monocular paresis of the gaze downwards with an ipsilateral or contralateral lesion, described in thalamomesencephalic lesions, explanation for the exposed case. The other is due to bilateral mesodiencephalic infarctions. It is difficult to understand the relationship between topography and the vertical gaze circuit, showing that it is more complex than we imagine. It is probably an association of topographies, little described, but of paramount importance to be discussed and researched.

Binocular immobilization induced by paralysis of the extraocular muscles of one eye: evidence for an interocular proprioceptive mechanism

1. Spontaneous changes in the positions of both eyes were measured in anesthetized cats before and after infusion of paralytic or anesthetic agents directly into the extraocular muscle capsule behind one eye. 2. Before retrobulbar injection, large changes in eye position were observed in both eyes. The position changes of each eye were independent of each other and often in opposite directions. 3. Application of a paralytic agent into the orbit of one eye reduced the spontaneous position changes in that eye to a very low level. Unexpectedly, the changes in the position of the other, untreated eye were also greatly reduced. 4. Control experiments demonstrated that the binocular immobilization observed after monocular paralysis was not due to 1) leakage of the paralytic agent from the orbit of the treated eye to the orbit of the untreated eye or 2) systemic vascular transport of the paralytic agent. 5. Passive movement of the paralyzed eye did not induce movement of the untreated eye. 6. Application of a local anesthetic agent rather than a paralytic agent to one eye resulted in reversible reduction of movement only in the treated eye, but not in the untreated eye. 7. The results suggest that the reduction of movement in one eye produced by application of a paralytic agent to the other eye is mediated by an afferent neural signal derived from extraocular muscle proprioceptors possibly gated by a central motor control signal.