Open AccessSyndrome of one and middle of the vertical look: possible clinical entity associated with percheron artery ischemia: semiological and neuroanatomic aspects
Author(s) -
Raphael Palomo Barreira,
Vanessa Moraes Rossette,
Thomas Zurga Markus Torres,
Beatriz Medeiros Correa,
Thiago da Cruz Marques,
Clara Kimie Miyahira,
Nahir Miranda,
Natasha Soares Cutolo,
Fernando Pierini Costa,
Euldes Mendes,
Júlio César Claudino dos Santos
Publication year - 2021
Language(s) - English
Resource type - Conference proceedings
DOI - 10.5327/1516-3180.467
Subject(s) - posterior commissure , medial longitudinal fasciculus , anatomy , decussation , medicine , midbrain , psychology , neuroscience , central nervous system , nucleus
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.