Abstract

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.

Highlights

  • Capsaicin is able to induce mast cell degranulation, an event probably related to the pathophysiology of a migraine attack

  • Objectives: The present review study aimed to address the mechanisms of action of capsaicin and other chemical inducers in mast cell degranulation and an interaction of nerves and events that happen in the dura mater with the activation of mast cells

  • The analyses showed significantly higher frequency of the genotype VV in those who had depression, compared with the allele A

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Summary

Introduction

Capsaicin is able to induce mast cell degranulation, an event probably related to the pathophysiology of a migraine attack. Neuroinfections are pathologies that affect the CNS, for example, we have Murcomycosis, a progressive infection caused by opportunistic fungi of the order Mucorales, with high frequency in Immunodepressed patients, Diabetes Mellitus (DM) is the main underlying pathology associated with the development of Rhinocerebral Murcomycosis, which represents 50% of the cases, with a mortality rate of 70% (Sidrim, 2012, p.168). The COVID-19 pandemic has been alarming the world since its first outbreak in December 2019 In this scenario, the presence of aggravating factors such as the elevation of the D-dimer and the reduction of the angiotensin-converting enzyme 2 (ACE2) during the clinical course of the disease, collaborated in the appearance of thromboembolic events derived from inflammatory processes and extensive intravascular coagulation, contributing to the emergence of diseases such as Hemorrhagic Stroke (ICH), leading the patient to have a worse clinical prognosis and a consecutive worsening of their health. Despite being classically associated with this etiology, the finding may be present in other diseases, especially infiltrative ones

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