ABSTRACT
A primeira descrição de dor severa no trajeto do nervo glossofaríngeo foi realizada por Weisenberg, em 1910¹, em um paciente com tumor do ângulo ponto cerebelar. Entretanto, coube a Harris, em 1926², nomear como nevralgia do nervo glossofaríngeo esse raro quadro clínico, caracterizado por paroxismos de dor intensa, unilaterais, na região posterior da língua, no palato mole, na garganta e na região lateral e posterior da faringe, irradiando para o ouvido. A dor pode ser desencadeada por deglutição, tosse, bocejo ou mastigação e normalmente dura de segundos a minutos. A associação de nevralgia do glossofaríngeo e síncope é muito rara e se deve a breves períodos de bradicardia, assistolia ou hipotensão, sendo a primeira descrição dessa associação, com essa fisiopatologia, realizada por Riley e cols., em 1942.
The first description of severe pain in the distribution of the glossopharyngeal nerve is credited to Weisenberg, in 1910¹, in a patient with cerebellopontine angle tumor. However, it was Harris, in 1926², who coined the term glossopharyngeal neuralgia to describe this rare condition characterized by paroxysms of excruciating pain located laterally at the back of the tongue, soft palate, throat, and lateral and posterior pharynx, radiating to the ear. Swallowing, coughing, yawning or chewing may trigger pain, which usually lasts from seconds to minutes. The association between glossopharyngeal neuralgia and syncope is very rare, being identified by brief episodes of bradycardia, asystole, and hypotension. Such an association, with this same pathophysiology, was first described by Riley et al in 1942.
Subject(s)
Humans , Male , Aged , Glossopharyngeal Nerve Diseases/complications , Neuralgia/complications , Syncope/etiology , Follow-Up Studies , Pacemaker, Artificial , Syncope/diagnosis , Syncope/surgery , Treatment OutcomeABSTRACT
We report a 81 years old female with a severe aortic insufficiency, treated with diuretics and antidepressants admitted due to recurrent syncopal episodes. During the first syncopal episode, an atrioventricular block was detected and an endocavitary demand pacemaker implanted. Two years later, she had a new syncope without evidences of pacemaker failure. The EKG during pacemaker rhythm showed a prolonged QT interval. During hospital monitoring, she presented a self limited polymorphic ventricular tachycardia (Torsade de pointes). Consequently, the pacemaker was programmed at a greater frequency, and the QT interval shortened from 0.73 to 0.56 sec. Thereafter, the patient no longer had tachycardia or syncopal episodes, after one year of follow up