Dorsolateral medullary infarction registry: a study protocol for a prospective, multicentric registry

Background Dorsolateral medullary infarction is a typical cerebral infarction which is characterized by Wallenberg’s syndrome. Neurotrophic keratopathy is an uncommon consequence of dorsolateral medullary infarction. At present, the protocol is aimed to study the dynamic changes in corneal innervation and the ocular surface environment after dorsolateral medullary infarction. Methods This study will involve consecutive data from all medical records of patients within 7 days of acute dorsolateral medullary infarction onset at the Departments of Neurology from 10 collaborating stroke centers. Eligible patients will mainly be characterized based on detailed physical examinations, multimodal imaging, and corneal related examinations and patients will be followed-up for 2 years. Neurotrophic keratopathy after dorsolateral medullary infarction is the primary endpoint. The dynamic histological corneal innervation and ocular surface environment after dorsolateral medullary infarction will be observed during the follow-up period. Discussion This multicentric, prospective registry is the first to identify and characterize the dynamic changes of corneal innervation and the ocular surface environment after acute dorsolateral medullary infarction. The significance of the study is to emphasize that the curative effect is based on the doctors’ identification of the disease in the earliest stage before irreversible damage occurs to the cornea. Trial registration The registry was registered (ChiCTR-OPC-17,011,625) on June 11, 2017.

Dorsolateral Medullary Infarction: A Neurogenic Cause of a Contralateral, Large-Amplitude Vestibular Evoked Myogenic Potential

The vestibular evoked myogenic potential (VEMP) has become a useful tool to assess the saccule and inferior vestibular nerve function. Vestibulopathies involving the saccule or inferior vestibular nerve typically result in VEMP responses that are diminished or absent on the involved side. Abnormally large VEMPs are rare. Large VEMPs have been associated with superior canal dehiscence, Ménière's disease, and labyrinthine fistula. In all of these cases, the abnormally large VEMP can be explained on the basis of labyrinthine hydromechanical changes that result in excessive saccular displacement in response to intense sound. In this report, a case is presented of a 74-year-old male with dorsal lateral medullary infarction (Wallenberg's syndrome) who presented with an enlarged VEMP—a finding that has not been reported to date as a result of a brain stem lesion. Particularly perplexing, the enlarged VEMP was on the contralesional side. A proposed mechanism of contralateral vestibular nuclei disinhibition secondary to the brain stem stroke is discussed. El potencial miogénico vestibular evocado (VEMP) se ha convertido en una herramienta útil para evaluar el sáculo y la función del nervio vestibular inferior. Las vestibulopatías que involucran el sáculo y el nervio vestibular inferior típicamente generan respuestas del VEMP que están disminuidas o ausentes en lado involucrado. Los VEMP anormalmente grandes son raros. Los VEMP grandes se han asociado con dehiscencia del canal superior, con enfermedad de Ménière y con fístula del laberinto. En todos estos casos, el VEMP anormalmente grande puede explicarse sobre la base de cambios hidromecánicos del laberinto, que producen un desplazamiento excesivo del sáculo, en respuesta a un estímulo sonoro intenso. En este reporte, se presenta un caso de un hombre de 74 años de edad con un infarto medular dorsolateral (Síndrome de Wallenberg), quien mostró un VEMP grande—un hallazgo que a la fecha no ha sido reportado como resultado de una lesión del tallo cerebral. Sorprendentemente, el VEMP agrandado estaba en el lado contrario a la lesión. Se discute un mecanismo propuesto de desinhibición de los núcleos vestibulares contralaterales, producto de la apoplejía en el tallo cerebral.