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

Abstract

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.

Topical Nerve Growth Factor for the Treatment of Neurotrophic Keratopathy Caused by Wallenberg Syndrome

“…Wallenberg syndrome is a rare neurological syndrome whose spectrum is mostly due to a stroke in the dorsal medulla of the brain stem. 1 The trigeminal nuclei involvement is responsible for NK in WS because of trigeminal innervation of the cornea. WS is the most frequent cause of NK of central origin 2,3 and occurs secondarily to damage of trigeminal nucleus in the brain stem.…”