Tréchot F, Tonnelet R, Conart J-B, Legou F, Braun M, Angioi K
Département d'Ophtalmologie, CHU de Nancy, hôpitaux de Brabois, , 9, allée du Morvan, 54000 Vandœuvre-lès-Nancy, France; CIC-IT IADI, unité Inserm U-947, Université de Lorraine, 54500 Vandœuvre-lès-Nancy, France.
CIC-IT IADI, unité Inserm U-947, Université de Lorraine, 54500 Vandœuvre-lès-Nancy, France; Service de Neuroradiologie, CHU de Nancy, 29, avenue du Maréchal-de-Lattre-de-Tassigny, 54000 Nancy, France.
J Fr Ophtalmol. 2016 Jun;39(6):491-7. doi: 10.1016/j.jfo.2016.03.004. Epub 2016 Jun 1.
To describe a form of neurovascular compression of the third cranial nerve (CNIII) in idiopathic mydriasis, in which a neurovascular "conflict" exists between the oculomotor nerve, the posterior communicating artery and the clinoid process, using high-resolution magnetic resonance imaging (MRI) with fast imaging employing steady acquisition (FIESTA) sequences.
An 18-month prospective, observational and monocentric case series report was performed. MRI was performed on 5 consecutive patients with idiopathic, unilateral, persistent and nonreactive mydriasis (pure intrinsic palsy of the CNIII). Patients with diplopia, ptosis or ophthalmoplegia were excluded. Cerebral MRI focused on the CNIII pathway from the mesencephalon to the cavernous sinus entry, particularly on the cisternal segment: image acquisition was performed on a 3 Tesla MRI; the protocol included fast imaging employing steady acquisition (FIESTA) and three-dimension time of flight (3D TOF) sequences.
All patients presented a neurovascular compression point, involving the CNIII clamped between a tortuous posterior communicating artery (PCoA) and the posterior clinoid process at the entrance of the cavernous sinus. No cases occurred in the root entry zone. There was no compression on the contralateral side. No tumors or aneurysms were found. Thus, the mydriasis was caused by CNIII compression.
MRI, including FIESTA sequences, revealed a new type of neurovascular conflict between the CNIII, PCoA and posterior clinoid process in patients with incomplete oculomotor palsy. Non-aneurysmal CNIII compression should be considered as a differential diagnosis in the work-up of idiopathic mydriasis. The role of MRI in the work-up of anisocoria should be considered.
利用采用稳态采集快速成像(FIESTA)序列的高分辨率磁共振成像(MRI),描述特发性瞳孔散大中第三脑神经(CNIII)的一种神经血管压迫形式,其中动眼神经、后交通动脉和床突之间存在神经血管“冲突”。
进行了一项为期18个月的前瞻性、观察性单中心病例系列报告。对5例连续的特发性、单侧、持续性和无反应性瞳孔散大(CNIII单纯性固有麻痹)患者进行了MRI检查。排除有复视、上睑下垂或眼肌麻痹的患者。脑部MRI聚焦于从中脑到海绵窦入口的CNIII路径,特别是脑池段:在3特斯拉MRI上进行图像采集;方案包括稳态采集快速成像(FIESTA)和三维时间飞跃(3D TOF)序列。
所有患者均出现神经血管压迫点,涉及在海绵窦入口处夹在迂曲的后交通动脉(PCoA)和后床突之间的CNIII。在神经根入区未发生病例。对侧无压迫。未发现肿瘤或动脉瘤。因此,瞳孔散大是由CNIII压迫引起的。
包括FIESTA序列在内的MRI显示,不完全动眼神经麻痹患者的CNIII、PCoA和后床突之间存在一种新型神经血管冲突。在特发性瞳孔散大的检查中,应将非动脉瘤性CNIII压迫视为鉴别诊断。应考虑MRI在不等大瞳孔检查中的作用。