Castellucci Andrea, Botti Cecilia, Bettini Margherita, Fernandez Ignacio Javier, Malara Pasquale, Martellucci Salvatore, Crocetta Francesco Maria, Fornaciari Martina, Lusetti Francesca, Renna Luigi, Bianchin Giovanni, Armato Enrico, Ghidini Angelo
ENT Unit, Department of Surgery, Azienda USL-IRCCS di Reggio Emilia, Reggio Emilia, Italy.
PhD Proam in Clinical and Experimental Medicine, University of Modena and Reggio Emilia, Modena, Italy.
Front Neurol. 2021 Mar 29;12:634782. doi: 10.3389/fneur.2021.634782. eCollection 2021.
We describe a case series of labyrinthine fistula, characterized by Hennebert's sign (HS) elicited by tragal compression despite global hypofunction of semicircular canals (SCs) on a video-head impulse test (vHIT), and review the relevant literature. All three patients presented with different amounts of cochleo-vestibular loss, consistent with labyrinthitis likely induced by labyrinthine fistula due to different temporal bone pathologies (squamous cell carcinoma involving the external auditory canal in one case and middle ear cholesteatoma in two cases). Despite global hypofunction on vHIT proving impaired function for each SC for high accelerations, all patients developed pressure-induced nystagmus, presumably through spared and/or recovered activity for low-velocity canal afferents. In particular, two patients with isolated horizontal SC fistula developed HS with ipsilesional horizontal nystagmus due to resulting excitatory ampullopetal endolymphatic flows within horizontal canals. Conversely, the last patient with bony erosion involving all SCs developed mainly torsional nystagmus directed contralaterally due to additional inhibitory ampullopetal flows within vertical canals. Moreover, despite impaired measurements on vHIT, we found simultaneous direction-changing positional nystagmus likely due to a buoyancy mechanism within the affected horizontal canal in a case and benign paroxysmal positional vertigo involving the dehiscent posterior canal in another case. Based on our findings, we might suggest a functional dissociation between high (impaired) and low (spared/recovered) accelerations for SCs. Therefore, it could be hypothesized that HS in labyrinthine fistula might be due to the activation of regular ampullary fibers encoding low-velocity inputs, as pressure-induced nystagmus is perfectly aligned with the planes of dehiscent SCs in accordance with Ewald's laws, despite global vestibular impairment on vHIT. Moreover, we showed how pressure-induced nystagmus could present in a rare case of labyrinthine fistulas involving all canals simultaneously. Nevertheless, definite conclusions on the genesis of pressure-induced nystagmus in our patients are prevented due to the lack of objective measurements of both low-acceleration canal responses and otolith function.
我们描述了一组迷路瘘管病例系列,其特征为尽管视频头脉冲试验(vHIT)显示半规管(SC)整体功能减退,但压迫耳屏仍可引出亨内贝格征(HS),并回顾了相关文献。所有三名患者均出现不同程度的耳蜗 - 前庭功能丧失,这与可能由迷路瘘管引起的迷路炎相符,病因是不同的颞骨病变(1例为外耳道鳞状细胞癌,2例为中耳胆脂瘤)。尽管vHIT显示整体功能减退,表明每个SC在高加速度时功能受损,但所有患者均出现了压力诱发性眼震,推测是由于低速半规管传入神经的活动得以保留和/或恢复。特别是,两名孤立性水平半规管瘘管患者因水平半规管内产生兴奋性向壶腹内淋巴流而出现HS伴同侧水平眼震。相反,最后一名所有半规管均有骨质侵蚀的患者,由于垂直半规管内额外的抑制性向壶腹内淋巴流,主要出现了向对侧的扭转性眼震。此外,尽管vHIT测量结果受损,但我们发现1例患者可能因患侧水平半规管内的浮力机制出现了同时性变向位置性眼震,另1例患者出现了累及后半规管裂开的良性阵发性位置性眩晕。基于我们的研究结果,我们可能提示半规管在高(受损)加速度和低(保留/恢复)加速度之间存在功能分离。因此,可以假设迷路瘘管中的HS可能是由于编码低速输入的正常壶腹纤维被激活,因为尽管vHIT显示整体前庭功能受损,但压力诱发性眼震与裂开的半规管平面完全符合埃瓦尔德定律。此外,我们展示了压力诱发性眼震如何在罕见的同时累及所有半规管的迷路瘘管病例中出现。然而,由于缺乏对低加速度半规管反应和耳石功能的客观测量,我们无法对患者中压力诱发性眼震的发生机制得出明确结论。