1例右侧后半规管异位性BPPV初步模拟左侧前半规管BPPV

A. Vats, S. Kothari, A. Biswas
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引用次数: 2

摘要

在任何有由头部相对于重力位置变化引起的旋转性眩晕史的患者中,其动眼力模式引起位置向下跳动的眼球震颤(p-DBN),定位可能在脑干中央、小脑中线或颅脑交界处;或者由于一种罕见的良性阵发性垂直半规管位置性眩晕而引起的周围性眩晕。p-DBN患者中枢性眩晕的大多数严重原因可以通过后窝和颅椎交界处的磁共振成像来诊断。然而,外周p-DBN可能是由于前半规管良性阵发性位置性眩晕(ASC-BPPV)或最近描述的后半规管BPPV的向地性变异(apo-PSC-BPPV)引起的,两者最初几乎无法区分。apo-PSC-BPPV通常的临床情况是最初诊断为ASC-BPPV。然而,在诊断性或治疗性ASC- bppv的定位操作后,定位性动眼力模式改变为上震性眼球震颤,同时扭转方向也发生逆转,与最初诊断的ASC相比,定位于对侧PSC。在该患者的右侧Dix-Hallpike试验中观察到的最初的眼球运动模式,短潜伏期下跳动的左扭(从患者的角度来看)位置性眼球震颤提示诊断为左ASC-BPPV,因此在一周内每天进行多次反向Epley动作治疗。在一周结束时,一个验证性的右Dix-Hallpike测试引发了一个向上的右扭(从患者的角度来看)位置性眼球震颤。该患者的初始左侧ASC-BPPV不太可能在每天进行一周的反向Epley操作后得到解决,并立即出现右侧PSC-BPPV的普通地向变型(地理-PSC-BPPV)。我们可以合理地解释,该患者从一开始就患有右侧apo-PSC-BPPV,对左侧ASC-BPPV进行反向Epley操作导致耳锥体碎片从其非壶腹臂转移到壶腹臂,导致右侧地位psc - bppv。为什么这种情况下智胜临床医生导致不准确的定位和偏侧的原因进行了讨论。患者转化为geo-PSC-BPPV后,采用右Epley手法治疗成功,随访4周无症状。任何有体位性眩晕病史的患者有扭转成分的外周p-DBN可以是ASC-BPPV或apo-PSC-BPPV。在很短的时间间隔内进行非常密切的跟踪,并精心执行位置测试,是区分这两种情况的唯一确定方法。
本文章由计算机程序翻译,如有差异,请以英文原文为准。
A Case of Right Apogeotropic Posterior Semicircular Canal BPPV that Initially Emulated as Left Anterior Semicircular Canal BPPV
Abstract In any patient with a history of rotational vertigo triggered by changes in the position of head relative to the gravity, whose oculomotor patterns elicit a positional downbeating nystagmus (p-DBN), the localization could be either central in the brainstem, midline cerebellum, or at the craniocerebral junction; or else peripheral due to one of the rare variants of benign paroxysmal positional vertigo of vertical semicircular canals. Most serious causes of central vertigo in patients with p-DBN can be diagnosed by magnetic resonance imaging of the posterior fossa and craniovertebral junction. However, the peripheral p-DBN could be either due to anterior semicircular canal benign paroxysmal positional vertigo (ASC-BPPV) or a recently described apogeotropic variant of posterior semicircular canal BPPV (apo-PSC-BPPV) and the two are almost impossible to differentiate initially. The usual clinical scenario in apo-PSC-BPPV is diagnosing it initially as ASC-BPPV. However, following diagnostic or therapeutic positioning maneuvers for the purported ASC-BPPV, the positional oculomotor pattern changes to an upbeating nystagmus with the reversal in the direction of the torsion as well, localizing it to the contralateral PSC with respect to the ASC initially diagnosed. The initial oculomotor pattern observed on the right Dix–Hallpike test in this patient, of a short latency downbeating left torsional (from the patient’s perspective) positional nystagmus suggested a diagnosis of left ASC-BPPV, which was accordingly treated with multiple sessions of reverse Epley maneuvers daily for a week. At the end of the week, a verifying right Dix–Hallpike test elicited an upbeating right torsional (from the patient’s perspective) positional nystagmus. It is extremely unlikely that this patient had resolution of her initial left ASC-BPPV with the daily sessions of reverse Epley maneuvers carried over a week and immediately suffered from commoner geotropic variant of the right PSC-BPPV (geo-PSC-BPPV). It is plausible to interpret that this patient suffered from the right apo-PSC-BPPV from the very outset, and the reverse Epley maneuver performed for the ostensive left ASC-BPPV led to an intracanal shift of otoconial debris from its nonampullary to the ampullary arm resulting in right geo-PSC-BPPV. The reasons why situations like this outwit the clinician resulting in inaccurate localization as well as lateralization is discussed. The patient was successfully treated with right Epley maneuver after transformation to geo-PSC-BPPV and was asymptomatic at follow-up for 4 weeks. A peripheral p-DBN with torsional component in any patient with a history of positionally triggered vertigo can be either ASC-BPPV or apo-PSC-BPPV. A very close follow-up at a short interval of time with meticulously executed positional tests is the only definitive way to differentiate the two conditions.
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