Faralli M, Ricci G, Molini E, Bressi T, Simoncelli C, Frenguelli A
Department of Medical-Surgical Specialisation, Otolaryngology and Cervico-Facial Surgery Division, University of Perugia, Italy.
Acta Otorhinolaryngol Ital. 2006 Feb;26(1):25-31.
Aim of this study was to examine possible relationships between several clinical aspects of paroxysmal positional vertigo and factors better defined as "intrinsic" to the patient, above all age. The disorder can affect essentially all age groups; nevertheless, the onset of age-linked degenerative processes, such as vascular damage, can have a negative influence--at least in theory--on the pathogenic mechanisms of cupulolithiasis or canalolithiasis. The study was based on the review of 566 patients with the typical form of paroxysmal positional vertigo. Based on age, the patients were divided into two groups, respectively < or =50 years and > 50 years. For the purposes of this study, a series of clinical-laboratory conditions associated with the risk of, or clear, vascular damage were also considered. The results indicate that if there are no clinical or case-history elements that can be attributed to an aetiological hypothesis, the clinical behaviour of paroxysmal positional vertigo is not affected by the age factor. However, the existence of generic vascular damage, hypothesised by the presence of the above-mentioned conditions, influences certain clinical aspects of the disorder, particularly recovery time, the trend of the active phase and the number of relapses. In conclusion, paroxysmal positional vertigo with a presumed vascular aetiology, the incidence of which increases with age, presents a worse prognosis, not only with respect to the "idiopathic" form in childhood but also the "idiopathic" type in the elderly. The lithiasic model responds well to pathogenic interpretation requirements, which envisage macular degeneration with a vascular component. However, the observation, via imaging, of diffuse ischaemic lesions in critical areas of the brainstem and the cerebellum in many "vascular" patients, does not exclude the possibility of alternative pathogenic mechanisms that, in the final analysis, can lead to compromised VOR on a central level.
本研究的目的是探讨阵发性位置性眩晕的几个临床方面与更确切定义为患者“内在”因素（尤其是年龄）之间的可能关系。该疾病实际上可影响所有年龄组；然而，与年龄相关的退行性过程（如血管损伤）的发生，至少在理论上，可能对嵴顶结石症或半规管结石症的发病机制产生负面影响。本研究基于对566例典型阵发性位置性眩晕患者的回顾。根据年龄，患者被分为两组，分别为≤50岁和＞50岁。为了本研究的目的，还考虑了一系列与血管损伤风险相关或明确的临床实验室情况。结果表明，如果没有可归因于病因假设的临床或病史因素，阵发性位置性眩晕的临床行为不受年龄因素影响。然而，由上述情况推测的一般性血管损伤会影响该疾病的某些临床方面，特别是恢复时间、急性期趋势和复发次数。总之，假定有血管病因的阵发性位置性眩晕，其发病率随年龄增加而上升，不仅相对于儿童期的“特发性”形式，而且相对于老年人的“特发性”类型，预后都更差。结石模型很好地符合发病机制解释要求，该要求设想存在血管成分的黄斑变性。然而，通过影像学观察发现许多“血管性”患者脑干和小脑关键区域存在弥漫性缺血性病变，这并不排除最终可能导致中枢性VOR受损的其他发病机制的可能性。
