Cedras Assan Mary, Dion Jonathan, Saj Arnaud, Champoux François, Maheu Maxime
School of Speech Language Pathology and Audiology, Montreal University, Montreal, QC H3N 1X7, Canada.
Institut Universitaire sur la Réadaptation en Déficience Physique de Montréal (IURDPM), Pavillon Laurier, CIUSSS du Centre-Sud-de-l'Île-de-Montréal, Montreal, QC H2H 1C4, Canada.
Audiol Res. 2025 Feb 11;15(1):15. doi: 10.3390/audiolres15010015.
: Vestibular agnosia is characterized by a reduced or absent self-motion perception while demonstrating the presence of normal peripheral vestibular function following stimulation. This condition has previously been reported by previous authors in different populations and more recently in traumatic brain injury patients. However, the underlying mechanisms responsible for vestibular agnosia remain a matter of debate. The objective of this manuscript is to review and compare the behavioral and neuroanatomical findings in populations where vestibular agnosia has been demonstrated to better understand the underlying mechanism. : A review of the literature was conducted using four databases: Medline, Embase, Google Scholar, and PubMed. A normal vestibulo-ocular reflex function with an impaired self-motion perception following vestibular stimulation represented the inclusion criteria used. : Behavioral data reviewed in the studies revealed a clear association with postural instability. However, no consensus can be drawn from neuroanatomical data due to variability in brain impairments in those populations even though impairments in the parietal cortex are often reported. : In general, behavioral data and neuroanatomical data regarding vestibular agnosia have been poorly documented throughout the literature. However, vestibular agnosia can be observed in different populations and is present in concomitant postural control deficits, an important predictor of falls. Finally, even though the parietal cortex has been associated with vestibular agnosia, future studies are required to adequately identify the underlying mechanism. Indeed, the parietal cortex could be part of a larger network mediating vestibular agnosia. This review proposes various methods that future studies should use to overcome the present limitations.
前庭失认症的特征是自我运动感知减弱或缺失，同时在受到刺激后显示出正常的外周前庭功能。先前已有作者在不同人群中报道过这种情况，最近在创伤性脑损伤患者中也有发现。然而，导致前庭失认症的潜在机制仍存在争议。本手稿的目的是回顾和比较已证实存在前庭失认症的人群中的行为和神经解剖学发现，以便更好地理解其潜在机制。
医学文献数据库（Medline）、荷兰医学文摘数据库（Embase）、谷歌学术（Google Scholar）和美国国立医学图书馆生物医学文献数据库（PubMed）。纳入标准为前庭刺激后前庭眼反射功能正常但自我运动感知受损。
研究中回顾的行为数据显示与姿势不稳有明显关联。然而，由于这些人群脑损伤的变异性，神经解剖学数据无法得出一致结论，尽管经常报告顶叶皮质有损伤。
总体而言，关于前庭失认症的行为数据和神经解剖学数据在整个文献中记录较少。然而，前庭失认症可在不同人群中观察到，且伴有姿势控制缺陷，这是跌倒的一个重要预测因素。最后，尽管顶叶皮质与前庭失认症有关，但未来仍需开展研究以充分确定其潜在机制。事实上，顶叶皮质可能是介导前庭失认症的更大网络的一部分。本综述提出了未来研究应采用的各种方法，以克服当前的局限性。
