## 1 Introduction  
Multiple chemical sensitivity (MCS) is a chronic polysymptomatic, multisystem condition characterized by subjective susceptibility to low levels of a wide spectrum of environmental compounds (such as petrol, perfume or pesticides) [1; 2]. It constitutes a relatively common clinical diagnosis in western populations [2], considering that the prevalence of self-reported chemical sensitivity symptoms in population-based studies has been found to range from 9% to 33% [2]. Relapsing and remittingcentral nervous system (CNS) manifestations including difficulty concentrating, memory problems, fatigue, depression, daytime sleepiness, \"spaciness\" (derealisation), tension, irritability and dizziness are commonly referred to by the patients [2; 3]. Major criteria to define the clinical spectrum of MCS were introduced by [PERSON] [4]; however, the discussion on definition and nomenclature reflects the fact that the aetiology of MCS is still unclear and a matter of debate [2; 5]. The most frequently discussed aetiologies include neurogenic inflammation [6], classical conditioning [7] and biochemical disruptions [8]. According to the neural sensitization theory, MCS is attributed to a pathological hyper-reactivity of neurons in olfactory and limbic areas of the brain [9]. However, the altered CNS responses are hypothesized to be paralleled by increased anxiety, avoidance, anticipatory stress [9] and attention bias [6] to chemical exposure. According to these theories, several studies in the last few years have shown cerebral blood flow distribution abnormalities in patients with MCS, especially while processing odorous substances [10; 11; 12]. In particular, MCS sufferers have been seen to react peculiarly to sensory stimuli, with activation of brain areas connected with motivational, emotional and non-conscious processing of information, such as the amygdala and the hippocampus, encompassed in the limbic system [10; 11; 12; 13; 14], whose pathways are known to mediate CNS sensitization and their dysregulation contributes to abnormalities of behaviour and mood, endocrine, autonomic and immune function [15]. In turn, the same brain circuits seem to be pivotal in vestibular processing, given the fact that the limbic system--previously thought to be engaged in the physiopathological underpinning of this disorder [1]--receives neural input from the vestibular cortex, and therefore it could be involved in vestibular stream processing also below the level of awareness [16; 17]. To screen populations for MCS correctly, [PERSON] and [PERSON] developed the environment exposure sensitivity inventory (EESI) and its quick form (QEESI), which are considered the most reliable tools for research on patients complaining of chemical sensitivity [18]. For instance, researchers have investigated the association between chemical sensitivity and other kinds of environmental intolerances, including noise and olfactory sensitivity [19]. This has been carried out principally by means of questionnaire surveys in clusters of healthy and affected subjects (i.e., teenage students, twins) and, although overlapping phenomena involving physiopathological aspects of MCS and vestibular processing are possible, any research on intolerance to chemicals and vestibular disorder had been devised previously. Thus, due to (i) the overlapping psychogenic and organic burdens that, below the level of consciousness, are shared not only in MCS development but also in the vestibular disorders [1; 10; 11; 12; 13; 15; 16; 17; 20]; (ii) the number of previous studies describing central processing impairment related to inner ear inflow in this syndrome [21; 22]; and (iii) the lack of literature on clinical evidence of the presentation of dizziness [2; 3], the purpose of the present exploratory study was to highlight the possible MCS hidden clinical/subclinical aspects of vestibular impairment by inferential and principal component (PC) analysis applied on the contribution of recently implemented otoneurological testings.