Brain responses to sound evoked vestibular stimulation for the whole sample of participants (18 healthy controls and 18 CSD patients). Statistical parametric maps (p-corr < 0.05, cluster level corrected for multiple comparisons) for the contrast of STB100 vs. STB65 exclusively masked for white noise (above threshold t-values in red). Response of the PIVC localizer group is outlined in white for comparison. Response is projected onto flat maps of the left (LH) and right (RH) hemisphere of the human PALS atlas (Caret, Washington University School of Medicine, Department of Anatomy and Neurobiology, http://brainmap.wustl.edu).

Brain responses to sound evoked vestibular stimulation for the whole sample of participants (18 healthy controls and 18 CSD patients). Statistical parametric maps (p-corr < 0.05, cluster level corrected for multiple comparisons) for the contrast of STB100 vs. STB65 exclusively masked for white noise (above threshold t-values in red). Response of the PIVC localizer group is outlined in white for comparison. Response is projected onto flat maps of the left (LH) and right (RH) hemisphere of the human PALS atlas (Caret, Washington University School of Medicine, Department of Anatomy and Neurobiology, http://brainmap.wustl.edu).

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Chronic subjective dizziness (CSD) is a common vestibular disorder characterized by persistent non-vertiginous dizziness, unsteadiness, and heightened sensitivity to motion stimuli that may last for months to years after events that cause acute vestibular symptoms or disrupt balance. CSD is not associated with abnormalities of basic vestibular or o...

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... Anxiety-related personality traits and high levels of anxiety and vigilance about acute vestibular symptoms have been associated with the initial pathologic processes (1). Alterations in postural control strategies (31), shifts in multi-sensory information (32), and reduced cortical integration of spatial orientation (33) have been considered as the underlying mechanisms of sustained dizziness in PPPD. Previous studies have shown that patients with a history of anxiety disorders before the onset of vestibular symptoms were more at risk of developing chronic dizziness (34,35). ...
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Objective To investigate differences in the clinical characteristics of patients with persistent postural-perceptual dizziness (PPPD) according to age. Methods We retrospectively reviewed 143 patients diagnosed with PPPD. Patients were classified into three groups by age: young group (19 to 44 years, n = 60), middle-age group (45 to 64 years, n = 56), old group (65 to 85 years, n = 27). Demographic data, scores of the Dizziness Handicap Inventory (DHI), the Niigata PPPD Questionnaire (NPQ), the Hospital Anxiety and Depression Scale (HADS), precipitating conditions, and the results of vestibular function tests including caloric testing, video head impulse test (vHIT), cervical and ocular vestibular evoked myogenic potentials (cVEMPs and oVEMPs), and posturography, were compared among the three groups. Results While there were no significant differences in the scores of the DHI or NPQ, the total score and anxiety score in HADS in the young group were significantly higher than in the old group (p < 0.05, each). On the other hand, for precipitating conditions, the rate of peripheral vestibular diseases was significantly greater in the old group (77.8%) compared to the young group (41.7%, p < 0.01). There was no significant difference in the results of caloric testing, vHIT, cVEMPs, or oVEMPs among the three groups. For posturography, the velocity of the center of pressure with eyes-open as well as with eyes-closed was significantly greater in the old group compared to the young group and the middle-age group (p < 0.005, respectively). Conclusion The clinical characteristics of PPPD were different according to age. Young patients tended to have stronger anxiety than old patients whereas the old patients had a higher proportion of peripheral vestibular diseases among the precipitating conditions compared to young patients.
... The research on the pathogenesis of PPPD included structural and functional neuroimaging. Using sound-evoked vestibular stimulation, one study examined changes in brain activation and connectivity in patients with PPPD (115). Patients with PPPD displayed lower activity than healthy controls in the parieto-insular vestibular cortex (PIVC), hippocampus, inferior frontal gyrus, the posterior and the anterior insula, and the anterior cingulate cortex. ...
... Additional research revealed decreased functional connectivity between PIVC with the hippocampus, inferior frontal gyrus and anterior cingulate cortex. In addition, hippocampal hypofunction in subjects with chronic subjective dizziness may make it harder for them to put space-motion stimuli in the correct context while also making it harder for them to judge the importance of this information due to decreased activity in the anterior insula and anterior cingulate cortex (115). The frontal operculum and anterior tissues play a part in determining the prominence of sensory stimuli (120). ...
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The vestibular system may have a critical role in the integration of sensory information and the maintenance of cognitive function. A dysfunction in the vestibular system has a significant impact on quality of life. Recent research has provided evidence of a connection between vestibular information and cognitive functions, such as spatial memory, navigation and attention. Although the exact mechanisms linking the vestibular system to cognition remain elusive, researchers have identified various pathways. Vestibular dysfunction may lead to the degeneration of cortical vestibular network regions and adversely affect synaptic plasticity and neurogenesis in the hippocampus, ultimately contributing to neuronal atrophy and cell death, resulting in memory and visuospatial deficits. Furthermore, the extent of cognitive impairment varies depending on the specific type of vestibular disease. In the present study, the current literature was reviewed, potential causal relationships between vestibular dysfunction and cognitive performance were discussed and directions for future research were proposed.
... Previous studies on functional neuroimaging methods reported that the symptoms of dizziness and vertigo affected the activation of the cortical vestibular area [17][18][19][20][21][22]. Therefore, the purpose of this study was to confirm the effect of tDCS on clinical features of dizziness and changes in cortical activation in a patient with VM using neuroimaging techniques. ...
... The fNIRS results indicated that the significant HbO and HbT responses in the MTG and ITG of the left hemisphere before the intervention uniformly decreased after the intervention, and the significant HbO and HbT responses in the STG, MTG, and ITG of the right hemisphere decreased after the intervention, except in the MTG. The reduced hemodynamic responses in the STG and MTG related to dizziness can be taken to indicate improved clinical features after the intervention period [17][18][19][20][21][22]. However, the redetected significant response in the MTG of the left hemisphere 6 weeks after the intervention and the continuous significant response in the MTG of the right hemisphere during the intervention period were in line with a previous study reporting increased blood flow in chronic dizziness patients [30]. ...
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Background: Vestibular migraine (VM) is common migraine that occurs in patients with dizziness. Vestibular rehabilitation for managing VM generally remains unclear. Recently, it has been reported that transcranial direct current stimulation (tDCS) has positive effects in alleviating dizziness. This study investigated the effects of tDCS on dizziness and cortical activation in a patient with VM. Methods: We recruited a male patient aged 31 years with no dizziness. The patient watched a video to induce dizziness using a virtual reality device. The study applied the intervention using tDCS for 4 weeks and measured 4 assessments: functional near-infrared spectroscopy (fNIRS), quantitative electroencephalography (qEEG), dizziness handicap inventory, and visual vertigo analog scale. Results: We showed the activation in the middle temporal gyrus and inferior temporal gyrus (ITG) of the left hemisphere and in the superior temporal gyrus and ITG of the right hemisphere in the pre-intervention. After the intervention, the activation of these areas decreased. In the results of qEEG, excessive activation of C3, P3, and T5 in the left hemisphere and C4 in the right hemisphere before intervention disappeared after the intervention. Conclusions: This study indicated that tDCS-based intervention could be considered a viable approach to treating patients with vestibular dysfunction and dizziness caused by VM.
... PPPD is a new diagnostic term for dizziness that was proposed on the basis of PPV and CSD (Staab et al., 2017), and its resting-state functional magnetic resonance imaging (rsfMRI) ndings show that patients with PPPD exhibit decreased connectivity between regions involved in multisensory vestibular processing and spatial cognition, but increased connectivity of networks linking visual and emotional processing (Lee et al., 2018 relative to controls, patients with CSD had reduced activation of the parietal-insula vestibular cortex (including the posterior insula), the anterior insula, the inferior frontal gyrus, the hippocampus, and anterior cingulate cortex by auditory stimuli, and that patients with CSD exhibited reduced activation of the anterior insula and parietal-insula vestibular cortex, altered connectivity between the anterior insula and midoccipital cortex, hippocampus and parietal-insular vestibular cortex, and anterior cingulate cortex and parietal-insular vestibular cortex. And connectivity changes between these regions may be associated with long-term vestibular symptoms in patients (Indovina et al., 2015). Imaging studies on dizziness are few and mostly in the preliminary stage of exploration, and the neural mechanisms of dizziness have not been fully elucidated. ...
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Background Dizziness is one of the most prevalent clinical symptoms in neurology clinics. Nevertheless, the neural mechanisms of dizziness, especially the characterization of EEG microstates, remain incompletely elucidated. Objectives This study aimed to explore the potential characteristics of EEG microstate in patients with Chronic Subjective Dizziness (CSD) and the relationship between dizziness handicaps and EEG microstate parameters. Methods We recruited 29 patients with CSD and 31 age-matched healthy adults. The 128-channel EEG recording of all participants at resting state with eyes closed was performed. Dizziness handicap Inventory (DHI) was used to evaluate patients’ dizziness related handicaps. The EEG microstates was clustered into four classes (A, B, C, and D) and we identified their parameters for logistic analysis. Results The CSD group scored higher on BAI, BDI-13, and the time coverage and occurrence of Microstate B compared to the HC group. And the time coverage and occurrence of Microstate B were also significantly associated with dizziness handicaps in CSD patients. Logistic regression analysis showed that the occurrence of class B microstates (OR = 0.058, 95%CI: 0.005 ~ 0.744) was a significant indicator for distinguishing the CSD group from the HC group. Conclusion The temporal dynamic alternations of EEG microstates and the relationship between dizziness handicaps and Microstate B in patients with CSD may reflect anomalies in their visual network. These neurophysiological characteristics of EEG microstates could be significant for auxiliary diagnosis of dizziness.
... Gray matter (GM) in the cerebellum, multisensory vestibular cortices, visual cortex, and anxiety-related network was structurally altered, according to structural neuroimaging [21,22]. Functional imaging during particular tasks or at rest has also shown abnormal functional activation and connectivity in the previously mentioned areas and in the parieto-insular vestibular cortex (PIVC) as well [22][23][24][25][26][27]. These studies offer strong proof of anatomical and functional abnormalities in the multimodal vestibular cortex in PPPD. ...
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Persistent postural-perceptual dizziness (PPPD) is a chronic functional vestibular disorder, not a structural or psychiatric condition, presented by one or more dizziness, unsteadiness, or non-spinning vertigo symptoms. These symptoms will worsen with upright posture, movements, and exposure to complex visual stimuli. PPDD may be precipitated by disorders that impair balance or induce vestibular symptoms, such as peripheral or central vestibular diseases, other medical conditions, or psychological illness The exact pathophysiological mechanism is unknown, and it might result from functional adjustments to the postural control systems—alterations in the way multisensory information are processed or the integration of spatial orientation and danger perception in the cortex. PPPD is usually associated with co morbidities like anxiety. Subtypes of PPPD are phobic postural vertigo, space and motion discomfort, visual vertigo, and chronic subjective dizziness. PPPD is diagnosed according to the diagnostic criteria of the Barany society. Physical examination and diagnostic investigation are not pathognomic to PPPD. Treatment approaches include patient counseling, vestibular rehabilitation therapy, cognitive behavioral therapy, and medications.
... This is consistent with Frontiers in Neurology 10 frontiersin.org previous reports where decreased FC was found between the vestibular cortex, represented by the posterior perisylvian regions, and visual areas such as the extrastriate areas when evaluating FC in patients with PPPD or predecessors of PPPD relative to HCs (36,37). Moreover, in our study, a higher FC was observed between the PostCG of the left dominant side (38), a somatosensory cortex, and toMTG/ toITG of the right dominant side (39), upstream of the visual pathway ( Figure 3; Table 3). ...
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Introduction Persistent postural-perceptual dizziness (PPPD) is a functional chronic vestibular syndrome with symptom exacerbation by upright posture, motion, and complex visual stimuli. Among these exacerbating factors, visual exacerbation is the most specific characteristic of PPPD requiring further investigation. We hypothesized that stimulus-induced changes occur in the functional connectivity (FC) rather than simple neural activation that is involved in visual stimulation. The present study aimed to identify the neural basis of PPPD by investigating FC before and after visual stimulation. Methods Eleven patients with PPPD and 11 age- and sex-matched healthy controls (HCs) underwent resting-state fMRI (rs-fMRI) before and after task-based fMRI with visual stimuli. Results At pre-stimulus, FC between the vestibular cortex and visual areas was low, while that between the somatosensory and visual areas was high in PPPD compared with that in HCs. FC between the visuospatial (parahippocampal gyrus) and spatial cognitive areas (inferior parietal lobule) was elevated in PPPD even in the pre-stimulus condition, which no longer increased at post-stimulus as observed in HCs. In the post-stimulus condition, FC between the visual and spatial cognitive areas and that between the visual and prefrontal areas increased compared with that in the pre-stimulus condition in PPPD. Task-based fMRI demonstrated that no brain regions showed different activities between the HC and PPPD groups during visual stimulation. Discussion In PPPD, vestibular inputs may not be fully utilized in the vestibulo-visuo-somatosensory network. Given that the FC between visuospatial and spatial cognitive areas increased even in HCs after visual stimuli, elevated status of this FC in combination with the high FC between the somatosensory and visual areas would be involved in the visual exacerbation in PPPD. An increase in FC from the visual areas to spatial cognitive and prefrontal areas after visual stimuli may account for the prolonged symptoms after visual exacerbation and anxious status in PPPD.
... These long-term effects of patients with PPPD are also associated with a reduced local gyrification index in posterior insular cortices, supramarginal gyri, and posterior superior temporal gyri (Nigro et al., 2019), as well as with decreased grey substance in the left middle temporal gyrus, the right anterior insular cortex, the secondary visual cortex, the right superior temporal gyrus, the cerebellum, different areas of the prefrontal cortex, the left posterior hippocampus, and the left anterior cingulate cortex (Wurthmann et al., 2012). Indovina and Riccelli et al. (2015) found a reduced connectivity in patients with CSD compared to a healthy control group between the left anterior insula/inferior frontal gyrus (IFG) and the right superior temporal gyrus (STG), between the left IFG and the right middle occipital gyrus, between the right STG and the hippocampus, and between the right STG and the ACC. Riccelli et al. (2017) found an increased connectivity between the right amygdala and the left PIVC in patients with CSD, with high anxiety-related personality traits (high neuroticism, high introversion) compared to HC group during a virtual reality rollercoaster task. ...
... It is also related to the anxiety-network, because of its strong functional connectivity to the amygdala (Zhao et al., 2014). There is evidence for its involvement in patients with CSD as well: Indovina and Riccelli et al. (2015) found an increase of functional connectivity between the insula and the STG, and between the hippocampus and the STG. We found a stronger activation in the STG in the PPPD group in comparison to both ANX and HC group, which we interpret as an increased neural response to vestibular and emotional stimuli. ...
... An increase of activity in this area might be associated with an increased emotional reaction in patients with PPPD. Another assumption could apply, e.g., an increased activity in the PPPD group may be due to vestibular related processes (Indovina et al., 2015). However, due to the multi-functionality of the hippocampus and selected neuroimaging methods, it is uncertain whether this activation pattern is due to their role in processing anxiety or vestibulo-spatial information. ...
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Introduction: Persistent postural-perceptual dizziness (PPPD) (ICD-11) and anxiety disorders (ANX) share behavioural symptoms like anxiety, avoidance, social withdrawal, hyperarousal, or palpitation as well as neurological symptoms like vertigo, stance and gait disorders. Furthermore, previous studies have shown a bidirectional link between vestibulo-spatial and anxiety neural networks. So far, there have been no neuroimaging-studies comparing these groups. Objectives: The aim of this explorative study was to investigate differences and similarities of neural correlates between these two patient groups and to compare their findings with a healthy control group. Methods: 63 participants, divided in two patient groups (ANX = 20 and PPPD = 14) and two sex and age matched healthy control groups (HC-A = 16, HC-P = 13) were included. Anxiety and dizziness related pictures were shown during fMRI-measurements in a block-design in order to induce emotional responses. All subjects filled in questionnaires regarding vertigo (VSS, VHQ), anxiety (STAI), depression (BDI-II), alexithymia (TAS), and illness-perception (IPQ). After modelling the BOLD response with a standard canonical HRF, voxel-wise t-tests between conditions (emotional-negative vs neutral stimuli) were used to generate statistical contrast maps and identify relevant brain areas (pFDR < 0.05, cluster size >30 voxels). ROI-analyses were performed for amygdala, cingulate gyrus, hippocampus, inferior frontal gyrus, insula, supramarginal gyrus and thalamus (p ≤ 0.05). Results: Patient groups differed from both HC groups regarding anxiety, dizziness, depression and alexithymia scores; ratings of the PPPD group and the ANX group did differ significantly only in the VSS subscale 'vertigo and related symptoms' (VSS-VER). The PPPD group showed increased neural responses in the vestibulo-spatial network, especially in the supramarginal gyrus (SMG), and superior temporal gyrus (STG), compared to ANX and HC-P group. The PPPD group showed increased neural responses compared to the HC-P group in the anxiety network including amygdala, insula, lentiform gyrus, hippocampus, inferior frontal gyrus (IFG) and brainstem. Neuronal responses were enhanced in visual structures, e.g. fusiform gyrus, middle occipital gyrus, and in the medial orbitofrontal cortex (mOFC) in healthy controls compared to patients with ANX and PPPD, and in the ANX group compared to the PPPD group. Conclusions: These findings indicate that neuronal responses to emotional information in the PPPD and the ANX group are comparable in anxiety networks but not in vestibulo-spatial networks. Patients with PPPD revealed a stronger neuronal response especially in SMG and STG compared to the ANX and the HC group. These results might suggest higher sensitivity and poorer adaptation processes in the PPPD group to anxiety and dizziness related pictures. Stronger activation in visual processing areas in HC subjects might be due to less emotional and more visual processing strategies.
... As a newly de ned syndrome, PPPD encompasses the main characteristics of the lesions, including PPV (fear postural vertigo),CSD(chronic subjective dizziness), and related disorders [17] , which is more comprehensive and speci c than previous de nitions. Although the exact pathophysiological mechanism of PPPD has not been clari ed in academic circles, three key mechanisms for the occurrence and development of PPPD are: excessively rigid posture when walking or standing, excessive dependence on visual information rather than vestibular input information when processing spatial orientation information, and failure of the higher cortex in regulating the rst two processes [4,23] . The cognitive behavioral response to this state is often followed by psychological and functional disorders such as fear of falling, anxiety or depression disorders, and postural gait abnormalities [24,25] . ...
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Background: Persistent postural-perceptual dizziness (PPPD) is a disorder of vestibular dysfunction in which chronic dizziness leads to limitations in daily life. Although pharmacology, vestibular rehabilitation, and cognitive behavioral therapy have been suggested to have some efficacy, they have certain limitations. Some patients with PPPD report that square dance can effectively relieve the symptoms of dizziness and instability, and their mood also improves. However, to date, there has been no research about the effect of square dance Exercise on people of PPPD,not to mention the middle-aged and older women who are more interested in square dance. Objective: To evaluate the effects of square dance on the subjective sensations of dizziness, balance enhancement, anxiety, and depressive symptom regulation in middle-aged and older women with PPPD. Materials and Methods: In this trial, a total of 124 patients diagnosed with PPPD were enrolled, among whom 64 were randomly assigned to square dance training as the experimental group (EG), and the other 60 cases were the control group (CG) without square dance training. To evaluate the effect of square dancing on middle-aged and elderly women with PPPD, data from the Dizziness Handicap Inventory (DHI), Hospital Anxiety and Depression Scale (HADS), Active-specific Balance Confidence Scale (ABC), and Vestibular Disorder Activities of Daily Living Scale (VADL) were collected and compared at the beginning and at three and six months of the trial. Results: Before the trial, there were no significant differences between the EG and CG. Compared with baseline measures, DHI, HADS, ABC, and VADL scores improved as the experiment progressed, and the improvements were more pronounced in the EG. Conclusion: Square dance has a positive impact on the subjective sensation of dizziness, balance enhancement, anxiety, and depressive symptom regulation in middle-aged and older women with PPPD.
... [14][15][16] Evidence also points to the direct impact of vestibular dysfunction on mental well-being, with studies reporting links between the vestibular system and brain areas involved in emotional and cognitive processing. [17][18][19] Despite the need for early intervention, routine vestibular assessment and treatment during aTBI does not appear to be commonplace. Previous studies noted long delays to diagnosis and treatment, 8 and large discrepancies in assessment and treatment practices between trauma centres. ...
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Objectives Vestibular dysfunction is common in patients with acute traumatic brain injury (aTBI). Persisting vestibular symptoms (ie, dizziness and imbalance) are linked to poor physical, psychological and socioeconomic outcomes. However, routine management of vestibular dysfunction in aTBI is not always standard practice. We aimed to identify and explore any healthcare professional barriers or facilitators to managing vestibular dysfunction in aTBI. Design A qualitative approach was used. Data were collected using face to face, semi-structured interviews and analysed using the Framework approach. Setting Two major trauma centres in London, UK. Participants 28 healthcare professionals participated: 11 occupational therapists, 8 physiotherapists and 9 surgical/trauma doctors. Results Vestibular assessment and treatment were not routinely undertaken by trauma ward staff. Uncertainty regarding responsibility for vestibular management on the trauma ward was perceived to lead to gaps in patient care. Interestingly, the term dizziness was sometimes perceived as an ‘invisible’ and vague phenomenon, leading to difficulties identifying or ‘proving’ dizziness and a tendency for making non-specific diagnoses. Barriers to routine assessment and treatment included limited knowledge and skills, a lack of local or national guidelines, insufficient training and concerns regarding the practical aspects of managing vestibular dysfunction. Of current trauma ward staff, therapists were identified as appropriate healthcare professionals to adopt new behaviours regarding management of a common form of vestibular dysfunction (benign paroxysmal positional vertigo). Strategies to support this behaviour change include heightened clarity around role, implementation of local or national guidelines, improved access to training and multidisciplinary support from experts in vestibular dysfunction. Conclusions This study has highlighted that role and knowledge barriers exist to multidisciplinary management of vestibular dysfunction in aTBI. Trauma ward therapists were identified as the most appropriate healthcare professionals to adopt new behaviours. Several strategies are proposed to facilitate such behaviour change. Trial registration number ISRCTN91943864 .
... Likewise, other functional connectivity studies have provided convincing evidence for vestibular-cingulate interaction via vestibular dysfunction studies. Indeed, reduced connectivity between the anterior cingulate cortex and the posterior insula has been associated with vertigo, suggesting (mis)-communication between the areas [14]. ...
... Given the recent interest in neuromodulation, our findings apply to the clinic. Several neurological deficits have been linked to vestibular malfunctioning [14,[23][24][25]. Because the Cingulate Gyrus is involved in vestibular processing, this region provides an inviting potential target for treating several disorders. ...
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Background and objectives The cingulate gyrus (CG) is a frequently studied yet not wholly understood area of the human cerebrum. Previous studies have implicated CG in different adaptive cognitive–emotional functions and fascinating or debilitating symptoms. We describe an unusual loss of gravity perception/floating sensation in consecutive persons with drug-resistant epilepsy undergoing electrical cortical stimulation (ECS), network analysis, and network robustness mapping. Methods Using Intracranial–EEG, Granger causality analysis, cortico-cortical evoked potentials, and fMRI, we explicate the functional networks arising from this phenomenon's anterior, middle, and posterior cingulate cortex. Results Fifty-four icEEG cases from 2013 to 2019 were screened. In 40.7% of cases, CG was sampled and in 22.2% the sampling was bilateral. ECS mapping was carried out in 18.5% of the entire cohort and 45.4% of the cingulate sampled cases. Five of the ten CG cases experienced symptoms during stimulation. A total of 1942 electrodes were implanted with a median number of 182 electrode contacts per patient (range: 106–274). The electrode contacts sampled all major cortex regions. Sixty-three contacts were within CG. Of those, 26 were electrically stimulated; 53.8% of the stimulated contacts produced positive responses, whereas 46.2% produced no observable responses. Our study reports a unique perceptive phenomenon of a subjective sense of weightlessness/floating sensation triggered by anterior and posterior CG stimulation, in 30% of cases and 21.42% of electrode stimulation sites. Notable findings include functional connections between the insula, the posterior and anterior cingulate cortex, and networks between the middle cingulate and the frontal and temporal lobes and the cerebellum. We also postulate a vestibular–cerebral–cingulate network responsible for the perception of gravity while suggesting that cingulate functional connectivity follows a long-term developmental trajectory as indicated by a robust, positive correlation with age and the extent of Granger connectivity (r = 0.82, p = 0.0035). Discussion We propose, in conjunction with ECS techniques, that a better understanding of the underlying gravity perception networks can lead to promising neuromodulatory clinical applications. Classification of evidence This study provides Class II evidence for CG's involvement in the higher order processing of gravity perception and related actions.