Illusions of Self-Motion during Magnetic Resonance-Guided Focused Ultrasound Thalamotomy for Tremor.

OBJECTIVE: Brain networks mediating vestibular perception of self-motion overlap with those mediating balance. A systematic mapping of vestibular perceptual pathways in the thalamus may reveal new brain modulation targets for improving balance in neurological conditions. METHODS: Here, we systematically report how magnetic resonance-guided focused ultrasound surgery of the nucleus ventralis intermedius of the thalamus commonly evokes transient patient-reported illusions of self-motion. In 46 consecutive patients, we linked the descriptions of self-motion to sonication power and 3-dimensional (3D) coordinates of sonication targets. Target coordinates were normalized using a standard atlas, and a 3D model of the nucleus ventralis intermedius and adjacent structures was created to link sonication target to the illusion. RESULTS: A total of 63% of patients reported illusions of self-motion, which were more likely with increased sonication power and with targets located more inferiorly along the rostrocaudal axis. Higher power and more inferiorly targeted sonications increased the likelihood of experiencing illusions of self-motion by 4 and 2 times, respectively (odds ratios = 4.03 for power, 2.098 for location). INTERPRETATION: The phenomenon of magnetic vestibular stimulation is the most plausible explanation for these illusions of self-motion. Temporary unilateral modulation of vestibular pathways (via magnetic resonance-guided focused ultrasound) unveils the central adaptation to the magnetic field-induced peripheral vestibular bias, leading to an explicable illusion of motion. Consequently, systematic mapping of vestibular perceptual pathways via magnetic resonance-guided focused ultrasound may reveal new intracerebral targets for improving balance in neurological conditions. ANN NEUROL 2024;96:121-132.

We should be screening for benign paroxysmal positional vertigo (BPPV) in all older adults at risk of falling: a commentary on the World Falls Guidelines.

Benign paroxysmal positional vertigo (BPPV) is amongst the commonest causes of dizziness and falls in older adults. Diagnosing and treating BPPV can reduce falls, and thereby reduce fall-related morbidity and mortality. Recent World Falls Guidelines recommend formal assessment for BPPV in older adults at risk of falling, but only if they report vertigo. However, this recommendation ignores the data that (i) many older adults with BPPV experience dizziness as vague unsteadiness (rather than vertigo), and (ii) others may experience no symptoms of dizziness at all. BPPV without vertigo is due to an impaired vestibular perception of self-motion, termed 'vestibular agnosia'. Vestibular agnosia is found in ageing, neurodegeneration and traumatic brain injury, and results in dramatically increased missed BPPV diagnoses. Patients with BPPV without vertigo are typically the most vulnerable for negative outcomes associated with this disorder. We thus recommend simplifying the World Falls Guidelines: all older adults (>60 years) with objective or subjective balance problems, irrespective of symptomatic complaint, should have positional testing to examine for BPPV.

Spinal Cord Stimulation for Gait Disorders in Parkinson's Disease and Atypical Parkinsonism: A Systematic Review of Preclinical and Clinical Data.

BACKGROUND: Falls in extrapyramidal disorders, particularly Parkinson's disease (PD), multisystem atrophy (MSA), and progressive supranuclear palsy (PSP), are key milestones affecting patients' quality of life, incurring increased morbidity/mortality and high healthcare costs. Unfortunately, gait and balance in parkinsonisms respond poorly to currently available treatments. A serendipitous observation of improved gait and balance in patients with PD receiving spinal cord stimulation (SCS) for back pain kindled an interest in using SCS to treat gait disorders in parkinsonisms. OBJECTIVES: We reviewed preclinical and clinical studies of SCS to treat gait dysfunction in parkinsonisms, covering its putative mechanisms and efficacies. MATERIALS AND METHODS: Preclinical studies in animal models of PD and clinical studies in patients with PD, PSP, and MSA who received SCS for gait disorders were included. The main outcome assessed was clinical improvement in gait, together with outcome measures used and possible mechanism of actions. RESULTS: We identified 500 references, and 45 met the selection criteria and have been included in this study for analysis. Despite positive results in animal models, the outcomes in human studies are inconsistent. CONCLUSIONS: The lack of blind and statistically powered studies, the heterogeneity in patient selection and study outcomes, and the poor understanding of the underlying mechanisms of action of SCS are some of the limiting factors in the field. Addressing these limitations will allow us to draw more reliable conclusions on the effects of SCS on gait and balance in extrapyramidal disorders.

Vestibular agnosia in traumatic brain injury and its link to imbalance.

Vestibular dysfunction, causing dizziness and imbalance, is a common yet poorly understood feature in patients with TBI. Damage to the inner ear, nerve, brainstem, cerebellum and cerebral hemispheres may all affect vestibular functioning, hence, a multi-level assessment-from reflex to perception-is required. In a previous report, postural instability was the commonest neurological feature in ambulating acute patients with TBI. During ward assessment, we also frequently observe a loss of vertigo sensation in patients with acute TBI, common inner ear conditions and a related vigorous vestibular-ocular reflex nystagmus, suggesting a 'vestibular agnosia'. Patients with vestibular agnosia were also more unbalanced; however, the link between vestibular agnosia and imbalance was confounded by the presence of inner ear conditions. We investigated the brain mechanisms of imbalance in acute TBI, its link with vestibular agnosia, and potential clinical impact, by prospective laboratory assessment of vestibular function, from reflex to perception, in patients with preserved peripheral vestibular function. Assessment included: vestibular reflex function, vestibular perception by participants' report of their passive yaw rotations in the dark, objective balance via posturography, subjective symptoms via questionnaires, and structural neuroimaging. We prospectively screened 918 acute admissions, assessed 146 and recruited 37. Compared to 37 matched controls, patients showed elevated vestibular-perceptual thresholds (patients 12.92°/s versus 3.87°/s) but normal vestibular-ocular reflex thresholds (patients 2.52°/s versus 1.78°/s). Patients with elevated vestibular-perceptual thresholds [3 standard deviations (SD) above controls' average], were designated as having vestibular agnosia, and displayed worse posturography than non-vestibular-agnosia patients, despite no difference in vestibular symptom scores. Only in patients with impaired postural control (3 SD above controls' mean), whole brain diffusion tensor voxel-wise analysis showed elevated mean diffusivity (and trend lower fractional anisotropy) in the inferior longitudinal fasciculus in the right temporal lobe that correlated with vestibular agnosia severity. Thus, impaired balance and vestibular agnosia are co-localized to the inferior longitudinal fasciculus in the right temporal lobe. Finally, a clinical audit showed a sevenfold reduction in clinician recognition of a common peripheral vestibular condition (benign paroxysmal positional vertigo) in acute patients with clinically apparent vestibular agnosia. That vestibular agnosia patients show worse balance, but without increased dizziness symptoms, explains why clinicians may miss treatable vestibular diagnoses in these patients. In conclusion, vestibular agnosia mediates imbalance in traumatic brain injury both directly via white matter tract damage in the right temporal lobe, and indirectly via reduced clinical recognition of common, treatable vestibular diagnoses.

Consensus on Virtual Management of Vestibular Disorders: Urgent Versus Expedited Care.

The virtual practice has made major advances in the way that we care for patients in the modern era. The culture of virtual practice, consulting, and telemedicine, which had started several years ago, took an accelerated leap as humankind was challenged by the novel coronavirus pandemic (COVID19). The social distancing measures and lockdowns imposed in many countries left medical care providers with limited options in evaluating ambulatory patients, pushing the rapid transition to assessments via virtual platforms. In this novel arena of medical practice, which may form new norms beyond the current pandemic crisis, we found it critical to define guidelines on the recommended practice in neurotology, including remote methods in examining the vestibular and eye movement function. The proposed remote examination methods aim to reliably diagnose acute and subacute diseases of the inner-ear, brainstem, and the cerebellum. A key aim was to triage patients into those requiring urgent emergency room assessment versus non-urgent but expedited outpatient management. Physicians who had expertise in managing patients with vestibular disorders were invited to participate in the taskforce. The focus was on two topics: (1) an adequate eye movement and vestibular examination strategy using virtual platforms and (2) a decision pathway providing guidance about which patient should seek urgent medical care and which patient should have non-urgent but expedited outpatient management.

Abnormal visuo-vestibular interactions in vestibular migraine: a cross sectional study.

Vestibular migraine is among the commonest causes of episodic vertigo. Chronically, patients with vestibular migraine develop abnormal responsiveness to both vestibular and visual stimuli characterized by heightened self-motion sensitivity and visually-induced dizziness. Yet, the neural mechanisms mediating such symptoms remain unknown. We postulate that such symptoms are attributable to impaired visuo-vestibular cortical interactions, which in turn disrupts normal vestibular function. To assess this, we investigated whether prolonged, full-field visual motion exposure, which has been previously shown to modulate visual cortical excitability in both healthy individuals and avestibular patients, could disrupt vestibular ocular reflex and vestibular-perceptual thresholds of self-motion during rotations. Our findings reveal that vestibular migraine patients exhibited abnormally elevated reflexive and perceptual vestibular thresholds at baseline. Following visual motion exposure, both reflex and perceptual thresholds were significantly further increased in vestibular migraine patients relative to healthy controls, migraineurs without vestibular symptoms and patients with episodic vertigo due to a peripheral inner-ear disorder. Our results provide support for the notion of altered visuo-vestibular cortical interactions in vestibular migraine, as evidenced by vestibular threshold elevation following visual motion exposure.

Dopamine Activation Preserves Visual Motion Perception Despite Noise Interference of Human V5/MT.

UNLABELLED: When processing sensory signals, the brain must account for noise, both noise in the stimulus and that arising from within its own neuronal circuitry. Dopamine receptor activation is known to enhance both visual cortical signal-to-noise-ratio (SNR) and visual perceptual performance; however, it is unknown whether these two dopamine-mediated phenomena are linked. To assess this, we used single-pulse transcranial magnetic stimulation (TMS) applied to visual cortical area V5/MT to reduce the SNR focally and thus disrupt visual motion discrimination performance to visual targets located in the same retinotopic space. The hypothesis that dopamine receptor activation enhances perceptual performance by improving cortical SNR predicts that dopamine activation should antagonize TMS disruption of visual perception. We assessed this hypothesis via a double-blinded, placebo-controlled study with the dopamine receptor agonists cabergoline (a D2 agonist) and pergolide (a D1/D2 agonist) administered in separate sessions (separated by 2 weeks) in 12 healthy volunteers in a William's balance-order design. TMS degraded visual motion perception when the evoked phosphene and the visual stimulus overlapped in time and space in the placebo and cabergoline conditions, but not in the pergolide condition. This suggests that dopamine D1 or combined D1 and D2 receptor activation enhances cortical SNR to boost perceptual performance. That local visual cortical excitability was unchanged across drug conditions suggests the involvement of long-range intracortical interactions in this D1 effect. Because increased internal noise (and thus lower SNR) can impair visual perceptual learning, improving visual cortical SNR via D1/D2 agonist therapy may be useful in boosting rehabilitation programs involving visual perceptual training. SIGNIFICANCE STATEMENT: In this study, we address the issue of whether dopamine activation improves visual perception despite increasing sensory noise in the visual cortex. We show specifically that dopamine D1 (or combined D1/D2) receptor activation enhances the cortical signal-to-noise-ratio to boost perceptual performance. Together with the previously reported effects of dopamine upon brain plasticity and learning (Wolf et al., 2003; Hansen and Manahan-Vaughan, 2014), our results suggest that combining rehabilitation with dopamine agonists could enhance both the saliency of the training signal and the long-term effects on brain plasticity to boost rehabilitation regimens for brain injury.

Intratympanic methylprednisolone versus gentamicin in patients with unilateral Ménière's disease: a randomised, double-blind, comparative effectiveness trial.

BACKGROUND: Ménière's disease is characterised by severe vertigo attacks and hearing loss. Intratympanic gentamicin, the standard treatment for refractory Ménière's disease, reduces vertigo, but damages vestibular function and can worsen hearing. We aimed to assess whether intratympanic administration of the corticosteroid methylprednisolone reduces vertigo compared with gentamicin. METHODS: In this double-blind comparative effectiveness trial, patients aged 18-70 years with refractory unilateral Ménière's disease were enrolled at Charing Cross Hospital (London, UK) and Leicester Royal Infirmary (Leicester, UK). Patients were randomly assigned (1:1) by a block design to two intratympanic methylprednisolone (62·5 mg/mL) or gentamicin (40 mg/mL) injections given 2 weeks apart, and were followed up for 2 years. All investigators and patients were masked to treatment allocation. The primary outcome was vertigo frequency over the final 6 months (18-24 months after injection) compared with the 6 months before the first injection. Analyses were done in the intention-to-treat population, and then per protocol. This trial is registered with ClinicalTrials.gov, number NCT00802529. FINDINGS: Between June 19, 2009, and April 15, 2013, 256 patients with Ménière's disease were screened, 60 of whom were enrolled and randomly assigned: 30 to gentamicin and 30 to methylprednisolone. In the intention-to-treat analysis (ie, all 60 patients), the mean number of vertigo attacks in the final 6 months compared with the 6 months before the first injection (primary outcome) decreased from 19·9 (SD 16·7) to 2·5 (5·8) in the gentamicin group (87% reduction) and from 16·4 (12·5) to 1·6 (3·4) in the methylprednisolone group (90% reduction; mean difference -0·9, 95% CI -3·4 to 1·6). Patients whose vertigo did not improve after injection (ie, non-responders) after being assessed by an unmasked clinician were eligible for additional injections given by a masked clinician (eight patients in the gentamicin group vs 15 in the methylprednisolone group). Two non-responders switched from methylprednisolone to gentamicin. Both drugs were well tolerated with no safety concerns. Six patients reported one adverse event each: three in the gentamicin group and three in the methylprednisolone group. The most common adverse event was minor ear infections, which was experienced by one patient in the gentamicin group and two in the methylprednisolone group. INTERPRETATION: Methylprednisolone injections are a non-ablative, effective treatment for refractory Ménière's disease. The choice between methylprednisolone and gentamicin should be made based on clinical knowledge and patient circumstances. FUNDING: Ménière's Society and National Institute for Health Research Imperial Biomedical Research Centre.

Temporoparietal encoding of space and time during vestibular-guided orientation.

When we walk in our environment, we readily determine our travelled distance and location using visual cues. In the dark, estimating travelled distance uses a combination of somatosensory and vestibular (i.e., inertial) cues. The observed inability of patients with complete peripheral vestibular failure to update their angular travelled distance during active or passive turns in the dark implies a privileged role for vestibular cues during human angular orientation. As vestibular signals only provide inertial cues of self-motion (e.g., velocity, °/s), the brain must convert motion information to distance information (a process called 'path integration') to maintain our spatial orientation during self-motion in the dark. It is unknown, however, what brain areas are involved in converting vestibular-motion signals to those that enable such vestibular-spatial orientation. Hence, using voxel-based lesion-symptom mapping techniques, we explored the effect of acute right hemisphere lesions in 18 patients on perceived angular position, velocity and motion duration during whole-body angular rotations in the dark. First, compared to healthy controls' spatial orientation performance, we found that of the 18 acute stroke patients tested, only the four patients with damage to the temporoparietal junction showed impaired spatial orientation performance for leftward (contralesional) compared to rightward (ipsilesional) rotations. Second, only patients with temporoparietal junction damage showed a congruent underestimation in both their travelled distance (perceived as shorter) and motion duration (perceived as briefer) for leftward compared to rightward rotations. All 18 lesion patients tested showed normal self-motion perception. These data suggest that the cerebral cortical regions mediating vestibular-motion ('am I moving?') and vestibular-spatial perception ('where am I?') are distinct. Furthermore, the congruent contralesional deficit in time (motion duration) and position perception, seen only in temporoparietal junction patients, may reflect a common neural substrate in the temporoparietal junction that mediates the encoding of motion duration and travelled distance during vestibular-guided navigation. Alternatively, the deficits in timing and spatial orientation with temporoparietal junction lesions could be functionally linked, implying that the temporoparietal junction may act as a cortical temporal integrator, combining estimates of self-motion velocity over time to derive an estimate of travelled distance. This intriguing possibility predicts that timing abnormalities could lead to spatial disorientation.

The neuroanatomical correlates of training-related perceptuo-reflex uncoupling in dancers.

Sensory input evokes low-order reflexes and higher-order perceptual responses. Vestibular stimulation elicits vestibular-ocular reflex (VOR) and self-motion perception (e.g., vertigo) whose response durations are normally equal. Adaptation to repeated whole-body rotations, for example, ballet training, is known to reduce vestibular responses. We investigated the neuroanatomical correlates of vestibular perceptuo-reflex adaptation in ballet dancers and controls. Dancers' vestibular-reflex and perceptual responses to whole-body yaw-plane step rotations were: (1) Briefer and (2) uncorrelated (controls' reflex and perception were correlated). Voxel-based morphometry showed a selective gray matter (GM) reduction in dancers' vestibular cerebellum correlating with ballet experience. Dancers' vestibular cerebellar GM density reduction was related to shorter perceptual responses (i.e. positively correlated) but longer VOR duration (negatively correlated). Contrastingly, controls' vestibular cerebellar GM density negatively correlated with perception and VOR. Diffusion-tensor imaging showed that cerebral cortex white matter (WM) microstructure correlated with vestibular perception but only in controls. In summary, dancers display vestibular perceptuo-reflex dissociation with the neuronatomical correlate localized to the vestibular cerebellum. Controls' robust vestibular perception correlated with a cortical WM network conspicuously absent in dancers. Since primary vestibular afferents synapse in the vestibular cerebellum, we speculate that a cerebellar gating of perceptual signals to cortical regions mediates the training-related attenuation of vestibular perception and perceptuo-reflex uncoupling.

The cognitive neurology of the vestibular system.

PURPOSE OF REVIEW: The aim is to reappraise the current state about what we know of vestibular cognition. The review focuses on cognition and perception, and hence the stress on human studies. In addition, the cerebral cortex is the main but not exclusive brain region of interest. There is a brief mention of vestibular ocular function if only to demonstrate the differential processing between reflex and perception. The effect of vestibular activation on some aspects of cognition, for example neglect, is not reviewed, as there have been no recent landmark findings in this area. RECENT FINDINGS: The vestibular cerebellum is pivotal in the differential gating of vestibular perceptual and ocular signals to the cerebral cortex. The neuroanatomical correlates mediating vestibular sensations of self-motion ('am I moving?') and spatial orientation ('where am I now?') are distinct. Vestibular-motion perception is supported by a widespread white matter network. Vestibular activation specifically reduces visual motion cortical excitability, whereas other visual cortical regions show an increase in excitability. SUMMARY: As the vestibular ocular reflex (VOR) and self-motion perception can be uncoupled both behaviourally and in neural correlate, deficits underlying vestibular patients' symptoms may not be revealed by simple VOR assessment. Given the pivotal cerebellar role in gating vestibular signals to perceptual regions, modulating mechanisms of cerebellar plasticity, for example by combining training with medication or brain stimulation, may prove fruitful in treating the symptoms of chronic dizzy patients.

Vestibular activation differentially modulates human early visual cortex and V5/MT excitability and response entropy.

Head movement imposes the additional burdens on the visual system of maintaining visual acuity and determining the origin of retinal image motion (i.e., self-motion vs. object-motion). Although maintaining visual acuity during self-motion is effected by minimizing retinal slip via the brainstem vestibular-ocular reflex, higher order visuovestibular mechanisms also contribute. Disambiguating self-motion versus object-motion also invokes higher order mechanisms, and a cortical visuovestibular reciprocal antagonism is propounded. Hence, one prediction is of a vestibular modulation of visual cortical excitability and indirect measures have variously suggested none, focal or global effects of activation or suppression in human visual cortex. Using transcranial magnetic stimulation-induced phosphenes to probe cortical excitability, we observed decreased V5/MT excitability versus increased early visual cortex (EVC) excitability, during vestibular activation. In order to exclude nonspecific effects (e.g., arousal) on cortical excitability, response specificity was assessed using information theory, specifically response entropy. Vestibular activation significantly modulated phosphene response entropy for V5/MT but not EVC, implying a specific vestibular effect on V5/MT responses. This is the first demonstration that vestibular activation modulates human visual cortex excitability. Furthermore, using information theory, not previously used in phosphene response analysis, we could distinguish between a specific vestibular modulation of V5/MT excitability from a nonspecific effect at EVC.

Brain Mechanisms Explaining Postural Imbalance in Traumatic Brain Injury: A Systematic Review.

Introduction: Persisting imbalance and falls in community-dwelling traumatic brain injury (TBI) survivors are linked to reduced long-term survival. However, a detailed understanding of the impact of TBI upon the brain mechanisms mediating imbalance is lacking. To understand the state of the art concerning the brain mechanisms mediating imbalance in TBI, we performed a systematic review of the literature. Methods: PubMed, Web of Science, and Scopus were searched and peer-reviewed research articles in humans, with any severity of TBI (mild, moderate, severe, or concussion), which linked a postural balance assessment (objective or subjective) with brain imaging (through computed tomography, T1-weighted imaging, functional magnetic resonance imaging [fMRI], resting-state fMRI, diffusion tensor imaging, magnetic resonance spectroscopy, single-photon emission computed tomography, electroencephalography, magnetoencephalography, near-infrared spectroscopy, and evoked potentials) were included. Out of 1940 articles, 60 were retrieved and screened, and 25 articles fulfilling inclusion criteria were included. Results: The most consistent finding was the link between imbalance and the cerebellum; however, the regions within the cerebellum were inconsistent. Discussion: The lack of consistent findings could reflect that imbalance in TBI is due to a widespread brain network dysfunction, as opposed to focal cortical damage. The inconsistency in the reported findings may also be attributed to heterogeneity of methodology, including data analytical techniques, small sample sizes, and choice of control groups. Future studies should include a detailed clinical phenotyping of vestibular function in TBI patients to account for the confounding effect of peripheral vestibular disorders on imbalance and brain imaging.

Electrophysiological markers of vestibular-mediated self-motion perception - A pilot study.

Peripheral vestibular activation results in multi-level responses, from brainstem-mediated reflexes (e.g. vestibular ocular reflex - VOR) to perception of self-motion. While VOR responses indicate preserved vestibular peripheral and brainstem functioning, there are no automated measures of vestibular perception of self-motion - important since some patients with brain disconnection syndromes manifest a vestibular agnosia (intact VOR but impaired self-motion perception). Electroencephalography ('EEG') - may provide a surrogate marker of vestibular perception of self-motion. A related objective is obtaining an EEG marker of vestibular sensory signal processing, distinct from vestibular-motion perception. We performed a pilot study comparing EEG responses in the dark when healthy participants sat in a vibrationless computer-controlled motorised rotating chair moving at near threshold of self-motion perception, versus a second situation in which subjects sat in the chair at rest in the dark who could be induced (or not) into falsely perceiving self-motion. In both conditions subjects could perceive self-motion perception, but in the second there was no bottom-up reflex-brainstem activation. Time-frequency analyses showed: (i) alpha frequency band activity is linked to vestibular sensory-signal activation; and (ii) theta band activity is a marker of vestibular-mediated self-motion perception. Consistent with emerging animal data, our findings support the role of theta activity in the processing of self-motion perception.

Treating benign paroxysmal positional vertigo in acute traumatic brain injury: a prospective, randomised clinical trial assessing safety, feasibility, and efficacy.

Background: Benign paroxysmal positional vertigo (BPPV) affects approximately half of acute, moderate-severe traumatic brain injury (TBI) patients. To date, there have been no rigorous studies of BPPV assessment or treatment in this cohort. We aimed to determine the safety, practicability, and efficacy of therapist-led BPPV management in acute TBI and the feasibility of a larger effectiveness trial. Methods: This was a multi-centre, three-arm, parallel-groups, randomised, feasibility trial. Recruitment was via convenience sampling. The main inclusion criteria were age over 18 years and a confirmed, non-penetrating, acute TBI. BPPV-positive patients were randomly allocated to one of three interventions (repositioning manoeuvres, Brandt-Daroff exercises or advice) using minimisation criteria. Outcome assessors were blinded to the intervention. Results: Of 2014 patients screened for inclusion, 180 were assessed for BPPV. Of those assessed, 34% (62/180) had BPPV, and 58 patients received an intervention. Therapist-led interventions were delivered safely and accurately according to intervention monitoring criteria. Resolution of BPPV was observed in 35/58 (60%) patients. The resolution rate was highest following repositioning manoeuvres (78%), followed by the advice (53%) and Brandt-Daroff interventions (42%). 10 patients experienced recurrence. This was observed more frequently in those with skull fractures and bilateral or mixed BPPV. Conclusions: Overall, the results provide strong evidence for the feasibility of a future trial. Therapist-led management of BPPV in acute TBI was safe and practicable. Repositioning manoeuvres seemingly yielded a superior treatment effect. However, given the high recurrence rate of post-traumatic BPPV, the optimal time to treat according to patients' specific recurrence risk requires further investigation. Trial registration: ISRCTN91943864, https://doi.org/10.1186/ISRCTN91943864.

Why are patients with acute traumatic brain injury not routinely assessed or treated for vestibular dysfunction in the UK? A qualitative study.

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.