Developing an implementation intervention for managing acute vertigo in the emergency department.

BACKGROUND: There are evidence-based bedside tests for diagnosing acute vertigo, but no evidence-based strategies to support clinicians in implementing them. The purpose of this study was to design an implementation strategy for treating acute vertigo by examining current facilitators and barriers to using these tests in the ED using the principles of implementation science. METHODS: A survey was developed using the Theoretical Domains Framework and Consolidated Framework for Implementation Research to examine barriers and facilitators for using HINTS+ (head impulse, nystagmus, test of skew, plus hearing) and Dix-Hallpike tests. The survey was sent to emergency clinicians (ECs) in a teaching hospital in London, UK, between May and September 2022. Semistructured interviews were conducted simultaneously, and data examined using direct content analysis. Implementation strategies were then selected based on the Expert Recommendations for Implementing Change framework. RESULTS: Fifty-one ECs responded to the survey and six ECs volunteered for interview. Less than half reported using the bedside tests to make a diagnosis. The most common barriers were beliefs about complexity, a lack of supporting materials, memory, lack of skills and negative experiences. The interview data revealed negative beliefs about the necessity, validity, safety and practicality. There were also barriers in the ED environment (eg, lack of space). There was a strong perception that the current approach to managing acute vertigo needed to change and ECs view this as part of their professional role and responsibility. Based on clinician input, the authors selected strategies to improve diagnostic efforts, which included guidelines for training, developing vertigo champions, protocols, memory aids, audit and feedback. CONCLUSION: This study found several barriers to managing acute vertigo such as memory constraints, and inadequate supporting materials and training, although a robust desire for change. The implementation strategy's initial phase is described, which must now be tested.

Reframing postconcussional syndrome as an interface disorder of neurology, psychiatry and psychology.

Persistent symptoms following a minor head injury can cause significant morbidity, yet the underlying mechanisms for this are poorly understood. The shortcomings of the current terminology that refer to non-specific symptom clusters is discussed. This update considers the need for a multi-dimensional approach for the heterogenous mechanisms driving persistent symptoms after mild traumatic brain injury. Relevant pathophysiology is discussed to make the case for mild traumatic brain injury to be conceptualized as an interface disorder spanning neurology, psychiatry and psychology. The relevance of pre-injury factors, psychological co-morbidities and their interaction with the injury to produce persistent symptoms are reviewed. The interplay with psychiatric diagnoses, functional and somatic symptom disorder presentations and the influence of the medicolegal process is considered. The judicious use and interpretation of investigations given the above complexity is discussed, with suggestions of how the explanation of the diagnostic formulation to the patient can be tailored, including insight into the above processes, to aid recovery. Moving beyond the one-dimensional concept of 'postconcussional syndrome' and reframing the cause of persistent symptoms following mild traumatic brain injury in a bio-psycho-socio-ecological model will hopefully improve understanding of the underlying contributory mechanistic interactions and facilitate treatment.

Trial Of Neurostimulation In Conversion Symptoms (TONICS): a feasibility randomised controlled trial of transcranial magnetic stimulation for functional limb weakness.

OBJECTIVES: Transcranial magnetic stimulation (TMS) has been used therapeutically for functional (conversion) motor symptoms but there is limited evidence for its efficacy and the optimal protocol. We examined the feasibility of a novel randomised controlled trial (RCT) protocol of TMS to treat functional limb weakness. DESIGN: A double-blind (patient, outcome assessor) two parallel-arm, controlled RCT. SETTING: Specialist neurology and neuropsychiatry services at a large National Health Service Foundation Trust in London, UK. PARTICIPANTS: Patients with a diagnosis of functional limb weakness (Diagnostic and Statistical Manual of Mental Disorders - Fifth Edition). Exclusion criteria included comorbid neurological or major psychiatric disorder, contraindications to TMS or previous TMS treatment. INTERVENTIONS: Patients were randomised to receive either active (single-pulse TMS to primary motor cortex (M1) above resting motor threshold) or inactive treatment (single-pulse TMS to M1 below resting motor threshold). Both groups received two TMS sessions, 4 weeks apart. OUTCOME MEASURES: We assessed recruitment, randomisation and retention rates. The primary outcome was patient-rated symptom change (Clinical Global Impression-Improvement scale, CGI-I). Secondary outcomes included clinician-rated symptom change, psychosocial functioning and disability. Outcomes were assessed at baseline, both TMS visits and at 3-month follow-up. RESULTS: Twenty-two patients were recruited and 21 (96%) were successfully randomised (active=10; inactive=11). Nineteen (91%) patients were included at follow-up (active=9; inactive=10). Completion rates for most outcomes were good (80%-100%). Most patients were satisfied/very satisfied with the trial in both groups, although ratings were higher in the inactive arm (active=60%, inactive=92%). Adverse events were not more common for the active treatment. Treatment effect sizes for patient-rated CGI-I scores were small-moderate (Cliff's delta=-0.1-0.3, CIs-0.79 to 0.28), reflecting a more positive outcome for the active treatment (67% and 44% of active arm-rated symptoms as 'much improved' at session 2 and follow-up, respectively, vs 20% inactive group). Effect sizes for secondary outcomes were variable. CONCLUSIONS: Our protocol is feasible. The findings suggest that supramotor threshold TMS of M1 is safe, acceptable and potentially beneficial as a treatment for functional limb weakness. A larger RCT is warranted. TRIAL REGISTRATION NUMBER: ISRCTN51225587.

Clinical and Functional Characterization of a Missense ELF2 Variant in a CANVAS Family.

Cerebellar ataxia with neuropathy and bilateral vestibular areflexia syndrome (CANVAS) is a rare disorder with an unknown etiology. We present a British family with presumed autosomal dominant CANVAS with incomplete penetrance and variable expressivity. Exome sequencing identified a rare missense variant in the ELF2 gene at chr4:g.140058846 C > T, c.10G > A, p.A4T which segregated in all affected patients. By using transduced BE (2)-M17 cells, we found that the mutated ELF2 (mt-ELF2) gene increased ATXN2 and reduced ELOVL5 gene expression, the causal genes of type 2 and type 38 spinocerebellar ataxias. Both, western blot and confocal microscopy confirmed an increase of ataxin-2 in BE(2)-M17 cells transduced with lentivirus expressing mt-ELF2 (CEE-mt-ELF2), which was not observed in cells transduced with lentivirus expressing wt-ELF2 (CEE-wt-ELF2). Moreover, we observed a significant decrease in the number and size of lipid droplets in the CEE-mt-ELF2-transduced BE (2)-M17 cells, but not in the CEE-wt-ELF2-transduced BE (2)-M17. Furthermore, changes in the expression of ELOVL5 could be related with the reduction of lipid droplets in BE (2)-M17 cells. This work supports that ELF2 gene regulates the expression of ATXN2 and ELOVL5 genes, and defines new molecular links in the pathophysiology of cerebellar ataxias.

Ramsay Hunt syndrome with cranial polyneuropathy with features of supraglottitis.

A 67-year-old woman presented with a 1-week history of left otalgia and a 1-day history of odynophagia, pain extending into the face and neck, and a productive cough. Flexible nasendoscopy showed features of supraglottitis, with swollen arytenoids and pooling of saliva in the piriform fossae. Laboratory investigations revealed a mildly raised C reactive protein. A CT scan of the neck supported the diagnosis of supraglottitis and pharyngitis, with thickening of the mucosa of the left piriform fossae and left oropharynx. Standard supraglottitis treatment was instigated, but on day 4 of the admission, a vesicular rash and features of cranial nerve involvement (V, VII, VIII, X) developed. A revised diagnosis of Ramsay Hunt syndrome with cranial polyneuropathy was made and later confirmed by varicella zoster virus PCR. After 4 weeks, facial nerve function normalised, but features of other cranial nerve palsies were persistent.

Downregulation of early visual cortex excitability mediates oscillopsia suppression.

OBJECTIVE: To identify in an observational study the neurophysiologic mechanisms that mediate adaptation to oscillopsia in patients with bilateral vestibular failure (BVF). METHODS: We directly probe the hypothesis that adaptive changes that mediate oscillopsia suppression implicate the early visual-cortex (V1/V2). Accordingly, we investigated V1/V2 excitability using transcranial magnetic stimulation (TMS) in 12 avestibular patients and 12 healthy controls. Specifically, we assessed TMS-induced phosphene thresholds at baseline and cortical excitability changes while performing a visual motion adaptation paradigm during the following conditions: baseline measures (i.e., static), during visual motion (i.e., motion before adaptation), and during visual motion after 5 minutes of unidirectional visual motion adaptation (i.e., motion adapted). RESULTS: Patients had significantly higher baseline phosphene thresholds, reflecting an underlying adaptive mechanism. Individual thresholds were correlated with oscillopsia symptom load. During the visual motion adaptation condition, no differences in excitability at baseline were observed, but during both the motion before adaptation and motion adapted conditions, we observed significantly attenuated cortical excitability in patients. Again, this attenuation in excitability was stronger in less symptomatic patients. CONCLUSIONS: Our findings provide neurophysiologic evidence that cortically mediated adaptive mechanisms in V1/V2 play a critical role in suppressing oscillopsia in patients with BVF.

Predictors of clinical recovery from vestibular neuritis: a prospective study.

We sought to identify predictors of symptomatic recovery in vestibular neuritis. Forty VN patients were prospectively studied in the acute phase (median = 2 days) and 32 in the recovery phase (median = 10 weeks) with vestibulo-ocular reflex, vestibular-perceptual, and visual dependence tests and psychological questionnaires. Clinical outcome was Dizziness Handicap Inventory score at recovery phase. Acute visual dependency and autonomic arousal predicted outcome. Worse recovery was associated with a combination of increased visual dependence, autonomic arousal, anxiety/depression, and fear of bodily sensations, but not with vestibular variables. Findings highlight the importance of early identification of abnormal visual dependency and concurrent anxiety.

Differential effect of visual motion adaption upon visual cortical excitability.

The objectives of this study were 1) to probe the effects of visual motion adaptation on early visual and V5/MT cortical excitability and 2) to investigate whether changes in cortical excitability following visual motion adaptation are related to the degree of visual dependency, i.e., an overreliance on visual cues compared with vestibular or proprioceptive cues. Participants were exposed to a roll motion visual stimulus before, during, and after visual motion adaptation. At these stages, 20 transcranial magnetic stimulation (TMS) pulses at phosphene threshold values were applied over early visual and V5/MT cortical areas from which the probability of eliciting a phosphene was calculated. Before and after adaptation, participants aligned the subjective visual vertical in front of the roll motion stimulus as a marker of visual dependency. During adaptation, early visual cortex excitability decreased whereas V5/MT excitability increased. After adaptation, both early visual and V5/MT excitability were increased. The roll motion-induced tilt of the subjective visual vertical (visual dependence) was not influenced by visual motion adaptation and did not correlate with phosphene threshold or visual cortex excitability. We conclude that early visual and V5/MT cortical excitability is differentially affected by visual motion adaptation. Furthermore, excitability in the early or late visual cortex is not associated with an increase in visual reliance during spatial orientation. Our findings complement earlier studies that have probed visual cortical excitability following motion adaptation and highlight the differential role of the early visual cortex and V5/MT in visual motion processing.NEW & NOTEWORTHY We examined the influence of visual motion adaptation on visual cortex excitability and found a differential effect in V1/V2 compared with V5/MT. Changes in visual excitability following motion adaptation were not related to the degree of an individual's visual dependency.

Chronic Symptoms After Vestibular Neuritis and the High-Velocity Vestibulo-Ocular Reflex.

HYPOTHESIS: As the anterior and posterior semicircular canals are vital to the regulation of gaze stability, particularly during locomotion or vehicular travel, we tested whether the high-velocity vestibulo-ocular reflex (VOR) of the three ipsilesional semicircular canals elicited by the modified Head Impulse Test would correlate with subjective dizziness or vertigo scores after vestibular neuritis (VN). BACKGROUND: Recovery after acute VN varies with around half reporting persistent symptoms long after the acute episode. However, an unanswered question is whether chronic symptoms are associated with impairment of the high-velocity VOR of the anterior or posterior canals. METHODS: Twenty patients who had experienced an acute episode of VN at least 3 months earlier were included in this study. Participants were assessed with the video head impulse test (vHIT) of all six canals, bithermal caloric irrigation, the Dizziness Handicap Inventory (DHI), and the Vertigo Symptoms Scale short-form (VSS). RESULTS: Of these 20 patients, 12 thought that they had recovered from the initial episode whereas 8 did not and reported elevated DHI and VSS scores. However, we found no correlation between DHI or VSS scores and the ipsilesional single or combined vHIT gain, vHIT gain asymmetry orcaloric paresis. The high-velocity VOR was not different between patients who thought they had recovered and patients who thought they had not. CONCLUSION: Our findings suggest that chronic symptoms of dizziness after VN are not associated with the high-velocity VOR of the single or combined ipsilesional horizontal, anterior, or posterior semicircular canals.

Are white matter abnormalities associated with "unexplained dizziness"?

INTRODUCTION: Although cerebral small vessel disease is a significant contributor to the development of imbalance and falls in the elderly, whether it causes dizziness is not known. METHODS: A retrospective case analysis was conducted for 122 dizzy patients referred to two neuro-otology tertiary centres in London and Pisa. Patients were divided into 'explained' causes of dizziness (e.g. benign positional vertigo, vestibular neuritis, orthostatic hypotension, cerebellar ataxias) and 'unexplained' dizziness. White matter hyperintensities (WMH) in MRI (T2 weighted and FLAIR sequences) were blindly rated according to the Fazekas scale. RESULTS: 122 patients; 58 (mean age=72, SD=7.95 years) in the 'unexplained' group and 64 (mean age=72.01, SD=8.28 years) in the 'explained' group were recruited. The overall frequency of lesions (Fazekas 1-3) significantly differed between groups (p=0.011). The frequency of severe lesions (Fazekas 3) was significantly higher in the 'unexplained' group (22%) than in the 'explained' group (5%; p=0.003). CONCLUSION: Increased severity of WMH in cases of unexplained dizziness suggests that such abnormalities are likely contributory to the development of dizziness. WM lesions may induce dizziness either because patients perceive a degree of objective unsteadiness or by a disconnection syndrome involving vestibular or locomotor areas of the brain.

Locomotor adaptation is modulated by observing the actions of others.

Observing the motor actions of another person could facilitate compensatory motor behavior in the passive observer. Here we explored whether action observation alone can induce automatic locomotor adaptation in humans. To explore this possibility, we used the "broken escalator" paradigm. Conventionally this involves stepping upon a stationary sled after having previously experienced it actually moving (Moving trials). This history of motion produces a locomotor aftereffect when subsequently stepping onto a stationary sled. We found that viewing an actor perform the Moving trials was sufficient to generate a locomotor aftereffect in the observer, the size of which was significantly correlated with the size of the movement (postural sway) observed. Crucially, the effect is specific to watching the task being performed, as no motor adaptation occurs after simply viewing the sled move in isolation. These findings demonstrate that locomotor adaptation in humans can be driven purely by action observation, with the brain adapting motor plans in response to the size of the observed individual's motion. This mechanism may be mediated by a mirror neuron system that automatically adapts behavior to minimize movement errors and improve motor skills through social cues, although further neurophysiological studies are required to support this theory. These data suggest that merely observing the gait of another person in a challenging environment is sufficient to generate appropriate postural countermeasures, implying the existence of an automatic mechanism for adapting locomotor behavior.