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Vestibular migraine is amongst the commonest causes of vertigo, but the regions underlying the development of symptoms including enhanced self-motion sensitivity and visually induced dizziness remain unknown. Bednarczuk et al. provide evidence for an abnormal interaction between visual and vestibular cortical regions in vestibular migraine., 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.

Background: A battery of stance and gait tasks can be used to quantify functional deficits and track improvement in balance control following peripheral vestibular loss. An improvement could be due to at least 3 processes: partial peripheral recovery of sensory responses eliciting canal or otolith driven vestibular reflexes; central compensation of vestibular reflex gains, including substitution of intact otolith responses for pathological canal responses; or sensory substitution of visual and proprioceptive inputs for vestibular contributions to balance control. Results: We describe the presumed action of all 3 processes observed for a case of sudden incapacitating acute bilateral peripheral loss probably due to vestibular neuritis. Otolith responses were largely unaffected. However, pathological decreases in all canal-driven vestibular ocular reflex (VOR) gains were observed. After 3 months of vestibular rehabilitation, balance control was normal but VOR gains remained low. Conclusions: This case illustrates the difficulty in predicting balance control improvements from tests of the 10 vestibular end organs and emphasizes the need to test balance control function directly in order to determine if balance control has improved and is normal again despite remaining vestibular sensory deficits. This case also illustrates that the presence of residual otolithic function may be crucial for balance control improvement in cases of bilateral vestibular hypofunction.

Traumatic brain injury (TBI) is the commonest cause of disability in under-40-year-olds. Vestibular features of dizziness (illusory self-motion) or imbalance which affects 50% of TBI patients at 5 years, increases unemployment threefold in TBI survivors. Unfortunately, vestibular diagnoses are cryptogenic in 25% of chronic TBI cases, impeding therapy. We hypothesized that chronic adaptive brain mechanisms uncouple vestibular symptoms from signs. This predicts a masking of vestibular diagnoses chronically but not acutely. Hence, defining the spectrum of vestibular diagnoses in acute TBI should clarify vestibular diagnoses in chronic TBI. There are, however, no relevant acute TBI data. Of 111 Major Trauma Ward adult admissions screened (median 38-years-old), 96 patients (87%) had subjective dizziness (illusory self-motion) and/or objective imbalance were referred to the senior author (BMS). Symptoms included: feeling unbalanced (58%), headache (50%) and dizziness (40%). In the 47 cases assessed by BMS, gait ataxia was the commonest sign (62%) with half of these cases denying imbalance when asked. Diagnoses included BPPV (38%), acute peripheral unilateral vestibular loss (19%), and migraine phenotype headache (34%), another potential source of vestibular symptoms. In acute TBI, vestibular signs are common, with gait ataxia being the most frequent one. However, patients underreport symptoms. The uncoupling of symptoms from signs likely arises from TBI affecting perceptual mechanisms. Hence, the cryptogenic nature of vestibular symptoms in TBI (acute or chronic) relates to a complex interaction between injury (to peripheral and central vestibular structures and perceptual mechanisms) and brain-adaptation, emphasizing the need for acute prospective, mechanistic studies.

In this paper we postulate that disruption of connectivity in the human brain can lead to dizziness, a symptom normally associated with focal disease of the vestibular system. The specific case that we will examine is the development of "unexplained" dizziness in the elderly-an extremely common clinical problem. Magnetic resonance imaging of the brain in the elderly usually show variable degrees of multifocal micro-angiopathy (small vessel white matter disease, SVD); thus, we review the literature, present a conceptual model and report preliminary quantitative EEG data in support of the hypothesis that such hemispheric SVD leads to central nervous system disconnection that elderly patients report as dizziness. Loss of connectivity by age-related build-up of SVD could lead to dizzy feelings through one or more of the following mechanisms: disconnection of cortical vestibular centers, disconnection between frontal gait centers and the basal ganglia, and disconnection between intended motor action (efference copy) and sensory re-afference. Finally, we propose that SVD-mediated dysregulation of cerebral blood pressure is linked to dizziness during standing and walking in elderly patients with "unexplained" dizziness.

This review provides an update on interdisciplinary treatment for dizziness. Dizziness can have various causes and the treatment offered should depend on the cause. After reading this article, the clinician will have an overview of current treatment recommendations. Recommendations are made for the most prevalent causes of dizziness including acute and chronic vestibular syndromes, vestibular neuritis, benign paroxysmal positional vertigo, endolymphatic hydrops and Menière’s disease, vestibular paroxysmia and vestibular migraine, cardiac causes, transient ischaemic attacks and strokes, episodic ataxia type 2, persistent postural-perceptual dizziness, bilateral vestibulopathy, degenerative, autoimmune and neoplastic diseases, upbeat- and downbeat nystagmus. Recommendations include clinical approaches (repositioning manoeuvres), medication (adding, removing or changing current medication depending on aetiology), vestibular physiotherapy, ergotherapy and rehabilitation, treatment of chest pain or stroke units and surgical interventions. If symptoms are acute and severe, medication with antivertigo agents is recommended as a first step, for a maximum period of 3 days. Following initial symptom control, treatment is tailored depending on aetiology. To assist the clinician in obtaining a useful overview, the level of evidence and number needed to treat are reported whenever possible based on study characteristics. In addition, warnings about possible arrhythmias due to medication are issued, and precautions to enable these to be avoided are discussed.

This review aims to assist emergency physicians in finding the underlying aetiology when a patient presents with dizziness to the emergency department. After reading this review, the emergency physician will be able to consider the most relevant differential diagnoses and have an idea about dangerous aetiologies that require immediate action. The emergency physician will also know what diagnostic steps need to be taken at what time, such as the three-component HINTS Test (Head Impulse, Nystagmus, and Test-of-Skew), which helps with distinguishing central from peripheral causes of the acute vestibular syndrome. Furthermore, episodic vestibular syndromes and chronic vestibular syndromes are discussed in detail. The five most frequent categories of dizziness are vasovagal syncope / orthostatic hypotension (22.3%), vestibular causes (19.9%), fluid and electrolyte disorders (17.5%), circulatory/pulmonary causes (14.8%) and central vascular causes (6.4%). Given that it would neither be economical nor practical to send all patients to specialists from the start, we present general guidelines for the diagnostic workup of patients presenting with dizziness to the emergency department. This review will focus on epidemiology, aetiologies, differential diagnoses and diagnostics. Treatment is described in a separate article.

A 31-year-old woman (figure) with relapsing-remitting multiple sclerosis (MS) (first symptoms February 1994, first diagnosis August 1994, Expanded Disability Status Scale [EDSS] 3.0) was diagnosed with breast cancer in January 2014. The last relapse had occurred in August 2007. Under treatment with natalizumab from August 2007 to June 2013, the patient was clinically stable and the brain MRI showed no signs of disease activity. Because of a positive JC virus antibody test, the immunomodulatory therapy was changed to fingolimod in July 2013. The patient remained clinically stable during the switching period and thereafter. In January 2014, a brain MRI showed 2 new lesions without contrast enhancement. After diagnosis of breast cancer in January 2014 and subsequent surgery in February 2014, adjuvant chemotherapy with cyclophosphamide, doxorubicin, and docetaxel was started (March–July 2014). Fingolimod was stopped in March 2014 considering the strong immunosuppressive effect of cyclophosphamide. The patient received granulocyte colony-stimulating factor (G-CSF; pegfilgrastim) 6 mg subcutaneously at each of the 6 cycles of chemotherapy to reduce the risk of infection during the phase of chemotherapy-induced neutropenia. In July 2014, the patient experienced a numbness and tingling in her right leg, which progressed to a severe hemiparesis (EDSS 7.0) leading to hospitalization. The MRI scan of the brain revealed several new lesions including a lesion with contrast enhancement. An IV steroid pulse therapy was administered. She recovered partially (EDSS 6.5). Fingolimod was started again in August 2014. Subsequently the patient developed another relapse with a worsening of the atactic hemiparesis on the left side, resulting in an inability to walk (EDSS 7.5). Again an IV steroid pulse therapy was administered. The patient recovered partially until the end of August 2014, when she was discharged from rehabilitation. At that time, she was able to walk for 50 meters without aid (EDSS 6.0). Another brain MRI in September 2014 revealed confluent progressive lesions in the white matter with partial contrast enhancement. The patient was referred to our inpatient clinic, where again a steroid pulse therapy was administered. In the following months, the patient recovered to a clinical condition similar to that before the start of the chemotherapy (as of August 2015, EDSS 3.0). An MRI scan of the brain in September 2015 did not show new lesions or contrast enhancement compared to the preceding MRI examination in September 2014.

Background Patients with multiple sclerosis (MS) suffer from diminished balance control due to slowed sensory conduction and possibly delayed central processing. Vibrotactile biofeedback of trunk sway has been shown to improve balance control in patients with peripheral and central vestibular disorders. Here, the effects of vibrotactile feedback training on trunk sway and a possible carry-over effect was measured in MS patients during stance and gait. Methods Ten MS patients (mean age 46.8±7.7 years, 40% male) participated in a crossover study in which 7 different stance and gait tasks were trained with and without angle feedback for stance and angular velocity feedback for gait. An assessment sequence of 12 tasks was performed once before and twice after the training sequence. Trunk sway was measured with body-worn gyroscopes. Head mounted vibrotactile biofeedback of trunk sway was provided during one crossover training arm and the following second assessment sequence. Results Biofeedback generally leads to a decrease in sway but an increase in sway angular velocities during some stance tasks compared to training without biofeedback. Biofeedback while walking eyes open resulted in a decreased sway angular velocity. The greatest changes were found in the pitch direction of trunk sway. Effects diminished after biofeedback was removed. Conclusions This study showed that vibrotactile biofeedback of trunk sway beneficially effects stance and provides significant improvement in gait compared to training without biofeedback in MS patients.