[Update on central oculomotor disorders and nystagmus]. / Okulomotorikstörungen und Nystagmus.

The diagnosis of ocular motor disorders and the different forms of a nystagmus is based on a systematic clinical examination of all types of eye movements: eye position, spontaneous nystagmus, range of eye movements, smooth pursuit, saccades, gaze-holding function, vergence, optokinetic nystagmus, as well as testing of the function of the vestibulo-ocular reflex (VOR) and visual fixation suppression of the VOR. Relevant anatomical structures are the midbrain, pons, medulla, cerebellum, and cortex. There is a simple clinical rule: vertical and torsional eye movements are generated in the midbrain, horizontal in the pons. The cerebellum is relevant for almost all types of eye movements; typical pathological findings are saccadic smooth pursuit, gaze-evoked nystagmus or dysmetric saccades.Nystagmus is defined as a rhythmic, most often involuntary eye movement. It normally consists of a slow (pathological) drift of the eyes and a fast central compensatory movement of the eyes back to the primary position (re-fixation saccade). There are three major categories: first, spontaneous nystagmus, i. e. nystagmus which occurs in the gaze straight ahead position as upbeat or downbeat nystagmus; second, nystagmus that becomes visible at eccentric gaze only and third, nystagmus which can be elicited by certain maneuvers, e. g. head-shaking, head positioning, air pressure or hyperventilation, most of which are of peripheral vestibular origin. The most frequent central types of spontaneous nystagmus are downbeat and upbeat, infantile, pure torsional, pendular fixation, periodic alternating, and seesaw nystagmus. Many types of central nystagmus allow a precise neuroanatomical localization: for instance, downbeat nystagmus, which is most often caused by a bilateral floccular lesion or dysfunction, or upbeat nystagmus, which is caused by a lesion in the mesencephalon or medulla oblongata. Examples of pharmacotherapy are the use of 4-aminopyridine for downbeat and upbeat nystagmus, memantine or gabapentin for fixation pendular nystagmus or baclofen for periodic alternating nystagmus.

Dizziness and benign paroxysmal positional vertigo among retirement home residents: a cross-sectional descriptive and interventional study.

BACKGROUND: The prevalence of dizziness increases with age. We aimed to determine the point prevalence of dizziness and, in particular, of benign paroxysmal positional vertigo (BPPV) among retirement home residents. Furthermore, we aimed to evaluate the efficacy of a 2-axis turntable based BPPV treatment. METHODS: We contacted all large retirement homes in or around the city of Zurich (Switzerland). 10 retirement homes (with a total of 536 residents) agreed to participate in this study. 83 rejected inquiries by residents led to a potential study population of 453 residents. After a structured interview evaluating the presence and characteristics of dizziness, all willing patients were tested for positional vertigo and nystagmus on a portable and manually operated 2-axis turntable that was transported to the retirement home. Testing consisted of the Dix-Hallpike and supine roll maneuvers to both sides. Participants were immediately treated with the appropriate liberation maneuver whenever BPPV was diagnosed. Otherwise, taking the resident's medical history, a neuro-otological bedside examination, and a review of the available medical documentation was used to identify other causes of dizziness. RESULTS: Out of the 453 residents, 75 (16.6%; average age: 87.0 years; 68% female) were suffering from dizziness presently or in the recent past and gave their consent to participate in this study. Among the participants tested on the turntable (n = 71), BPPV was present in 11.3% (point prevalence). Time-related properties, triggering factors and qualitative attributes of vertigo or dizziness were not significantly different between the dizzy participants with and those without BPPV. In all BPPV patients, appropriate liberation maneuvers were successful. CONCLUSIONS: BPPV could be demonstrated in about one tenth of retirement home residents with dizziness or recent dizziness. Such point prevalence of BPPV translates to a much higher yearly prevalence if one assumes that BPPV is not present on every day. Our finding suggests that retirement home residents suffering from dizziness should be regularly tested for BPPV and treated with appropriate liberation maneuvers, ideally on turntable to reduce strain. TRIAL REGISTRATION: ClinicalTrials.gov Identifier NCT03643354 .

Cerebellar Rebound Nystagmus Explained as Gaze-Evoked Nystagmus Relative to an Eccentric Set Point: Implications for the Clinical Examination.

A brain stem/cerebellar neural integrator enables stable eccentric gaze. Cerebellar loss-of-function can cause an inability to maintain gaze eccentrically (gaze-evoked nystagmus). Moreover, after returning gaze to straight ahead, the eyes may drift toward the prior eye position (rebound nystagmus). Typically, gaze-evoked nystagmus decays during continuously held eccentric gaze. We hypothesized this adaptive behavior to be prerequisite for rebound nystagmus and thus predicted a correlation between the velocity decay of gaze-evoked nystagmus and the initial velocity of rebound nystagmus. Using video-oculography, eye position was measured in 11 patients with cerebellar degeneration at nine horizontal gaze angles (15° nasal to 25° temporal) before (baseline), during, and after attempted eccentric gaze at ± 30° for 20 s. We determined the decrease of slow-phase velocity at eccentric gaze and the slow-phase velocity of the subsequent rebound nystagmus relative to the baseline. During sustained eccentric gaze, eye drift velocity of gaze-evoked nystagmus decreased by 2.40 ± 1.47°/s. Thereafter, a uniform change of initial eye drift velocity relative to the baseline (2.40 ± 1.35°/s) occurred at all gaze eccentricities. The velocity decrease during eccentric gaze and the subsequent uniform change of eye drift were highly correlated (R2 = 0.80, p < 0.001, slope = 1.09). Rebound nystagmus can be explained as gaze-evoked nystagmus relative to a set point (position with least eye drift) away from straight-ahead eye position. To improve detection at the bedside, we suggest testing rebound nystagmus not at straight-ahead eye position but at an eccentric position opposite of prior eccentric gaze (e.g., 10°), ideally using quantitative video-oculography to facilitate diagnosis of cerebellar loss-of-function.

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.

Nystagmus: Diagnosis, Topographic Anatomical Localization and Therapy. / Nystagmus: Diagnose, anatomische Zuordnung und Therapie.

Nystagmus is defined as rhythmic, most often involuntary eye movements. It normally consists of a slow (pathological) drift of the eyes, followed by a fast central compensatory movement back to the primary position (refixation saccade). The direction, however, is reported according to the fast phase. The cardinal symptoms are, on the one hand, blurred vision, jumping images (oscillopsia), reduced visual acuity and, sometimes, double vision; many of these symptoms depend on the eye position. On the other hand, depending on the etiology, patients may suffer from the following symptoms: 1. permanent dizziness, postural imbalance, and gait disorder (typical of downbeat and upbeat nystagmus); 2. if the onset of symptoms is acute, the patient may experience spinning vertigo with a tendency to fall to one side (due to ischemia in the area of the brainstem or cerebellum with central fixation nystagmus or as acute unilateral vestibulopathy with spontaneous peripheral vestibular nystagmus); or 3. positional vertigo. There are two major categories: the first is spontaneous nystagmus, i.e., nystagmus which occurs in the primary position as upbeat or downbeat nystagmus; and the second includes various types of nystagmus which are induced or modified by certain factors. Examples are gaze-evoked nystagmus, head-shaking nystagmus, positional nystagmus, and hyperventilation-induced nystagmus. In addition, there are disorders similar to nystagmus, such as ocular flutter or opsoclonus. The most common central types of spontaneous nystagmus are downbeat and upbeat, infantile, pure torsional, pendular fixation, periodic alternating, and seesaw nystagmus. Many types of nystagmus allow a precise neuroanatomical localization: for instance, downbeat nystagmus, which is most often caused by a bilateral floccular lesion or dysfunction, or upbeat nystagmus, which is caused by a lesion in the midbrain or medulla. Examples of drug treatment are the use of 4-aminopyridine for downbeat and upbeat nystagmus, memantine or gabapentin for pendular fixation nystagmus, or baclofen for periodic alternating nystagmus. In this article we are focusing on nystagmus. In a second article we will focus on central ocular motor disorders, such as saccade or gaze palsy, internuclear ophthalmoplegia, and gaze-holding deficits. Therefore, these types of eye movements will not be described here in detail.

Central Ocular Motor Disorders: Clinical and Topographic Anatomical Diagnosis, Syndromes and Underlying Diseases. / Zentrale Okulomotorikstörungen: klinische Diagnose, anatomische Zuordnung, Syndrome und zugrunde liegende Erkrankungen.

The key to the diagnosis of ocular motor disorders is a systematic clinical examination of the different types of eye movements, including eye position, spontaneous nystagmus, range of eye movements, smooth pursuit, saccades, gaze-holding function, vergence, optokinetic nystagmus, as well as testing of the function of the vestibulo-ocular reflex (VOR) and visual fixation suppression of the VOR. This is like a window which allows you to look into the brain stem and cerebellum even if imaging is normal. Relevant anatomical structures are the midbrain, pons, medulla, cerebellum and rarely the cortex. There is a simple clinical rule: vertical and torsional eye movements are generated in the midbrain, horizontal eye movements in the pons. For example, isolated dysfunction of vertical eye movements is due to a midbrain lesion affecting the rostral interstitial nucleus of the medial longitudinal fasciculus (riMLF), with impaired vertical saccades only or vertical gaze-evoked nystagmus due to dysfunction of the Interstitial nucleus of Cajal (INC). Lesions of the lateral medulla oblongata (Wallenberg syndrome) lead to typical findings: ocular tilt reaction, central fixation nystagmus and dysmetric saccades. The cerebellum is relevant for almost all types of eye movements; typical pathological findings are saccadic smooth pursuit, gaze-evoked nystagmus or dysmetric saccades. The time course of the development of symptoms and signs is important for the diagnosis of underlying diseases: acute: most likely stroke; subacute: inflammatory diseases, metabolic diseases like thiamine deficiencies; chronic progressive: inherited diseases like Niemann-Pick type C with typically initially vertical and then horizontal saccade palsy or degenerative diseases like progressive supranuclear palsy. Treatment depends on the underlying disease. In this article, we deal with central ocular motor disorders. In a second article, we focus on clinically relevant types of nystagmus such as downbeat, upbeat, fixation pendular, gaze-evoked, infantile or periodic alternating nystagmus. Therefore, these types of nystagmus will not be described here in detail.

Gentle rocking movements during sleep in the elderly.

Vestibular stimulation in the form of rocking movements could be a promising non-pharmacological intervention for populations with reduced sleep quality, such as the elderly. We hypothesized that rocking movements influence sleep by promoting comfort. We assessed whether gentle rocking movements can facilitate the transition from wake to sleep, increase sleep spindle density and promote deep sleep in elderly people. We assessed self-reported comfort using a pilot protocol including translational movements and movements along a pendulum trajectory with peak linear accelerations between 0.10 and 0.20 m/s2 . We provided whole-night stimulation using the settings rated most comfortable during the pilot study (movements along a pendulum trajectory with peak linear acceleration of 0.15 m/s2 ). Sleep measures (polysomnography) of two baseline and two movement nights were compared. In our sample (n = 19; eight female; mean age: 66.7 years, standard deviation: 3 years), vestibular stimulation using preferred stimulation settings did not improve sleep. A reduction of delta power was observed, suggesting reduced sleep depth during rocking movements. Sleep fragmentation was similar in both conditions. We did not observe a sleep-promoting effect using settings optimized to be comfortable. This finding could imply that comfort is not the underlying mechanism. At frequencies below 0.3 Hz, the otoliths cannot distinguish tilt from translation. Translational movement trajectories, such as used in previous studies reporting positive effects of rocking, could have caused sensory confusion due to a mismatch between vestibular and other sensory information. We propose that this sensory confusion might be essential to the sleep-promoting effect of rocking movements described in other studies.

Recommendations for initial examination, differential diagnosis, and management of concussion and other head injuries in high-level football.

Head injuries can result in substantially different outcomes, ranging from no detectable effect to transient functional impairments to life-threatening structural lesions. In high-level international football (soccer) tournaments, on average, one head injury occurs in every third match. Making the diagnosis and determining the severity of a head injury immediately on-pitch or off-field is a major challenge for team physicians, especially because clinical signs of a brain injury can develop over several minutes, hours, or even days after the injury. A standardized approach is useful to support team physicians in their decision whether the player should be allowed to continue to play or should be removed from play after head injury. A systematic, football-specific procedure for examination and management during the first 72 hours after head injuries and a graduated Return-to-Football program for high-level players have been developed by an international group of experts based on current national and international guidelines for the management of acute head injuries. The procedure includes seven stages from the initial on-pitch examination to the graduated Return-to-Football program. Details of the assessments and the consequences of different outcomes are described for each stage. Criteria for emergency management (red flags), removal from play (orange flags), and referral to specialists for further diagnosis and treatment (persistent orange flags) are provided. The guidelines for return to sport after concussion-type head injury are specified for football. Thus, the present paper presents a comprehensive procedure for team physicians after a head injury in high-level football.

Case Studies in Neuroscience: Instability of the visual near triad in traumatic brain injury-evidence for a putative convergence integrator.

Deficits of convergence and accommodation are common following traumatic brain injury, including mild traumatic brain injury, although the mechanism and localization of these deficits have been unclear and supranuclear control of the near-vision response has been incompletely understood. We describe a patient who developed profound instability of the near-vision response with inability to maintain convergence and accommodation following mild traumatic brain injury, who was identified to have a structural lesion on brain MRI in the pulvinar of the caudal thalamus, the pretectum, and the rostral superior colliculus. We discuss the potential relationship between posttraumatic clinical near-vision response deficits and the MRI lesion in this patient. We further propose that the MRI lesion location, specifically the rostral superior colliculus, participates in neural integration for convergence holding, given its proven anatomic connections with the central mesencephalic reticular formation and C-group medial rectus motoneurons in the oculomotor nucleus, which project to extraocular muscle nontwitch fibers specialized for fatigue-resistant, slow, tonic activity such as vergence holding.NEW & NOTEWORTHY Supranuclear control of the near-vision response has been incompletely understood to date. We propose, based on clinical and anatomic evidence, functional pathways for vergence that participate in the generation of the near triad, "slow vergence," and vergence holding.

Nystagmus.

PURPOSE OF REVIEW: The clinical and laboratory assessment of nystagmus in patients with neurologic disorders can provide crucial elements for a state-of-the-art differential diagnosis. An increasing number of publications in the fields of neuro-otology and neuro-ophthalmology have nystagmus in the center of interest, which makes frequent updates on the diagnostic and therapeutic relevance of these contributions indispensable. This review covers important clinical studies and studies in basic research relevant for the neurologist published from January 2016 to August 2017. RECENT FINDINGS: Current themes include vestibular nystagmus, positional nystagmus, optokinetic nystagmus and after-nystagmus, vibration-induced nystagmus, head-shaking nystagmus, postrotatory nystagmus, caloric nystagmus, nystagmus in cerebellar disorders, differential diagnosis of nystagmus and treatment approaches (whereas infantile nystagmus syndrome is not addressed in this review). These studies address mechanisms/pathomechanisms, differential diagnoses and treatment of different forms of nystagmus. SUMMARY: In clinical practice, a structured description of nystagmus including its three-dimensional beating direction, trigger factors and duration is of major importance. The differential diagnosis of downbeat nystagmus is broad and includes acute intoxications, neurodegenerative disorders and cerebrovascular causes amongst others. In patients with positional nystagmus, the distinction between frequent benign peripheral and rare but dangerous central causes is imperative.

The Most Common Causes of Eye Pain at 2 Tertiary Ophthalmology and Neurology Clinics.

BACKGROUND: Eye pain is a common complaint, but no previous studies have determined the most common causes of this presenting symptom. Our objective was to determine the most common causes of eye pain in 2 ophthalmology and neurology departments at academic medical centers. METHODS: This was a retrospective cross-sectional analysis and chart review at the departments of ophthalmology and neurology at the University Hospital Zurich (USZ), University of Zürich, Switzerland, and the University of Utah (UU), USA. Data were analyzed from January 2012 to December 2013. We included patients aged 18 years or older presenting with eye pain as a major complaint. RESULTS: Two thousand six hundred three patient charts met inclusion criteria; 742 were included from USZ and 1,861 were included from UU. Of these, 2,407 had been seen in an ophthalmology clinic and 196 had been seen in a neurology clinic. Inflammatory eye disease (conjunctivitis, blepharitis, keratitis, uveitis, dry eye, chalazion, and scleritis) was the underlying cause of eye pain in 1,801 (69.1%) of all patients analyzed. Although only 71 (3%) of 2,407 patients had migraine diagnosed in an ophthalmology clinic as the cause of eye pain, migraine was the predominant cause of eye pain in the neurology clinics (100/196; 51%). Other causes of eye pain in the neurology clinics included optic neuritis (44 patients), trigeminal neuralgia, and other cranial nerve disorders (8 patients). CONCLUSIONS: Eye pain may be associated with a number of different causes, some benign and others sight- or life-threatening. Because patients with eye pain may present to either a neurology or an ophthalmology clinic and because the causes of eye pain may be primarily ophthalmic or neurologic, the diagnosis and management of these patients often requires collaboration and consultation between the 2 specialties.

Gaze-evoked nystagmus induced by alcohol intoxication.

KEY POINTS: The cerebellum is the core structure controlling gaze stability. Chronic cerebellar diseases and acute alcohol intoxication affect cerebellar function, inducing, among others, gaze instability as gaze-evoked nystagmus. Gaze-evoked nystagmus is characterized by increased centripetal eye-drift. It is used as an important diagnostic sign for patients with cerebellar degeneration and to assess the 'driving while intoxicated' condition. We quantified the effect of alcohol on gaze-holding using an approach allowing, for the first time, the comparison of deficits induced by alcohol intoxication and cerebellar degeneration. Our results showed that alcohol intoxication induces a two-fold increase of centripetal eye-drift. We establish analysis techniques for using controlled alcohol intake as a model to support the study of cerebellar deficits. The observed similarity between the effect of alcohol and the clinical signs observed in cerebellar patients suggests a possible pathomechanism for gaze-holding deficits. ABSTRACT: Gaze-evoked nystagmus (GEN) is an ocular-motor finding commonly observed in cerebellar disease, characterized by increased centripetal eye-drift with centrifugal correcting saccades at eccentric gaze. With cerebellar degeneration being a rare and clinically heterogeneous disease, data from patients are limited. We hypothesized that a transient inhibition of cerebellar function by defined amounts of alcohol may provide a suitable model to study gaze-holding deficits in cerebellar disease. We recorded gaze-holding at varying horizontal eye positions in 15 healthy participants before and 30 min after alcohol intake required to reach 0.6‰ blood alcohol content (BAC). Changes in ocular-motor behaviour were quantified measuring eye-drift velocity as a continuous function of gaze eccentricity over a large range (±40 deg) of horizontal gaze angles and characterized using a two-parameter tangent model. The effect of alcohol on gaze stability was assessed analysing: (1) overall effects on the gaze-holding system, (2) specific effects on each eye and (3) differences between gaze angles in the temporal and nasal hemifields. For all subjects, alcohol consumption induced gaze instability, causing a two-fold increase [2.21 (0.55), median (median absolute deviation); P = 0.002] of eye-drift velocity at all eccentricities. Results were confirmed analysing each eye and hemifield independently. The alcohol-induced transient global deficit in gaze-holding matched the pattern previously described in patients with late-onset cerebellar degeneration. Controlled intake of alcohol seems a suitable disease model to study cerebellar GEN. With alcohol resulting in global cerebellar hypofunction, we hypothesize that patients matching the gaze-holding behaviour observed here suffered from diffuse deficits in the gaze-holding system as well.

Motion Illusion-Evidence towards Human Vestibulo-Thalamic Projections.

Contemporary studies speculated that cerebellar network responsible for motion perception projects to the cerebral cortex via vestibulo-thalamus. Here, we sought for the physiological properties of vestibulo-thalamic pathway responsible for the motion perception. Healthy subjects and the patient with focal vestibulo-thalamic lacunar stroke spun a hand-held rheostat to approximate the value of perceived angular velocity during whole-body passive earth-vertical axis rotations in yaw plane. Vestibulo-ocular reflex was simultaneously measured with high-resolution search coils (paradigm 1). In primates, the vestibulo-thalamic projections remain medial and then dorsomedial to the subthalamus. Therefore, the paradigm 2 assessed the effects of high-frequency subthalamic nucleus electrical stimulation through the medial and caudal deep brain stimulation electrode in five subjects with Parkinson's disease. Paradigm 1 discovered directional mismatch of perceived rotation in a patient with vestibulo-thalamic lacune. There was no such mismatch in vestibulo-ocular reflex. Healthy subjects did not have such directional discrepancy of perceived motion. The results confirmed that perceived angular motion is relayed through the thalamus. Stimulation through medial and caudal-most electrode of subthalamic deep brain stimulator in paradigm 2 resulted in perception of rotational motion in the horizontal semicircular canal plane. One patient perceived riding a swing, a complex motion, possibly the combination of vertical canal and otolith-derived signals representing pitch and fore-aft motion, respectively. The results examined physiological properties of the vestibulo-thalamic pathway that passes in proximity to the subthalamic nucleus conducting pure semicircular canal signals and convergent signals from the semicircular canals and the otoliths.

Cold Thermal Irrigation Decreases the Ipsilateral Gain of the Vestibulo-Ocular Reflex.

OBJECTIVES: During head rotations, neuronal firing rates increase in ipsilateral and decrease in contralateral vestibular afferents. At low accelerations, this "push-pull mechanism" is linear. At high accelerations, however, the change of firing rates is nonlinear in that the ipsilateral increase of firing rate is larger than the contralateral decrease. This mechanism of stronger ipsilateral excitation than contralateral inhibition during high-acceleration head rotation, known as Ewald's second law, is implemented within the nonlinear pathways. The authors asked whether caloric stimulation could provide an acceleration signal high enough to influence the contribution of the nonlinear pathway to the rotational vestibulo-ocular reflex gain (rVOR gain) during head impulses. DESIGN: Caloric warm (44°C) and cold (24, 27, and 30°C) water irrigations of the left ear were performed in 7 healthy human subjects with the lateral semicircular canals oriented approximately earth-vertical (head inclined 30° from supine) and earth-horizontal (head inclined 30° from upright). RESULTS: With the lateral semicircular canal oriented earth-vertical, the strongest cold caloric stimulus (24°C) significantly decreased the rVOR gain during ipsilateral head impulses, while all other irrigations, irrespective of head position, had no significant effect on rVOR gains during head impulses to either side. CONCLUSIONS: Strong caloric irrigation, which can only be achieved with cold water, reduces the rVOR gain during ipsilateral head impulses and thus demonstrates Ewald's second law in healthy subjects. This unilateral gain reduction suggests that cold-water caloric irritation shifts the set point of the nonlinear relation between head acceleration and the vestibular firing rate toward a less acceleration-sensitive zone.

What domains of clinical function should be assessed after sport-related concussion? A systematic review.

BACKGROUND: Sport-related concussion (SRC) is a clinical diagnosis made after a sport-related head trauma. Inconsistency exists regarding appropriate methods for assessing SRC, which focus largely on symptom-scores, neurocognitive functioning and postural stability. DESIGN: Systematic literature review. DATA SOURCES: MEDLINE, EMBASE, PsycINFO, Cochrane-DSR, Cochrane CRCT, CINAHL, SPORTDiscus (accessed July 9, 2016). ELIGIBILITY CRITERIA FOR SELECTING STUDIES: Original (prospective) studies reporting on postinjury assessment in a clinical setting and evaluation of diagnostic tools within 2 weeks after an SRC. RESULTS: Forty-six studies covering 3284 athletes were included out of 2170 articles. Only the prospective studies were considered for final analysis (n=33; 2416 athletes). Concussion diagnosis was typically made on the sideline by an (certified) athletic trainer (55.0%), mainly on the basis of results from a symptom-based questionnaire. Clinical domains affected included cognitive, vestibular and headache/migraine. Headache, fatigue, difficulty concentrating and dizziness were the symptoms most frequently reported. Neurocognitive testing was used in 30/33 studies (90.9%), whereas balance was assessed in 9/33 studies (27.3%). SUMMARY/CONCLUSIONS: The overall quality of the studies was considered low. The absence of an objective, gold standard criterion makes the accurate diagnosis of SRC challenging. Current approaches tend to emphasise cognition, symptom assessment and postural stability with less of a focus on other domains of functioning. We propose that the clinical assessment of SRC should be symptom based and interdisciplinary. Whenever possible, the SRC assessment should incorporate neurological, vestibular, ocular motor, visual, neurocognitive, psychological and cervical aspects.

Dissociating vestibular and somatosensory contributions to spatial orientation.

Inferring object orientation in the surroundings heavily depends on our internal sense of direction of gravity. Previous research showed that this sense is based on the integration of multiple information sources, including visual, vestibular (otolithic), and somatosensory signals. The individual noise characteristics and contributions of these sensors can be studied using spatial orientation tasks, such as the subjective visual vertical (SVV) task. A recent study reported that patients with complete bilateral vestibular loss perform similar as healthy controls on these tasks, from which it was conjectured that the noise levels of both otoliths and body somatosensors are roll-tilt dependent. Here, we tested this hypothesis in 10 healthy human subjects by roll tilting the head relative to the body to dissociate tilt-angle dependencies of otolith and somatosensory noise. Using a psychometric approach, we measured the perceived orientation, and its variability, of a briefly flashed line relative to the gravitational vertical (SVV). Measurements were taken at multiple body-in-space orientations (-90 to 90°, steps of 30°) and head-on-body roll tilts (30° left ear down, aligned, 30° right ear down). Results showed that verticality perception is processed in a head-in-space reference frame, with a systematic SVV error that increased with larger head-in-space orientations. Variability patterns indicated a larger contribution of the otolith organs around upright and a more substantial contribution of the body somatosensors at larger body-in-space roll tilts. Simulations show that these findings are consistent with a statistical model that involves tilt-dependent noise levels of both otolith and somatosensory signals, confirming dynamic shifts in the weights of sensory inputs with tilt angle.

The cerebellar nodulus: perceptual and ocular processing of graviceptive input.

Current concepts postulate a decisive role of the cerebellar nodulus in the processing of otolith input. We hypothesized that nodular lesions abolish otolith-perceptual integration, predicting alignment of perceived direction of earth vertical with the z-axis of the head and not with gravity. In an 80-year-old patient with acute heminodular infarction, the subjective visual vertical deviated contralesionally by -21.1° when the patient was upright. After subtracting this offset, perceived vertical closely matched the patient's head orientation when the patient was roll-tilted. Otolith-ocular reflexes remained normal. This is the first report on abolished earth verticality perception in heminodular stroke and underlines the importance of the nodulus in spatial orientation.

Multiple timescales in the adaptation of the rotational VOR.

Goal-directed movements, such as pointing and saccades, have been shown to share similar neural architectures, in spite of the different neuromuscular systems producing them. Such structure involve an inverse model of the actuator being controlled, which produces the commands innervating the muscles, and a forward model of the actuator, which predicts the sensory consequences of such commands and allows online movement corrections. Recent studies have shown that goal-directed movements also share similar motor-learning and motor-memory mechanisms, which are based on multiple timescales. The hypothesis that also the rotational vestibulo-ocular reflex (rVOR) may be based on a similar architecture has been presented recently. We hypothesize that multiple timescales are the brain's solution to the plasticity-stability dilemma, allowing adaptation to temporary and sudden changes while keeping stable motor-control abilities. If that were the case, then we would also expect the adaptation of reflex movements to follow the same principles. Thus we studied rVOR gain adaptation in eight healthy human subjects using a custom paradigm aimed at investigating the existence of spontaneous recovery, which we considered as the hallmark of multiple timescales in motor learning. Our experimental results show that spontaneous recovery occurred in six of eight subjects. Thus we developed a mathematical model of rVOR adaptation based on two hidden-states processes, which adapts the cerebellar-forward model of the ocular motor plant, and show that it accurately simulates our experimental data on rVOR gain adaptation, whereas a single timescale learning process fails to do so.

Binding body and self in visuo-vestibular conflicts.

Maintenance of the bodily self relies on the accurate integration of multisensory inputs in which visuo-vestibular cue integration is thought to play an essential role. Here, we tested in healthy volunteers how conflicting visuo-vestibular bodily input might impact on body self-coherence in a full body illusion set-up. Natural passive vestibular stimulation was provided on a motion platform, while visual input was manipulated using virtual reality equipment. Explicit (questionnaire) and implicit (skin temperature) measures were employed to assess illusory self-identification with either a mannequin or a control object. Questionnaire results pointed to a relatively small illusion, but hand skin temperature, plausibly an index of illusory body ownership, showed the predicted drop specifically in the condition when participants saw the mannequin moving in congruence with them. We argue that this implicit measure was accessible to visuo-vestibular modulation of the sense of self, possibly mediated by shared neural processes in the insula involved in vestibular and interoceptive signalling, thermoregulation and multisensory integration.

Discriminant validity and test re-test reproducibility of a gait assessment in patients with vestibular dysfunction.

BACKGROUND: Gait function may be impaired in patients with vestibular disorders, making gait assessment in the clinical setting relevant for this patient population. The purpose of this study was to evaluate the discriminant validity of a gait assessment protocol between patients with vestibular disorders and healthy participants. Furthermore, test re-test reproducibility and the measurement error of gait performance measures in patients with vestibular lesions was performed under different walking conditions. METHODS: Gait parameters of thirty-five patients with vestibular disorders and twenty-seven healthy controls were assessed twice with the GAITRite® system. Discriminant validity, reproducibility (intra class correlation [ICC]) and the measurement error (standard error of measurement [SEM], smallest detectable change [SDC]) were determined for gait speed, cadence and step length. Bland-Altman plots were made to assess systematic bias between tests. RESULTS: A significant effect of grouping on gait performance indicates discriminant validity of gait assessment. All tests revealed differences between patients and healthy controls (p < 0.01). The ICCs for test re-test reproducibility were excellent (0.70-0.96) and measurement error showed acceptable SDC values for gait parameters derived from three walking conditions (9-19 %). Bland-Altman plots indicated no systematic bias. CONCLUSIONS: Good validity and reproducibility of GAITRite® system measurements suggest that this system could facilitate the study of gait in patients with vestibular disorders in clinical settings. The SDC values for gait are generally small enough to detect changes after a rehabilitation program for patients with vestibular disorders.