Acute Unilateral Vestibular Loss Research Articles

Weak nystagmus in the dark persists for months after acute unilateral vestibular loss.

Weak nystagmus with fixation removed can be seen both in normal individuals and in recovery from a unilateral vestibular insult, thus its clinical significance is unclear in patients with dizziness. We thus sought to compare features of nystagmus at various stages following unilateral vestibular loss (UVL). We enrolled thirty consecutive patients after acute UVL with impaired vestibulo-ocular reflex (VOR) gain. The patients were allocated into three groups according to time from onset of symptoms: acute (1-7 days), subacute (8-30 days), and chronic (>30 days). Patients underwent video-oculography (with and without fixation) and video head impulse testing (vHIT) to determine VOR gain. We examined the relationships amongst SPV, VOR gain, and time from symptom onset across groups. There were 11, 10, and 9 patients in the acute, subacute, and chronic stages of UVL, respectively. With visual fixation, only 8 patients (26.7%) demonstrated nystagmus, all from the acute group. With fixation removed, 26 patients (86.7%) exhibited spontaneous nystagmus, including 90.9%, 90%, and 77.8% of the patients from the acute, subacute, and chronic groups, respectively. Horizontal nystagmus was paralytic (i.e., fast phase contralesional) in 25 (96.7%) cases. Horizontal SPV was negatively correlated with logarithm of time from onset to examination (r = -0.48, p = 0.007) and weakly negatively correlated with ipsilesional VOR gain (r = -0.325, p = 0.08). In the subacute or chronic stages of UVL, paralytic nystagmus with fixation removed persisted at a low intensity. Therefore, weak nystagmus in the dark may have diagnostic value in chronic dizziness.

Delay and Acceleration Threshold of Movement Perception in Patients Suffering from Vertigo or Dizziness.

The objective was to evaluate the delay and the acceleration threshold (AT) of movement perception in a population of patients suffering from dizziness and analyze the factors influencing these parameters. This prospective study included 256 adult subjects: 16 control and 240 patients (5 acute unilateral vestibular loss, 13 compensated unilateral loss, 32 Meniere diseases, 48 persistent postural-perceptual dizziness (PPPD), 95 benign paroxysmal positional vertigo (BPPV), 10 central cases, 19 bilateral vestibulopathy, 14 vestibular migraine, and 4 age-related dizziness). Patients were evaluated for the sound-movement synchronicity perception (maximum delay between the bed oscillation peak and a beep perceived as synchronous, PST) and AT during a pendular movement on a swinging bed. We observed higher PST in women and in senior patients regardless of etiology. AT was higher in senior patients. AT was not influenced by etiology except in patients with bilateral vestibulopathy who had higher thresholds. AT was related to unipodal stance performance, past history of fall, and stop-walking-when-talking test. Delay and acceleration thresholds appear to be coherent with clinical findings and open insights on the exploration of symptoms that cannot be explained by routine otoneurological tests.

Acute unilateral vestibular neuritis contributes to alterations in vestibular function modulating circumvention around obstacles: A pilot study suggesting a role for vestibular signals in the spatial perception of orientation during circumvention.

Walking among crowds avoiding colliding with people is described by patients with vestibular disorders as vertigo-inducing. Accurate body motion while circumventing an impeding obstacle in the gait pathway is dependent on an integration of multimodal sensory cues. However, a direct role of vestibular signals in spatial perception of distance or orientation during obstacle circumvention has not been investigated to date. We examined trunk yaw motion during circumvention in patients with acute unilateral vestibular loss (aUVL) and compared their results with age-matched healthy controls (HCs). Subjects performed five gait tasks with eyes open two times: walk 6 m in total, but after 3 m, circumvent to the left or right, as closely as possible, a cylindrical obstacle representing a person, and then veer back to the original path; walk 6 m, but after left and right circumvention at 3 m, veer, respectively, to the right, and left 45 deg; and walk 6 m without circumvention. Trunk yaw angular velocities (YAVs) were measured using a gyroscope system. Yaw angular velocity peak amplitudes approaching to, and departing from, the circumvented object were always greater for patients with aUVL compared to HCs, regardless of whether passing was to the aUVLs' deficit or normal side. The departing peak YAV was always greater, circa 52 and 87%, than the approaching YAV for HCs when going straight and veering 45 deg (p ≤ 0.0006), respectively. For patients with aUVL, departing velocities were marginally greater (12%) than approaching YAVs when going straight (p < 0.05) and were only 40% greater when veering 45 deg (p = 0.05). The differences in departing YAVs resulted in significantly lower trajectory-end yaw angles for veering trials to the deficit side in patients with aUVL (34 vs. 43 degs in HCs). The results demonstrate the effects of vestibular loss on yaw velocity control during the three phases of circumvention. First, approaching an obstacle, a greater YAV is found in patients with aUVL. Second, the departing YAV is found to be less than in HCs with respect to the approaching velocity, resulting in larger deficit side passing yaw angles. Third, patients with UVLs show yaw errors returning to the desired trajectory. These results could provide a basis for rehabilitation protocols helping to avoid collisions while walking in crowded spaces.

Head-shaking-induced nystagmus reflects dynamic vestibular compensation: A 2-year follow-up study.

PurposeWe aimed to assess the ability of a head-shaking test (HST) to reflect vestibular compensation in patients after unilateral peripheral vestibular loss and to provide missing evidence and new insights into the features of head-shaking-induced nystagmus (HSN) over a 2-year follow-up.BackgroundHSN may occur after a prolonged sinusoidal oscillation of the head. HSN is frequently observed in subjects with vestibular function asymmetry; it usually beats toward the functionally intact or “stronger” ear and can be followed by a reversal of its direction.Study designA prospective observational case-control study.SettingsA tertiary academic referral center.MethodsA total of 38 patients after acute unilateral vestibular loss (22 patients with vestibular neuronitis and 16 patients after vestibular neurectomy) and 28 healthy controls were followed for four consecutive visits over a 2-year period. A complex vestibular assessment was performed on all participants, which included spontaneous nystagmus (SPN), the caloric test, the head-shaking test (HST), the video head impulse test (vHIT), the Timed Up and Go (TUG) test, and the Dizziness Handicap Inventory (DHI) questionnaire. We established the criteria for the poorly compensated group to assess different compensatory behaviors and results.ResultsWe found a time-related decrease in HSN (ρ < −0.84, p < 0.001) after unilateral vestibular loss. After 2 years of follow-up, HSN intensity in compensated patients reached the level of the control group; TUG and DHI also improved to normal; however, the caloric and vHIT tests remained abnormal throughout all follow-ups, indicating a chronic vestibular deficit. Besides, poorly compensated patients had a well-detectable HSN throughout all follow-ups; TUG remained abnormal, and DHI showed at least a moderate deficit.ConclusionsOur study showed that, after a unilateral peripheral vestibular loss, the intensity of HSN decreased exponentially over time, reflecting an improvement in dynamic ability and self-perceived deficit. HSN tended to decline to the value of the control group once vestibular compensation was satisfactory and sufficient for a patient's everyday life. In contrast, well-detectable HSN in poorly compensated patients with insufficient clinical recovery confirmed the potential of HSN to reflect and distinguish between adequate and insufficient dynamic compensation. HSN could serve as an objective indicator of stable unilateral vestibular loss.

Vascular vertigo and dizziness: Diagnostic criteria.

This paper presents diagnostic criteria for vascular vertigo and dizziness as formulated by the Committee for the Classification of Vestibular Disorders of the Bárány Society. The classification includes vertigo/dizziness due to stroke or transient ischemic attack as well as isolated labyrinthine infarction/hemorrhage, and vertebral artery compression syndrome. Vertigo and dizziness are among the most common symptoms of posterior circulation strokes. Vascular vertigo/dizziness may be acute and prolonged (≥24 hours) or transient (minutes to < 24 hours). Vascular vertigo/dizziness should be considered in patients who present with acute vestibular symptoms and additional central neurological symptoms and signs, including central HINTS signs (normal head-impulse test, direction-changing gaze-evoked nystagmus, or pronounced skew deviation), particularly in the presence of vascular risk factors. Isolated labyrinthine infarction does not have a confirmatory test, but should be considered in individuals at increased risk of stroke and can be presumed in cases of acute unilateral vestibular loss if accompanied or followed within 30 days by an ischemic stroke in the anterior inferior cerebellar artery territory. For diagnosis of vertebral artery compression syndrome, typical symptoms and signs in combination with imaging or sonographic documentation of vascular compromise are required.

Evaluation of the Video Ocular Counter-Roll (vOCR) as a New Clinical Test of Otolith Function in Peripheral Vestibulopathy

Video-oculography (VOG) goggles have been integrated into the assessment of semicircular canal function in patients with vestibular disorders. However, a similar bedside VOG method for testing otolith function is lacking. To evaluate the use of VOG-based measurement of ocular counter-roll (vOCR) as a clinical test of otolith function. A case-control study was conducted to compare vOCR measurement among patients at various stages of unilateral loss of vestibular function with healthy controls. The receiver operating characteristic curve method was used to determine the diagnostic accuracy of the vOCR test in detecting loss of otolith function. Participants were recruited at a tertiary center including the Johns Hopkins outpatient clinic and Johns Hopkins Hospital, Baltimore, Maryland. Participants included 56 individuals with acute (≤4 weeks after surgery), subacute (4 weeks-6 months after surgery), and chronic (>6 months after surgery) unilateral vestibular loss as well as healthy controls. A simple bedside maneuver with en bloc, 30° lateral tilt of the head and trunk was used for vOCR measurement. The study was conducted from February 2, 2017, to March 10, 2019. In each participant vOCR was measured during static tilts of the head and trunk en bloc. The vOCR measurements and diagnostic accuracy of vOCR in detecting patients with loss of vestibular function from healthy controls. Of the 56 participants, 28 (50.0%) were men; mean (SD) age was 53.5 (11.4) years. The mean (SD) time of acute unilateral vestibular loss was 9 (7) days (range, 2-17 days) in the acute group, 61 (39) days (range, 28-172 days) in the subacute group, and 985 (1066) days (range 185-4200 days) in the chronic group. The vOCR test showed reduction on the side of vestibular loss, and the deficit was greater in patients with acute and subacute vestibular loss than in patients with chronic loss and healthy controls (acute vs chronic: -1.81°; 95% CI, -3.45° to -0.17°; acute vs control: -3.18°; 95% CI, -4.83° to -1.54°; subacute vs chronic: -0.63°; 95% CI, -2.28° to 1.01°; subacute vs control: -2.01°; 95% CI, -3.65° to -0.36°; acute vs subacute: -1.17°; 95% CI, -2.88° to 0.52°; and chronic vs control: -1.37°; 95% CI, -2.96° to 0.21°). The asymmetry in vOCR between the side of vestibular loss and healthy side was significantly higher in patients with acute vs chronic loss (0.28; 95% CI, 0.06-0.51). Overall, the performance of the vOCR test in discriminating between patients with vestibular loss and healthy controls was 0.83 (area under the receiver operating characteristic curve). The best vOCR threshold to detect vestibular loss at the 30° tilt was 4.5°, with a sensitivity of 80% (95% CI, 0.62%-0.88%) and specificity of 82% (95% CI, 0.57%-1.00%). The findings of this case-control study suggest that the vOCR test can be performed with a simple bedside maneuver and may be used to detect or track loss of otolith function.

Cognitive functions in acute unilateral vestibular loss

Cognitive deficits mainly involving visuospatial functions have been defined in patients with bilateral and even unilateral vestibular loss (UVL). We compared the cognitive test results of 21 patients with acute UVL with age- and education-matched healthy controls. The diagnosis of UVL was based on the clinical findings, a normal magnetic resonance imaging with diffusion-weighted sequence and canal paresis on the affected side on caloric testing. Cognitive tests assessing visuospatial functions (Benton’s Judgment of Line Orientation test, Verbal and non-verbal Cancellation tests, Rey–Osterrieth Complex Figure test) and global mental status, verbal memory, learning, retention of information, and recalling (Mini Mental State Examination, Oktem Verbal Memory Process Test, Forward and Backward Digit span) were used in addition to Beck depression and Anxiety inventories. Abnormalities in verbal and non-verbal cancellation tests (p < 0.005), Benton’s Judgment of Line Orientation test (p = 0.042) and backward digit span (p = 0.029) was found. A very prominent difference regarding Beck depression (p = 0.012) and anxiety inventories (p < 0.001) was present. On multiple regression analysis, the abovementioned cognitive tests’ results lost their statistical significance (p > 0.05) when depression and anxiety scores were taken into consideration. The severity of canal paresis was found to be correlated with Benton’s Judgment of Line Orientation test (p = 0.008, r = − 0.5639) and Rey–Osterrieth Complex Figure test copying scores (p = 0.029, r = − 0.477). Comparison of all the results in right- and left-sided lesions did not reveal a significant difference (p > 0.05). Vestibular patients are prone to develop anxiety, and depression. Deficits in visuospatial functions, mental manipulation, psychomotor speed and short-term memory detected in our patients with acute UVL seem to be enhanced by accompanying anxiety and depression. The extent of vestibular dysfunction was correlated with the severity of deficits in visuospatial skills. Lesion side did not cause alterations in cognitive or emotional status.

Effect of the novel histamine H4 receptor antagonist SENS-111 on spontaneous nystagmus in a rat model of acute unilateral vestibular loss.

Histamine H4 receptors are expressed in the peripheral vestibular system, and their selective inhibition improves vertigo symptoms in rats with unilateral vestibular lesions. The effects of SENS-111, a selective oral H4 receptor antagonist with high affinity to both animal and human receptors, on vertigo symptoms was evaluated in a translational in vivo model of unilateral vestibular loss. Pharmacokinetics of SENS-111 in rats was determined to aid dose selection for efficacy testing. Vestibular lesions were induced in rats by unilateral transtympanic injection of kainic acid. The effect of SENS-111 (10 or 20mg·kg-1 ) on spontaneous nystagmus was evaluated compared with placebo vehicle using video-nystagmography, and the effective dose was compared with those of similar drugs used clinically, as single agents or combined with SENS-111. Doses were selected for plasma exposure were consistent with published phase 1 results from healthy volunteers. SENS-111 of 10mg·kg-1 gave a 21-22% reduction in nystagmus at 1hr post-administration, whereas a loss of efficacy was seen with 20mg·kg-1 . Compared with SENS-111, meclizine and methylprednisolone had minimal effects on nystagmus as single agents, and meclizine abolished the effect of SENS-111 when combined with SENS-111. All evaluated drugs were well tolerated. The exposure-efficacy relationship for improved spontaneous nystagmus seen with SENS-111 in this in vivo model is consistent with phase 1 clinical results and provides preclinical support for pharmacokinetic/pharmacodynamic modelling and selection of effective clinical drug concentrations. This article is part of a themed section on New Uses for 21st Century. To view the other articles in this section visit http://onlinelibrary.wiley.com/doi/10.1111/bph.v177.3/issuetoc.

Vestibular dysfunction in acute traumatic brain injury

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.

TP1-9 Vestibular dysfunction in acute traumatic brain injury

ObjectivesVestibular dysfunction following traumatic brain injury (TBI) is a major cause of morbidity and unemployment and has impact on the patient’s ability to rehabilitate. Chronically, up to a quarter of TBI cases have cryptogenic dizziness and imbalance, possibly due to chronic brain adaptation that masks the diagnosis. Establishing the spectrum of vestibular diagnoses in acute TBI – when they may be more obvious – may aid diagnosis in chronic TBI cases.DesignProspective audit of referrals to specialist neuro-otology team.SubjectsConsecutive Major Trauma Ward TBI in-patients admitted between June 2014 and May 2015.MethodsAll cases were screened by the therapists for vestibular symptoms and/or signs and referred for specialist neuro-otology review.ResultsOf 111 patients screened, 96 had features of vestibular dysfunction. Of 96 cases, SYMPTOMS (i.e. subjective report) included: – imbalance (58.3%) – headache (50%) -dizziness (40%) Of 96 cases, SIGNS (i.e. examination) included: – gait ataxia (75.5%) – broken smooth pursuit (61.2%) – positive Hallpike (51%) – positive head impulse test (18%). The data indicate that BPPV affects 49% and headache with migraine-like features affect 40.8%. Acute peripheral unilateral vestibular loss affects 18% TBI cases.ConclusionsVestibular dysfunction in TBI is common, typically involving peripheral and central structures, often in the same case, and requires specialist neuro-otological management.

Vestibular paroxysmia in vestibular neuritis: A case report.

The term vestibular paroxysmia (VP) was introduced for the first time by Brandt and Dieterich in 1994. In 2016, the Barany Society formulated the International Classification of VP, focusing in particular on the number and duration of attacks, on the differential diagnosis and on the therapy. Ephaptic discharges in the proximal part of the eighth cranial nerve, which is covered by oligodendrocytes, are assumed to be the neural basis of VP. We report the first case in literature of an onset of symptoms and signs typical of VP in a young man following acute unilateral vestibular loss not combined with auditory symptoms. Indeed, the pathogenic mechanism affected only the vestibular nerve as confirmed by the presence of a stereotyped nystagmus pattern. The magnetic resonance imaging didn’t reveal any specific cause therefore we suggest the possible role of a neuritis triggering an ephaptic discharge as the neural mechanism of VP.

Reader response: Clinical Reasoning: Labyrinthine hemorrhage: An unusual etiology for peripheral vertigo.

I read with interest the Resident & Fellow Clinical Reasoning by Drs. Parikh and Frank.1 In differentiating peripheral (e.g., acute unilateral vestibular loss) from central causes of vertigo (e.g., acute posterior circulation stroke), the clinical head impulse test remains the most important clinical test. However, as a clinical test, it is subjective and, depending on examiner experience, its interpretation is variable. With the widespread availability of the video head impulse test, which provides quantitative information on the vestibulo-ocular reflex and catch-up saccade, the head impulse sign can be rapidly confirmed at point of care. This should now be considered part of the initial workup.

The Effect of Peripheral Vestibular Recovery on Improvements in Vestibulo-ocular Reflexes and Balance Control After Acute Unilateral Peripheral Vestibular Loss.

Patients with an acute unilateral peripheral vestibular deficit (aUPVD), presumed to be caused by vestibular neuritis, show asymmetrical vestibular ocular reflexes (VORs) that improve over time. Questions arise regarding how much of the VOR improvement is due to peripheral recovery or central compensation, and whether differences in peripheral recovery influence balance control outcomes. Thirty patients were examined at aUPVD onset and 3, 6, and 13 weeks later with four different VOR tests: caloric tests; rotating (ROT) chair tests performed in yaw with angular accelerations of 5 and 20 degrees/s; and video head impulse tests (vHIT) in the yaw plane. ROT and vHIT responses and balance control of 11 patients who had a caloric canal paresis (CP) more than 90% at aUPVD onset and no CP recovery (no-CPR) at 13 weeks in caloric tests were compared with those of 19 patients with CP recovery (CPR) to less than 30%, on average. Balance control was measured with a gyroscope system (SwayStar) recording trunk sway during stance and gait tasks. ROT and vHIT asymmetries of no-CPR and CPR patients reduced over time. The reduction was less at 13 weeks (36.2% vs. 83.5% on average) for the no-CPR patients. The no-CPR group asymmetries at 13 weeks were greater than those of CPR patients who had normal asymmetries. The greater asymmetries were caused by weaker deficit side responses which remained deficient in no-CPR patients at 13 weeks. Contra-deficit side vHIT and ROT responses remained normal. For all balance tests, sway was slightly greater for no-CPR compared with CPR patients at aUPVD onset and 3 weeks later. At 13 weeks, only sway during walking eyes closed was greater for the no-CPR group. A combination of 5 degrees/s ROT and balance tests could predict at onset (90% accuracy) which patients would have no-CPR at 13 weeks. These results indicate that for ROT and vHIT tests, central compensation is observed in CPR and no-CPR patients. It acts primarily by increasing deficit side responses. Central compensation provides approximately 60% of the VOR improvement for CPR patients. The rest of the improvement is due to peripheral recovery which appears necessary to reduce VOR asymmetry to normal at 13 weeks on average. Balance control improvement is more rapid than that of the VOR and marginally affected by the lack of peripheral recovery. Both VOR and balance control measures at onset provide indicators of future peripheral recovery. For these reasons VOR and balance control needs to be tested at aUPVD onset and at 13 weeks.

Saccadic entropy of head impulses in acute unilateral vestibular loss.

To evaluate the complexity of vestibular-ocular reflex (VOR) in patients with acute unilateral vestibular loss (AUVL) via entropy analysis of head impulses. Horizontal head impulse test (HIT) with high-velocity alternating directions was used to evaluate 12 participants with AUVL and 16 healthy volunteers. Wireless electro-oculography and electronic gyrometry were used to acquire eye positional signals and head velocity signals. The eye velocity signals were then obtained through differentiation, band-pass filtering. The approximate entropy of eye velocity to head velocity (RApEn) was used to evaluate chaos property. VOR gain, gain asymmetry ratio, and RApEn asymmetry ratio were also used to compare the groups. For the lesion-side HIT of the patient group, the mean VOR gain was significantly lower and the mean RApEn was significantly greater compared with both nonlesion-side HIT and healthy controls (p < 0.01, one-way analysis of variance). Both the RApEn asymmetry ratio and gain asymmetry ratio of the AUVL group were significantly greater compared with those of the control group (p < 0.05, independent sample t test). Entropy and gain analysis of HIT using wireless electro-oculography system could be used to detect the VOR dysfunctions of AUVL and may become effective methods for evaluating vestibular disorders.

Posture, balance control, movement: Involvement in vestibular rehabilitation

The ability to move upright maintaining balance is a pre-requisite for most human behavior and independence. To maintain balance and to orientate, we use sensory information from vestibular, visual and somatosensory receptors (see above). The information is coordinated and integrated in the central nervous system (CNS) and modifies the motor control efferent command, which regulates the muscles that keep us upright. The motor command leads to correcting movements, which lead to new information from the sensory systems. In this aspect, the vestibular senses have a special and non-complementary role. Thus, changes in afferent sensory information arising from one or more receptor systems may affect the motor control performance by evoking and modifying the motor output elicited at all levels from the spinal medulla to the cerebral cortex. However, it has become evident that the different sensory systems, the neural control as well as the cognitive attitude all interact in achieving and expressing what human postural control is. All these players operate in concert with overlap, redundancy and adaptive capacity. Therefore, a lesion of one function will most often have an effect on several other components. Thus, a more advanced research methodology is necessary to reach useful understanding and interventions. Therefore, we need a system-biology or system-medicine approach both to analyse and to treat loss of balance and especially when it depends on vestibular loss. Vestibular rehabilitation’ is a physiotherapeutic approach to help regain balance after vestibular lesions with maladaptation. In patients with Meniere's disease not responding to conservative treatment, vestibular nerve section or transtympanic gentamicin is the last option to achieve vestibular ablation. However, this causes the subjects to suffer from acute unilateral vestibular loss. In patients with vestibular schwannomas and with remaining vestibular function, surgery will cause a combined effect of an acute unilateral vestibular lesion and manipulation of the cerebellum with possibly compromised compensatory mechanisms. These patients form a model of vestibular rehabilitation. We therefore train patients with rehabilitation even before the treatment and lesion. Our experience is that we reduce the time for recovery. We have seen occasional patients that have gone through a gentamicin treatment without any sick leave! In schwannoma patients, we see stunning postoperative recovery and may postulate that we will avoid some cases of lifelong incapacity due to combined cerebello-vestibular lesions. Furthermore, both frequency and time dispersing in training seem to be of major importance. In postural training, it seems that a 3 times a day schedule is not surpassed by more frequent training, which is of importance for planning the rehabilitation.

EPV 20. Vascular encephalopathy is a major risk factor for poor vestibular compensation

Background and aim Acute unilateral vestibular loss leads to vertigo sensation, nystagmus and postural imbalance. As a rule, a behavioral recovery of the signs and symptoms follows over days to months due to central vestibular compensation (VC). The present study aimed to investigate the influence of cerebral vascular lesions on VC by following a large cohort of patients after vestibular neuritis. Methods 235 patients (mean age: 54.2 ± 15.2, 53.4% men) with the clinical picture or history of an acute unilateral vestibulopathy, who were seen at the Department of Neurology and the German Center for Vertigo and Balance Disorders over the last 10 years, were included in the study. All patients underwent a detailed neuro-ophthalmological and neurological examination, including measures of the subjective visual vertical (SVV), ocular torsion (OT), head impulse test (HIT), provocation nystagmus (PN), visual acuity and postural control and were followed along their course of VC (mean number of visits 3.5 ± 1.2, mean time of follow-up 217 ± 625 days). In all patients a cranial MRI was available at onset of vestibular failure. The MRI was assessed by a two senior neuro-radiologist. Extent of supra- and infratentorial vascular white matter lesions was classified by the ARWMC scale (0–3 points). Strategic lesions in the vestibular network (medulla, vestibulocerebellum, thalamus) were registered separately. Patients were indicated as poorly compensated, if deviation of SVV (>2.5°), PN and postural asymmetry persisted for longer than 3 months after vestibular failure. Results 13.3% of patients were classified as poorly compensated at 3 months (PN: 55%, SVV deviation: 36%, postural asymmetry: 22%), 12.8% at 6 months and 10.6% at 12 months after acute unilateral vestibulopathy. These patients had significantly higher ARWMC scales as compared to patients with regular VC ( p Conclusions About 10% of patients have an impeded course of VC after acute unilateral vestibulopathy. Supratentorial vascular encephalopathy is a major risk factor for poor VC and should be considered to guide the intensity of physical treatment following acute unilateral vestibulopathy.

Vestibular compensation: the neuro-otologist's best friend.

Why vestibular compensation (VC) after an acute unilateral vestibular loss is the neuro-otologist’s best friend is the question at the heart of this paper. The different plasticity mechanisms underlying VC are first reviewed, and the authors present thereafter the dual concept of vestibulo-centric versus distributed learning processes to explain the compensation of deficits resulting from the static versus dynamic vestibular imbalance. The main challenges for the plastic events occurring in the vestibular nuclei (VN) during a post-lesion critical period are neural protection, structural reorganization and rebalance of VN activity on both sides. Data from animal models show that modulation of the ipsilesional VN activity by the contralateral drive substitutes for the normal push–pull mechanism. On the other hand, sensory and behavioural substitutions are the main mechanisms implicated in the recovery of the dynamic functions. These newly elaborated sensorimotor reorganizations are vicarious idiosyncratic strategies implicating the VN and multisensory brain regions. Imaging studies in unilateral vestibular loss patients show the implication of a large neuronal network (VN, commissural pathways, vestibulo-cerebellum, thalamus, temporoparietal cortex, hippocampus, somatosensory and visual cortical areas). Changes in gray matter volume in these multisensory brain regions are structural changes supporting the sensory substitution mechanisms of VC. Finally, the authors summarize the two ways to improve VC in humans (neuropharmacology and vestibular rehabilitation therapy), and they conclude that VC would follow a “top-down” strategy in patients with acute vestibular lesions. Future challenges to understand VC are proposed.

The Effect of Age on Improvements in Vestibulo-Ocular Reflexes and Balance Control after Acute Unilateral Peripheral Vestibular Loss.

An acute unilateral peripheral vestibular loss (aUVL) initially causes severe gaze and balance control problems. However, vestibulo-ocular reflexes (VOR) and balance control are nearly normal 3 months later as a result of peripheral recovery and/or central compensation. As pre-existing vestibular sensory loss is assumed to be greater in the healthy elderly, this study investigated whether improvements in VOR and balance function over time after aUVL are different for the elderly than for the young. Thirty aUVL patients divided into three age-groups were studied (8 age range 23-35, 10 with range 43-58, and 12 with range 60-74 years). To measure VOR function eye movements were recorded during caloric irrigation, rotating chair (ROT), and head impulse tests. Balance control during stance and gait was recorded as lower trunk angular velocity in the pitch and roll planes. Measurements were taken at deficit onset, and 3, 6, and 13 weeks later. There was one difference in VOR improvements over time between the age-groups: Low acceleration ROT responses were less at onset in the elderly group. Deficit side VOR responses and asymmetries in each group improved to within ranges of healthy controls at 13 weeks. Trunk sway of the elderly was greater for stance and gait at onset when compared to healthy age-matched controls and the young and greater than that of the young and controls during gait tasks at 13 weeks. The sway of the young was not different from controls at either time point. Balance control for the elderly improved slower than for the young. These results indicate that VOR improvement after an aUVL does not differ with age, except for low accelerations. Recovery rates are different between age-groups for balance control tests. Balance control in the elderly is more abnormal at aUVL onset for stance and gait tasks with the gait abnormalities remaining after 13 weeks. Thus, we conclude that balance control in the elderly is more affected by the UVL than for the young, and the young overcome balance deficits more rapidly. These differences with age should be taken into account when planning rehabilitation.

Comparative analysis of pharmacological treatments with N-acetyl-dl-leucine (Tanganil) and its two isomers (N-acetyl-L-leucine and N-acetyl-D-leucine) on vestibular compensation: Behavioral investigation in the cat

Head roll tilt, postural imbalance and spontaneous nystagmus are the main static vestibular deficits observed after an acute unilateral vestibular loss (UVL). In the UVL cat model, these deficits are fully compensated over 6 weeks as the result of central vestibular compensation. N-Acetyl-dl-leucine is a drug prescribed in clinical practice for the symptomatic treatment of acute UVL patients. The present study investigated the effects of N-acetyl-dl-leucine on the behavioral recovery after unilateral vestibular neurectomy (UVN) in the cat, and compared the effects of each of its two isomers N-acetyl-L-leucine and N-acetyl-D-leucine. Efficacy of these three drug treatments has been evaluated with respect to a placebo group (UVN+saline water) on the global sensorimotor activity (observation grids), the posture control (support surface measurement), the locomotor balance (maximum performance at the rotating beam test), and the spontaneous vestibular nystagmus (recorded in the light). Whatever the parameters tested, the behavioral recovery was strongly and significantly accelerated under pharmacological treatments with N-acetyl-dl-leucine and N-acetyl-L-leucine. In contrast, the N-acetyl-D-leucine isomer had no effect at all on the behavioral recovery, and animals of this group showed the same recovery profile as those receiving a placebo. It is concluded that the N-acetyl-L-leucine isomer is the active part of the racemate component since it induces a significant acceleration of the vestibular compensation process similar (and even better) to that observed under treatment with the racemate component only.

Compensatory saccades benefit from prediction during head impulse testing in early recovery from vestibular deafferentation.

The head impulse test (HIT) can identify a deficient vestibulo-ocular reflex (VOR) by the compensatory saccade (CS) generated once the head stops moving. The inward HIT is considered safer than the outward HIT, yet might have an oculomotor advantage given that the subject would presumably know the direction of head rotation. Here, we compare CS latencies following inward (presumed predictable) and outward (more unpredictable) HITs after acute unilateral vestibular nerve deafferentation. Seven patients received inward and outward HITs delivered at six consecutive postoperative days (POD) and again at POD 30. All head impulses were recorded by portable video-oculography. CS included those occurring during (covert) or after (overt) head rotation. Inward HITs included mean CS latencies (183.48ms±4.47 SE) that were consistently shorter than those generated during outward HITs in the first 6 POD (p=0.0033). Inward HITs induced more covert saccades compared to outward HITs, acutely. However, by POD 30 there were no longer any differences in latencies or proportions of CS and direction of head rotation. Patients with acute unilateral vestibular loss likely use predictive cues of head direction to elicit early CS to keep the image centered on the fovea. In acute vestibular hypofunction, inwardly applied HITs may risk a preponderance of covert saccades, yet this difference largely disappears within 30days. Advantages of inwardly applied HITs are discussed and must be balanced against the risk of a false-negative HIT interpretation.